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Hlozhyk, I. Z. "Biochemical Markers of Free Radical Oxidation and Lipid Exchange in Rats with Obesity, Iodine Defficiency and Obesity in Combination with Iodine Defficiency". Ukraïnsʹkij žurnal medicini, bìologìï ta sportu 6, n.º 4 (20 de setembro de 2021): 166–71. http://dx.doi.org/10.26693/jmbs06.04.166.
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The purpose of the study was the content of lipid and protein peroxidation products, lipid spectrum parameters and the level of aminotransferases in obese, iodine deficient and obese rats in combination with iodine deficiency. Materials and methods. The study was performed on 45 white nonlinear rats weighing 120-180 g, which were divided into three experimental groups: obese rats (1st experimental group, n = 15), iodine-deficient animals (2nd experimental group), obese animals in combined with iodine deficiency (3rd experimental group, n = 15). The control group consisted of 15 intact rats. The content of products of lipid peroxidation and oxidative modification of proteins was determined in the blood and liver tissue of rats. Blood lipid spectrum was assessed by serum levels of triacylglycerols, total cholesterol, high-density lipoproteins and low-density lipoproteins, followed by calculation of the atherogenic factor. The activity of aspartate aminotransferase and alanine aminotransferase was determined in the blood. Results and discussion. It was found that in the liver tissue of rats and blood of experimental groups the content of lipid hydroperoxides and active products that react with thiobarbituric acid increases, which indicates the activation of lipoperoxidation processes. A variety of changes in protein peroxidation in both blood serum and liver tissue of animals of experimental groups was revealed. Regarding the lipid spectrum, the most pronounced differences in the indicators in relation to the control were found in obese animals in combination with iodine deficiency. In this group of animals, cholesterol was increased by 65% in reference to control, triacylglycerol content increased by 52%, low-density lipoprotein exceeded control by 60%, and high-density lipoprotein decreased by 61% in reference to control. The highest activity of aspartate aminotransferase was found in the group of animals with iodine deficiency, and alanine aminotransferase – in the group of obese animals. Conclusion. In the blood and liver tissue of rats with obesity, iodine deficiency and obesity in combination with iodine deficiency increases the content of products of free radical oxidation. The content of cholesterol, triacylglycerols, low-density lipoproteins increases in the blood, the content of high-density lipoproteins decreases, the activity of aspartate aminotransferase and alanine aminotransferase increases. The most pronounced differences in the indicators in reference to the control were found in obese animals in combination with iodine deficiency
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Valiyaveettil, Manojkumar, Niladri Kar, Mohammad Z. Ashraf, Tatiana V. Byzova, Maria Febbraio e Eugene A. Podrez. "Oxidized high-density lipoprotein inhibits platelet activation and aggregation via scavenger receptor BI". Blood 111, n.º 4 (15 de fevereiro de 2008): 1962–71. http://dx.doi.org/10.1182/blood-2007-08-107813.
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Numerous studies have reported the presence of oxidatively modified high-density lipoprotein (OxHDL) within the intima of atheromatous plaques as well as in plasma; however, its role in the pathogenesis of thrombotic disease is not established. We now report that OxHDL, but not native HDL, is a potent inhibitor of platelet activation and aggregation induced by physiologic agonists. This antithrombotic effect was concentration and time dependent and positively correlated with the degree of lipoprotein oxidation. Oxidized lipoproteins are known ligands for scavenger receptors type B, CD36 and scavenger receptor B type I (SR-BI), both of which are expressed on platelets. Studies using murine CD36−/− or SR-BI−/− platelets demonstrated that the antithrombotic activity of OxHDL depends on platelet SR-BI but not CD36. Binding to SR-BI was required since preincubation of human and murine platelets with anti–SR-BI blocking antibody abrogated the inhibitory effect of OxHDL. Agonist-induced aggregation of platelets from endothelial nitric oxide synthase (eNOS)−/−, Akt-1−/−, and Akt-2−/− mice was inhibited by OxHDL to the same degree as platelets from wild-type (WT) mice, indicating that the OxHDL effect is mediated by a pathway different from the eNOS/Akt pathway. These novel findings suggest that contrary to the prothrombotic activity of oxidized low-density lipoprotein (OxLDL), HDL upon oxidation acquires antithrombotic activity that depends on platelet SR-BI.
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Rüfer, Corinna E., Sabine E. Kulling, Jutta Möseneder, Peter Winterhalter e Achim Bub. "Role of plasma lipoproteins in the transport of the soyabean isoflavones daidzein and daidzein-7-O-β-d-glucoside". British Journal of Nutrition 102, n.º 6 (31 de março de 2009): 793–96. http://dx.doi.org/10.1017/s0007114509297224.
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Isoflavone intake is associated with various properties beneficial to human health which are related to their antioxidant activity, for example, to their ability to increase LDL oxidation resistance. However, the distribution of isoflavones among plasma lipoproteins has not yet been elucidated in vivo. Therefore, the objective of the present study was to investigate the association between daidzein (DAI) and lipoproteins in human plasma upon administration of the aglycone and glucoside form. Five men aged 22–30 years participated in a randomised, double-blind study in cross-over design. After ingestion of DAI and daidzein-7-O-β-d-glucoside (DG) (1 mg DAI aglycone equivalents/kg body weight) blood samples were drawn before isoflavone administration as well as 1, 2, 3, 4·5, 6, 8, 10, 12, 24 and 48 h post-dose. Concentrations of DAI in the different lipoprotein fractions (chylomicrons, VLDL, LDL, HDL) and in the non-lipoprotein fraction were analysed using isotope dilution capillary GC/MS. The lipoprotein fraction profiles were similar for all subjects and resembled those obtained for plasma in our previously published study. The lipoprotein distribution based on the area under the concentration–time profiles from 0 h to infinity in the different fractions were irrespective of the administered form: non-lipoprotein fraction (53 %) > LDL (20 %) > HDL (14 %) > VLDL (9·5 %) > chylomicrons (2·5 %). Of DAI present in plasma, 47 % was associated to lipoproteins. Concentrations in the different lipoprotein fractions as well as in the non-lipoprotein fraction were always higher after the ingestion of DG than of DAI. Taken together, these results demonstrate an association between isoflavones and plasma lipoproteins in vivo.
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Lankin, Vadim Z., Alla K. Tikhaze e Valeria Ya Kosach. "Comparative Susceptibility to Oxidation of Different Classes of Blood Plasma Lipoproteins". Biochemistry (Moscow) 87, n.º 11 (novembro de 2022): 1335–41. http://dx.doi.org/10.1134/s0006297922110128.
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Gorshunskaya., M. Yu. "Paraoxonase activity and lipid peroxidation in female patients with type 2 diabetes mellitus and without coronary heart disease". Problems of Endocrinology 49, n.º 1 (15 de fevereiro de 2003): 17–20. http://dx.doi.org/10.14341/probl11394.
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The rate of lipid peroxidation and the parameters of antioxida- tive defense, including the activity of paraoxonase that is essential for the prevention of low-density lipoprotein oxidation, was studied in 229female patients with type 2 diabetes mellitus with and without coronary heart disease (CHD) under varying glycemic control. Carbohydrate and lipid metabolisms were explored by unified biochemical studies, blood insulin levels were measured by radioimmunological assay. The activity of paraoxonase associated with high-density lipoproteins of ester hydrolase was spectrophotometrically determined by using paraoxan as a substrate. Along with dyslipoproteinemia and insulin resistance, there was a drastically reduced paraoxonase activity that was associated with the high-density lipoproteins of the antioxidant enzyme and more pronounced in diabetics with CHD. A highly significant inverse correlation of the activity of the enzyme with the rate of lipid peroxidation and a less close relationship to basal glycemia have been verified, which substantiates the polygenic nature of decreased paraoxonase activity in diabetes mellitus.
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Pethő, Dávid, Tamás Gáll, Zoltán Hendrik, Annamária Nagy, Lívia Beke, Attila Péter Gergely, Gábor Méhes et al. "Ferryl Hemoglobin and Heme Induce Α1-Microglobulin in Hemorrhaged Atherosclerotic Lesions with Inhibitory Function against Hemoglobin and Lipid Oxidation". International Journal of Molecular Sciences 22, n.º 13 (22 de junho de 2021): 6668. http://dx.doi.org/10.3390/ijms22136668.
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Infiltration of red blood cells into atheromatous plaques and oxidation of hemoglobin (Hb) and lipoproteins are implicated in the pathogenesis of atherosclerosis. α1-microglobulin (A1M) is a radical-scavenging and heme-binding protein. In this work, we examined the origin and role of A1M in human atherosclerotic lesions. Using immunohistochemistry, we observed a significant A1M immunoreactivity in atheromas and hemorrhaged plaques of carotid arteries in smooth muscle cells (SMCs) and macrophages. The most prominent expression was detected in macrophages of organized hemorrhage. To reveal a possible inducer of A1M expression in ruptured lesions, we exposed aortic endothelial cells (ECs), SMCs and macrophages to heme, Oxy- and FerrylHb. Both heme and FerrylHb, but not OxyHb, upregulated A1M mRNA expression in all cell types. Importantly, only FerrylHb induced A1M protein secretion in aortic ECs, SMCs and macrophages. To assess the possible function of A1M in ruptured lesions, we analyzed Hb oxidation and heme-catalyzed lipid peroxidation in the presence of A1M. We showed that recombinant A1M markedly inhibited Hb oxidation and heme-driven oxidative modification of low-density lipoproteins as well plaque lipids derived from atheromas. These results demonstrate the presence of A1M in atherosclerotic plaques and suggest its induction by heme and FerrylHb in the resident cells.
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Shrestha, Rojeet, Zhen Chen, Yusuke Miura, Yusuke Yamamoto, Toshihiro Sakurai, Hitoshi Chiba e Shu-Ping Hui. "Identification of molecular species of phosphatidylcholine hydroperoxides in native and copper-oxidized triglyceride-rich lipoproteins in humans". Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 57, n.º 1 (8 de outubro de 2019): 95–98. http://dx.doi.org/10.1177/0004563219880932.
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Background Triglyceride-rich lipoproteins are considered to be independent predictors of atherosclerotic cardiovascular disease. The molecular basis of its atherogenicity is uncertain. Here, we aim to identify molecular species of phosphatidylcholine hydroperoxides (PCOOH) in triglyceride-rich lipoproteins. For comparison, copper-oxidized triglyceride-rich lipoproteins were investigated as well. Methods A fasting EDTA blood sample was collected from six healthy human volunteers to isolate two major triglyceride-rich lipoproteins fractions – very low-density lipoproteins (VLDL) and intermediate-density lipoproteins (IDL) using sequential ultracentrifugation. Triglyceride-rich lipoproteins and plasma samples were studied for PCOOH by liquid chromatography (LC) coupled with Orbitrap mass spectrometry. Results Twelve molecular species of PCOOH in triglyceride-rich lipoproteins and/or plasma were identified using the following criteria: (1) high-resolution mass spectrometry (MS) with mass accuracy within 5 ppm, (2) retention time in LC and (3) fragmentation pattern in MS2 and MS3. PC36:4-OOH was most often detected in VLDL, IDL and plasma. The ratio of total PCOOH to phosphatidylcholine progressively increased with the duration of oxidation in both VLDL and IDL. Conclusion This study demonstrated the presence of 12 molecular species of PCOOH in native triglyceride-rich lipoproteins. The frequent detection of PCOOH in triglyceride-rich lipoproteins provides a molecular basis of the atherogenicity of triglyceride-rich lipoproteins. PCOOH in triglyceride-rich lipoproteins might serve as a molecular basis of the atherogenicity of triglyceride-rich lipoproteins.
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Frei, B., T. M. Forte, B. N. Ames e C. E. Cross. "Gas phase oxidants of cigarette smoke induce lipid peroxidation and changes in lipoprotein properties in human blood plasma. Protective effects of ascorbic acid". Biochemical Journal 277, n.º 1 (1 de julho de 1991): 133–38. http://dx.doi.org/10.1042/bj2770133.
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Cigarette smoke (CS) is known to contain a large number of oxidants. In order to assess the oxidative effects of CS on biological fluids, we exposed human blood plasma to filtered (gas phase) and unfiltered (whole) CS, and determined the rate of utilization of endogenous antioxidants in relation to the appearance of lipid hydroperoxides. Lipid peroxidation was measured with a specific and sensitive assay that can detect lipid hydroperoxides at plasma levels as low as 10 nM. We found that exposure of plasma to the gas phase of CS, but not to whole CS, induces lipid peroxidation once endogenous ascorbic acid has been oxidized completely. In addition, CS exposure caused oxidation of plasma protein thiols and albumin-bound bilirubin, whereas uric acid and alpha-tocopherol were not consumed at significant rates. In plasma exposed to the gas phase of CS, low-density lipoprotein exhibited slightly increased electrophoretic mobility, but there was no apparent degradation of apolipoprotein B. Our results support the concept of an increased vitamin C utilization in smokers, and suggest that lipid peroxidation induced by oxidants present in the gas phase of CS leads to potentially atherogenic changes in lipoproteins.
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Henein, Michael Y., Sergio Vancheri, Giovanni Longo e Federico Vancheri. "The Role of Inflammation in Cardiovascular Disease". International Journal of Molecular Sciences 23, n.º 21 (26 de outubro de 2022): 12906. http://dx.doi.org/10.3390/ijms232112906.
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Atherosclerosis is a chronic inflammatory disease, in which the immune system has a prominent role in its development and progression. Inflammation-induced endothelial dysfunction results in an increased permeability to lipoproteins and their subendothelial accumulation, leukocyte recruitment, and platelets activation. Recruited monocytes differentiate into macrophages which develop pro- or anti-inflammatory properties according to their microenvironment. Atheroma progression or healing is determined by the balance between these functional phenotypes. Macrophages and smooth muscle cells secrete inflammatory cytokines including interleukins IL-1β, IL-12, and IL-6. Within the arterial wall, low-density lipoprotein cholesterol undergoes an oxidation. Additionally, triglyceride-rich lipoproteins and remnant lipoproteins exert pro-inflammatory effects. Macrophages catabolize the oxidized lipoproteins and coalesce into a lipid-rich necrotic core, encapsulated by a collagen fibrous cap, leading to the formation of fibro-atheroma. In the conditions of chronic inflammation, macrophages exert a catabolic effect on the fibrous cap, resulting in a thin-cap fibro-atheroma which makes the plaque vulnerable. However, their morphology may change over time, shifting from high-risk lesions to more stable calcified plaques. In addition to conventional cardiovascular risk factors, an exposure to acute and chronic psychological stress may increase the risk of cardiovascular disease through inflammation mediated by an increased sympathetic output which results in the release of inflammatory cytokines. Inflammation is also the link between ageing and cardiovascular disease through increased clones of leukocytes in peripheral blood. Anti-inflammatory interventions specifically blocking the cytokine pathways reduce the risk of myocardial infarction and stroke, although they increase the risk of infections.
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Giglio, Rosaria Vincenza, Angelo Maria Patti, Arrigo F. G. Cicero, Giuseppe Lippi, Manfredi Rizzo, Peter P. Toth e Maciej Banach. "Polyphenols: Potential Use in the Prevention and Treatment of Cardiovascular Diseases". Current Pharmaceutical Design 24, n.º 2 (5 de abril de 2018): 239–58. http://dx.doi.org/10.2174/1381612824666180130112652.
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Background: Polyphenols are bioactive compounds that can be found mostly in foods like fruits, cereals, vegetables, dry legumes, chocolate and beverages such as coffee, tea and wine. They are extensively used in the prevention and treatment of cardiovascular disease (CVD) providing protection against many chronic illnesses. Their effects on human health depend on the amount consumed and on their bioavailability. Many studies have demonstrated that polyphenols have also good effects on the vascular system by lowering blood pressure, improving endothelial function, increasing antioxidant defences, inhibiting platelet aggregation and low-density lipoprotein oxidation, and reducing inflammatory responses. Methods: This review is focused on some groups of polyphenols and their effects on several cardiovascular risk factors such as hypertension, oxidative stress, atherogenesis, endothelial dysfunction, carotid artery intima-media thickness, diabetes and lipid disorders. Results: It is proved that these compounds have many cardio protective functions: they alter hepatic cholesterol absorption, triglyceride biosynthesis and lipoprotein secretion, the processing of lipoproteins in plasma, and inflammation. In some cases, human long-term studies did not show conclusive results because they lacked in appropriate controls and in an undefined polyphenol dosing regimen. Conclusion: Rigorous evidence is necessary to demonstrate whether or not polyphenols beneficially impact CVD prevention and treatment.
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Osipenko, Alexander N. "Fatty Acid Metabolism Disorder as a Factor in Atherogenesis". Romanian Journal of Diabetes Nutrition and Metabolic Diseases 25, n.º 3 (1 de setembro de 2018): 243–52. http://dx.doi.org/10.2478/rjdnmd-2018-0028.
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Abstract Background and aims: The study aims to analyze of fatty acid (FA) composition of arteries and blood plasma in atherosclerosis. Material and method: The blood plasma in patients with coronary atherosclerosis was studied, the blood from healthy volunteers was used as control. There were also analyzed arteries of patients with severe atherosclerotic lesions and arteries of people with significantly less atherosclerotic changes. Results: The received data indicates that there is a rather active penetration of FA from blood plasma lipoproteins into intima of arteries. Penetration of FA from blood lipoproteins into the depth of atherosclerotic aorta and an atherosclerotic plaque appears to be small and does not effect on their fatty acid composition, which is similar to that of free FA of blood plasma. The evidence of the increased activity of desaturases and fatty acid synthases in atherosclerotic and intact arteries in patients with severe atherosclerotic vascular lesions was obtained. This increase in activity may be related by relatively low content of polyunsaturated linoleic acid in blood plasma in atherosclerosis. Conclusions: The increased activity of desaturases and fatty acid synthases as well as arterial wall hypoxia must promote accumulation of lipids in vascular wall by increasing the synthesis and inhibition of FA oxidation including free FA coming from blood.
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Potte, Juan, e Victor Hinojoza. "Protective effects of Curcumin against development of atherosclerosis". American Journal of BioMedicine 7, n.º 4 (27 de dezembro de 2019): 333–41. http://dx.doi.org/10.18081/2333-5106/019-310-321.
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Atherosclerosis is characterized by oxidative damage, which affects lipoproteins, the walls of blood vessels, and subcellular membranes. The oxidation of low-density lipoproteins (LDLs) plays an important role in the development of atherosclerosis. Curcumin is a component of turmeric, a spice used in many types of cooking and gives the yellow color to turmeric, was first isolated almost two centuries ago, and its structure as diferuloylmethane was determined in 1910. Since the time of Ayurveda (1900 Bc) numerous therapeutic activities have been assigned to turmeric for a wide variety of diseases and conditions, including those of the skin, pulmonary, and gastrointestinal systems, aches, pains, wounds, sprains, and liver disorders. Curcumin has been known that turmeric exhibits anti-inflammatory activity, this activity of turmeric is due to curcumin, a diferuloylmethane, and has been shown to regulate numerous transcription factors, cytokines, protein kinases, adhesion molecules, redox status and enzymes that have been linked to inflammation. The process of inflammation has been shown to play a major role in most chronic illnesses, like atherosclerosis. The researchers showed that curcumin exhibited protective effects as indicated by inhibition of lipoperoxidation of subcellular membranes. Oral curcumin inhibits LDL oxidation and has hypocholesterolemic effects in rabbits with experimental atherosclerosis. In the current review, we provide evidence for the potential role of curcumin in the prevention and treatment of atherosclerosis and pharmacological safety and negligible cost.
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Gebicki, Janusz M., Alexander V. Babiy e David R. Sullivan. "Oxidation of blood lipoproteins by free radicals: Effects of vitamin E, glycosylation and probucol treatment". Free Radical Biology and Medicine 9 (janeiro de 1990): 69. http://dx.doi.org/10.1016/0891-5849(90)90412-c.
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Oostenbrug, G. S., R. P. Mensink, M. R. Hardeman, T. De Vries, F. Brouns e G. Hornstra. "Exercise performance, red blood cell deformability, and lipid peroxidation: effects of fish oil and vitamin E". Journal of Applied Physiology 83, n.º 3 (1 de setembro de 1997): 746–52. http://dx.doi.org/10.1152/jappl.1997.83.3.746.
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Oostenbrug, G. S., R. P. Mensink, M. R. Hardeman, T. De Vries, F. Brouns, and G. Hornstra. Exercise performance, red blood cell deformability, and lipid peroxidation: effects of fish oil and vitamin E. J. Appl. Physiol. 83(3): 746–752, 1997.—Previous studies have indicated that fish oil supplementation increases red blood cell (RBC) deformability, which may improve exercise performance. Exercise alone, or in combination with an increase in fatty acid unsaturation, however, may enhance lipid peroxidation. Effects of a bicycle time trial of ∼1 h on RBC characteristics and lipid peroxidation were, therefore, studied in 24 trained cyclists. After 3 wk of fish oil supplementation (6 g/day), without or with vitamin E (300 IU/day), trial performance, RBC characteristics, and lipid peroxidation were measured again. RBC deformability appeared to decrease during endurance exercise. After correction for hemoconcentration, plasma total tocopherol concentrations decreased by 0.77 μmol/l ( P = 0.012) or 2.9% and carotenoid concentrations by 0.08 μmol/l ( P = 0.0008) or 4.5%. Endurance exercise did not affect the lag time and rate of in vitro oxidation of low-density lipoproteins (LDLs), but the maximum amount of conjugated dienes formed decreased by 2.1 ± 1.0 μmol/mmol LDL cholesterol ( P= 0.042) or 1.2%. Fish oil supplementation with and without vitamin E did not affect RBC characteristics or exercise performance. Both supplements decreased the rate of LDL oxidation, and fish oil supplementation with vitamin E delayed oxidation. The amount of dienes, however, was not affected. The supplements also did not change effects of exercise. We conclude that the changes observed during endurance exercise may indicate increased oxidative stress, but further research is necessary to confirm this. Fish oil supplementation does not improve endurance performance, but it also does not cause or augment changes in antioxidant levels or LDL oxidation during exercise.
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Mortensen, Alicja, Birgit Fischer Hansen, Jørgen Fischer Hansen, Henrik Frandsen, Elzbieta Bartnikowska, Peder S. Andersen e Lone S. Bertelsen. "Comparison of the effects of fish oil and olive oil on blood lipids and aortic atherosclerosis in Watanabe heritable hyperlipidaemic rabbits". British Journal of Nutrition 80, n.º 6 (dezembro de 1998): 565–73. http://dx.doi.org/10.1017/s0007114598001664.
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To compare the effects of fish oil and olive oil on the development of atherosclerosis in Watanabe heritable hyperlipidaemic (WHHL) rabbits, 6-week-old animals were given a daily dose (1·5 ml/kg body weight) of fish oil (n 10) or olive oil (n 10) by oral administration for 16 weeks. Plasma cholesterol and triacylglycerols were measured once monthly, and their concentrations in lipoproteins, together with susceptibility of LDL to oxidation were measured in vitro at the termination of the experiment. Aortic atherosclerosis was quantified biochemically and microscopically. After 4 weeks of treatment, and throughout the study thereafter, blood lipids were significantly (P < 0·05) lower in the fish-oil group than in the olive-oil group (cholesterol: 17·0 v. 30·3 mmol/l, triacylglycerols 2·97 v. 6·25 mmol/l, at termination). In the fish-oil group cholesterol was significantly lower in intermediate-density lipoproteins (2·69 v. 6·76 mmol/l) and VLDL (3·36 v. 11·51 mmol/l). Triacylglycerol levels of intermediate-density lipoproteins and VLDL in the fish-oil group were also significantly lower when compared with the olive-oil group (0·54 v 1·36 mmol/l and 0·92 v. 2·87 mmol/l respectively). No group differences were recorded for LDL- and HDL-cholesterol or triacylglycerol levels. A significantly higher oxidation of LDL was recorded 1 h after exposure to CuSO4 in the fish-oil group when compared with the olive-oil group (0·465 v. 0·202, arbitrary units). The following indicators of atherosclerosis development were significantly lower in the fish-oil group than in the olive-oil group: the cholesterol content (mg/g tissue) in the ascending aorta (29·8 v.48·9), the intima:media value (4·81 v. 18·24) and the area of intima (0·10 v. 0·57 mm2) in the thoracic aorta. It was concluded that fish-oil treatment decreased blood lipids and the development of aortic atherosclerosis in WHHL rabbits when compared with olive-oil treatment.
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Zouaoui Boudjeltia, Karim, Cédric Delporte, Pierre Van Antwerpen, Thierry Franck, Didier Serteyn, Nicole Moguilevsky, Martine Raes et al. "Myeloperoxidase-Dependent LDL Modifications in Bloodstream Are Mainly Predicted by Angiotensin II, Adiponectin, and Myeloperoxidase Activity: A Cross-Sectional Study in Men". Mediators of Inflammation 2013 (2013): 1–4. http://dx.doi.org/10.1155/2013/750742.
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The present paradigm of atherogenesis proposes that low density lipoproteins (LDLs) are trapped in subendothelial space of the vascular wall where they are oxidized. Previously, we showed that oxidation is not restricted to the subendothelial location. Myeloperoxidase (MPO), an enzyme secreted by neutrophils and macrophages, can modify LDL (Mox-LDL) at the surface of endothelial cells. In addition we observed that the activation of the endothelial cells by angiotensin II amplifies this process. We suggested that induction of the NADPH oxidase complex was a major step in the oxidative process. Based on these data, we asked whether there was an independent association, in 121 patients, between NADPH oxidase modulators, such as angiotensin II, adiponectin, and levels of circulating Mox-LDL. Our observations suggest that the combination of blood angiotensin II, MPO activity, and adiponectin explains, at least partially, serum Mox-LDL levels.
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Ermeith, Enas, Ashraf Jamal Mahmoud e Buthaina Jassim Yousef. "The Effect of Infection by Toxocariasis on Some Biochemical Parameters in Some Areas of Salah Al-Din Governorate". Journal of Life and Bio Sciences Research 1, n.º 3 (14 de dezembro de 2020): 89–92. http://dx.doi.org/10.38094/jlbsr1329.
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The current study examined 277 blood samples of people, from both sexes of different ages, living in different areas of Salah Al-Din Governorate (Tikrit, Al-Alam and Baiji districts). The study was conducted from November, 2018 to June, 2019. All participants were secrened to investigate the incidence of toxocariasis using IgG TES-ELISA technique. The results showed that the rate of infection with toxocariasis was 22%. It was found an increase in cholesterol concentrations within age group 48-58 years and amounted to 185.8 mg/dl, and highest rate of increase in triglycerides was recorded within age group 15-25 years (168.1 mg/dl). The highest percentage of total protein was recorded within age group 26- 36 years (6.67 mg/dl). As for lipoprotein tests, highest percentage of high-density lipoproteins in age group 48-58 years was recorded (53 mg/dl), while low-density lipoproteins were highest in age group 48-58 years (100.8 mg/dl), and in very low-density lipoproteins the highest percentage within age group 15-25 years (33.5 mg/dl). The highest percentage of AST liver enzymes was recorded in age group 15-25 years and the percentage was 20.6 u/l. The highest percentage of ALT was recorded in age group 26-36 years (20.1 u/l) and 15-25 years (20 u/l). It is concluded that This age group continues to be exposed to infection with toxocariasis, which leads to presence large numbers of live larvae which secrete their antigens in the body and thus spread of toxoplasmosis, and the increase in proportion of fats is caused by poor oxidation of fatty acids and increased production of hepatic fatty acids Which leads to a delay in breakdown of lipoproteins, and the increase in level of AST, ALT enzyme occurs in cases of hepatitis and cirrhosis and may be associated with advanced cases of toxocariasis.
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Lindqvist, Helen M., Anna Maria Langkilde, Ingrid Undeland e Ann-Sofie Sandberg. "Herring (Clupea harengus) intake influences lipoproteins but not inflammatory and oxidation markers in overweight men". British Journal of Nutrition 101, n.º 3 (18 de julho de 2008): 383–90. http://dx.doi.org/10.1017/s0007114508003073.
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Fish consumption is associated with a lower incidence of CVD and decreases in risk factors for atherosclerosis. Although fish contains other interesting components than fish oil, few studies focus on total fish composition and the influence food preparation might have on health-beneficial components. In the present cross-over intervention study the effect of a 6-week herring diet compared with a reference diet on CVD risk factors was investigated. Thirty-five healthy, but overweight, men (mean BMI 28·3 kg/m2) were randomised to a 6-week herring diet (150 g baked herring fillets/d, 5 d/week) or a reference diet (150 g baked lean pork and chicken fillets/d, 5 d/week). Diets were switched after a 12-week washout period. Plasma total cholesterol, TAG, HDL, HDL2, HDL3, LDL, C-reactive protein, IL-6, IL-18, intercellular adhesion molecule-1, oxidised LDL, oxygen radical absorbance capacity using perchloric acid (ORACPCA), whole-blood fatty acids, bleeding time and blood pressure were measured at the beginning and end of each dietary period. HDL was significantly higher after the herring diet period compared with after the reference diet period: 1·04v.0·99 mmol/l. TAG decreased after both diets, with no significant difference between the two diets. ORACPCAvalues did not indicate lower concentrations of non-protein plasma antioxidants, and oxidised LDL was not higher after the herring diet than after the reference diet. To conclude, a 6-week herring-rich diet significantly raised HDL compared with a diet of matched lean pork and chicken dishes. No adverse effects onin vivooxidation or serum antioxidants were found after herring intake.
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Oteiza, Ana, Ruomei Li, Robert S. McCuskey, Bård Smedsrød e Karen Kristine Sørensen. "Effects of oxidized low-density lipoproteins on the hepatic microvasculature". American Journal of Physiology-Gastrointestinal and Liver Physiology 301, n.º 4 (outubro de 2011): G684—G693. http://dx.doi.org/10.1152/ajpgi.00347.2010.
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Oxidized low-density lipoproteins (oxLDLs) are involved in proinflammatory and cytotoxic events in different microcirculatory systems. The liver is an important scavenger organ for circulating oxLDLs. However, the interaction of oxLDL with the hepatic microcirculation has been poorly investigated. The present study was conducted to examine the effects of differently modified oxLDLs on the hepatic microvasculature. C57Bl/6J mice were injected intravenously with low-density lipoprotein (LDL), or LDL oxidized for 3 h (oxLDL3) or 24 h (oxLDL24), at doses resembling oxLDL plasma levels in cardiovascular disease patients. Radioiodinated ligands were used to measure blood decay and organ distribution, and nonlabeled ligands to evaluate microcirculatory responses, examined by in vivo microscopy 30–60 min after ligand injection, immunohistochemistry, and scanning and transmission electron microscopy. Mildly oxLDL (oxLDL3) was cleared from blood at a markedly slower rate than heavily oxLDL (oxLDL24), but significantly faster than LDL ( P < 0.01). Injected oxLDLs distributed to liver. OxLDL effects were most pronounced in central areas of the liver lobules where oxLDL3elicited a significant ( P < 0.05) reduction in perfused sinusoids, and both oxLDL3and oxLDL24significantly increased the numbers of swollen endothelial cells and adherent leukocytes compared with LDL ( P < 0.05). OxLDL-treated livers also exhibited increased intercellular adhesion molecule (ICAM)-1 centrilobular staining. Electron microscopy showed a 30% increased thickness of the liver sinusoidal endothelium in the oxLDL3group ( P < 0.05) and a reduced sinusoidal fenestration in centrilobular areas with increased oxidation of LDL ( P for linear trend <0.05). In conclusion, OxLDL induced several acute changes in the liver microvasculature, which may lead to sinusoidal endothelial dysfunction.
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Kullisaar, Tiiu, Epp Songisepp, Marika Mikelsaar, Kersti Zilmer, Tiiu Vihalemm e Mihkel Zilmer. "Antioxidative probiotic fermented goats' milk decreases oxidative stress-mediated atherogenicity in human subjects". British Journal of Nutrition 90, n.º 2 (agosto de 2003): 449–56. http://dx.doi.org/10.1079/bjn2003896.
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The increasing interest in a healthy diet is stimulating innovative development of novel scientific products in the food industry. The viable lactic acid bacteria in fermented milk products, such as yoghurt, have been associated with increased lactose tolerance, a well-balanced intestinal microflora, antimicrobial activity, stimulation of the immune system and antitumoural, anticholesterolaemic and antioxidative properties in human subjects. Recently, we have studied a humanLactobacillusspp. strain that possesses antioxidative activity. The aim of the present pilot study was to develop goats' milk fermented with the human antioxidative lactobacilli strain,Lactobacillus fermentumME-3, and to test the effect of the fermented probiotic goats' milk on oxidative stress markers (including markers for atherosclerosis) in human blood and urine and on the gut microflora. Twenty-one healthy subjects were assigned to two treatment groups: goats' milk group and fermented goats' milk group (150 g/d) for a period of 21 d. Consumption of fermented goats' milk improved anti-atherogenicity in healthy subjects: it prolonged resistance of the lipoprotein fraction to oxidation, lowered levels of peroxidized lipoproteins, oxidized LDL, 8-isoprostanes and glutathione redox ratio, and enhanced total antioxidative activity. The consumption of fermented goats' milk also altered both the prevalence and proportion of lactic acid bacteria species in the gut microflora of the subjects. We conclude that the goats' milk fermented with our special antioxidative lactobacilli strainLactobacillus fermentumME-3 exhibits anti-atherogenic effects.
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Makangali, Kadyrzhan, Aigul Taeva, Andrei Lisitsyn, Yasin Uzakov, Damilya Konysbaeva e Gorbula Victoria. "Study of the National Cooked Smoked Meat Products While Tests with Laboratory Animals at the Pathology Models with the Purpose to Confirm the set of Biocorrective Features". Current Research in Nutrition and Food Science Journal 6, n.º 2 (25 de agosto de 2018): 536–51. http://dx.doi.org/10.12944/crnfsj.6.2.28.
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Conducted physico-chemical and biological studies of Goji berries and national products made it possible to obtain information on the bioavailability of nutrients included in the product, to evaluate their food value and nutritional value, and their functional orientation. The study of the processes of digestibility and absorption of the developed products on the gastric invitro model and the monolayer of the intestinal wall epithelium showed high absorption and assimilability of the low molecular weight (from 30 kDa and below) protein fraction of the studied product. The detected acceleration of the absorption of nutrients of the tested products was reflected positively on the dynamics of changes in the biochemical composition of the blood, which, in turn, will lead to an acceleration of the biocorrecting action of functional biologically active substances. As a result of the experiment it was established that Goji berries, characterized by high catalase activity, have a prominent antioxidant effect, helping to control free radical oxidation in the rat organism with hyperlipidemia by decrease of MDA concentration (to 30%) and improvement of blood serum antioxidant activity (to 40 %). A prominent hipolipidemic (lipid-lowering) effect of berries has been established, which consists in normalization of the blood serum lipid profile of rats with hyperlipidemia 28 days after the beginning of feeding (decrease in total cholesterol (by 1.5 times), low density lipoproteins (to 40%) and blood serum atherogenity index (by more than 50%) with increase of high-density lipoproteins (up to 45%).
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Bozic, Tatjana, Jelka Stevanovic, Suncica Borozan, Slavoljub Jovic, Blagoje Dimitrijevic e Igor Ignjatovic. "Influence of oxidative stress on disease development". Veterinarski glasnik 67, n.º 1-2 (2013): 75–85. http://dx.doi.org/10.2298/vetgl1302075b.
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There is ever increasing data indicating the vmast contribution of oxidative stress to the pathogenesis of numerous diseases (atherosclerosis, hypertension, heart failure, diabetes mellitus, stroke, rheumatoid arthritis, and others). Thus, in the pathogenesis of atherosclerosis the primary role is held by reactive oxygen species that are synthetized by endothelial cells of arterial blood vessels, leukocytes and macrophages. Furthermore, native particles of lipoproteins of small density become atherogenic through oxidation caused by reactive oxygen species. The oxidation of small-density lipoproteins stimulates the inflammatory process, and it in turn steps up adhesion and the inflow of monocytes and affects the synthesis and release of numerous proinflammatory cytokines involved in the further course of the process. One of the reasons for the development of arterial hypertension is the simultaneous activation of NAD(P)H oxidase and 12/15-lipoxygenase, since it results in the stepped up production of reactive oxygen species. These stimulate the production of matrix metalloproteinase 2, which lead to vascular remodelling and to increased apoptosis of heart muscle cells. Stepped up apoptosis is linked with myocardial infarction, cardiomyopathies and the development of heart failure. The sensitivity of ?-cells of the endocrine part of the pancreas to reactive oxygen species favor the naturally low concentrations of the collectors of free radicals in them, as well as an increase in the concentration of proinflammatory cytokines, glucosis and lipids that induce a reduction in the mass and function of ?-cells. Hyperglycemia in diabetes mellitus causes tissue damage through non-enzyme glycosylation of intracellular and extracellular proteins, which results in: reduced enzyme activity, damaged nucleic acid, disrupted natural decomposition of proteins, and activation of cytotoxic pathways. These processes are the basis of the pathogenesis of numerous complications of diabetes mellitus. Since inducible nitrogen-oxide synthesis launches processes that stimulate apoptosis of cerebral endothelial cells, and superoxide-anion radicals, hypochloric acid and hydrogen peroxide damage the parenchyma of an ischemic brain and biomacromolecules (causing lipid peroxidation, oxidation of proteins and deoxyribonucleic acid), brain damage occurs during cerebral ischemia and reperfusion.
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Thomas, C. E., R. L. Jackson, D. F. Ohlweiler e G. Ku. "Multiple lipid oxidation products in low density lipoproteins induce interleukin-1 beta release from human blood mononuclear cells." Journal of Lipid Research 35, n.º 3 (março de 1994): 417–27. http://dx.doi.org/10.1016/s0022-2275(20)41193-9.
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Micheletta, Fausta, Luigi Iuliano e Francesco Violi. "Vitamin E, Atherosclerosis and Thrombosis". Thrombosis and Haemostasis 85, n.º 05 (2001): 766–70. http://dx.doi.org/10.1055/s-0037-1615715.
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SummaryVitamin E, a major lipid-soluble, chain-breaking antioxidant includes several tocopherols having the biological activity of RRR-alpha-tocopherol. Vitamin E circulates in the blood as free tocopherol bound to beta-lipoproteins and is present in cell membrane where it exerts a potent defence against lipid peroxidation (1). Blood concentration of vitamin E in humans ranges from 25 to 30 μM, depending on daily intake and body’s ability to absorb fat (1). In the last decade the scientific interest on biological activity of vitamin E increased because of a growing body of evidence linking this vitamin with atherosclerosis and its complications (2). Thus, the oxidative hypothesis of atherosclerosis suggests that LDL accumulates within vessel wall, in particular in the macrophages, as a consequence of its oxidative modification mediated by resident cells (3, 4). A reduced defence against LDL oxidation could favour this process and accelerate atherosclerotic progression. Accordingly, patients with coronary heart disease have lower plasma concentration of vitamin E than controls (2) and prospective studies demonstrated that a daily assumption of vitamin E reduces cardiovascular events (5). According to the oxidative hypothesis of atherosclerosis, this effect has been attributed to the inhibition of LDL oxidation. Alternative mechanism potentially implicated in the antiatherosclerotic activity of vitamin E includes its interference with the activity of platelet and monocyte, in which the intracellular redox status plays an important functional role (6, 7). As platelets and monocytes are both involved in the pathophysiologic process leading to atherosclerotic lesion, the interference of vitamin E with the biological function of these cells may represent another important tool to explore the anti-atherosclerotic activity of vitamin E. This review will focus on the open issues related to the use of vitamin E in clinical studies and the potential usefulness in investigating platelet function and clotting activation in patients treated with vitamin E.
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Sher, Elena A., Keren Hemi, Shai Efrati, Joshua Weissgarten, Matityahu Shaklai e Nurith Shaklai. "Hemopexin Is Protective Against Intravascular Hemolysis–Induced Vascular Damage". Blood 116, n.º 21 (19 de novembro de 2010): 3207. http://dx.doi.org/10.1182/blood.v116.21.3207.3207.
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Abstract Abstract 3207 Background: Intravascular hemolysis renders hemoglobin (Hb), usually protected by the red blood cell environment, susceptible to oxidation to its ferric (metHb) form. Haptoglobin (Hp) provides first aid to protect the vasculature from acellular metHb havoc. However, once Hp is consumed, ferrous Hb readily undergoes oxidation to metHb, in which the globin to heme affinity is reduced. MetHb releases the loosely bound heme allowing it to execute its oxidative activity. While nucleated cells, like endothelial cells, are equipped with the heme oxygenase-1 defence system, the nucleus lacking red blood cells (RBC) and low density lipoproteins (LDL) particles have no defence from heme-induced oxidation. Therefore the sole defence from heme oxidative damage remains the plasma protein hemopexin (Hx), which binds hemin with high affinity comparable to that of globin. Following hemin binding, Hx undergoes conformational changes rendering the heme inaccessible thereby inactive. Aim: The current study is focused on the ability of plasma Hx to defend the vasculature from acellular Hb induced damage. Results: Hx defence from metHb damage was studied in the following projects: a) preventing in vitro LDL oxidation by metHb, b) decreasing in vitro lysis of red cells created by hypotonic and mechanical stress. (c) Exploring consumption of Hx in hemodialysis (HD) treated patients by measuring their Hx levels. (a) Methemoglobin iron is a central cause of LDL oxidation. This process initiates formation of blood vessel plaques and atherosclerosis development. This part of the study examined the effect of apoHx (lacking heme) on LDL oxidation by metHb. Incubation of isolated native LDL (nLDL) or vitamin E depleted (dLDL) with low concentration of metHb range (1-10μM) resulted in covalent apoB inter-particle crosslinking in both LDL types, dLDL being more sensitive than nLDL to the oxidative crosslinking. Addition of apoHx abolished metHb-induced oxidation even in the dLDL. This Hx activity (comparable to that of haptoglobin) was confirmed by both SDS-PAGE and fluorescent assay of bityrosines formation. The fact that Hx protects LDL, especially vitamin E depleted particles, shed light on the controversial antioxidant vitamin E properties by indicating its efficacy in defence against acellular Hb induced LDL oxidation. (b) Like LDL the red cell membrane is exposed to metHb-induced oxidative damage. Acellular Hb was formed by hypotonic shock or mechanical shear stress to fresh whole blood of healthy donors. The effect of Hx on acellular Hb levels was measured spectrophotometrically. Reduction of osmotic pressure in fresh blood to 40% of its normal value resulted in formation of ∼300 μM acellular Hb. Supplementation of exogenous apoHx (20μM) to blood before exposure to hypotonicity reduced acellular Hb formation by half. The specificity of Hx was proved by addition of up to 80μM albumin, which had no effect on acellular Hb concentration. Acellular Hb was formed also by applying shear stress on circulating fresh blood in narrow channels using a peristaltic pump. Within 4 hours acellular Hb reached ∼500μM. However, in presence of 20μM apoHx hemolysis was significantly reduced (up to 50%). This reduction may be attributed to Hx's ability to block the hemolysis amplifying effect of metHb on the RBC membrane. (c) In HD treated patients RBCs are exposed to the effects of recurrent mechanical shear stress. The last part of the research was dedicated to quantisation of apoHx levels (by titration with hemin) in sera of HD patients (n=60) prior to and immediately after a single dialysis procedure versus normal controls (n=20). Sera apoHx levels in HD patients prior to a dialysis session were lower compared to healthy controls (10.91±3.19 μM vs. 14.95±2.63 μM, p<0.05) and were even lower (7.49±3.8 μM) immediately after the treatment. These findings indicate that in the plasma of HD treated patients Hx consumption rate exceeds synthesis rate leading to a chronically low level of Hx. Moreover, reduction of Hx was even more prominent in patients on long term HD treatment of above five years. Conclusion: Hx is specifically effective in attenuation of acellular Hb damage to the vasculature. These results point to the option that treating HD patients with exogenous Hx may slow down the rate of atherosclerotic cardiovascular disease development, the major cause of morbidity and mortality in these patients. Disclosures: No relevant conflicts of interest to declare.
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Ghibu, Steliana, Cristina Elena Craciun, Razvan Rusu, Claudiu Morgovan, Cristina Mogosan, Luc Rochette, Adrian Florin Gal e Maria Dronca. "Impact of Alpha-Lipoic Acid Chronic Discontinuous Treatment in Cardiometabolic Disorders and Oxidative Stress Induced by Fructose Intake in Rats". Antioxidants 8, n.º 12 (11 de dezembro de 2019): 636. http://dx.doi.org/10.3390/antiox8120636.
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Insulin resistance (IR) and cardiometabolic disorders are the main consequences of today’s alimentary behavior. This study evaluates the effects of a chronic-discontinuous treatment with alpha-lipoic acid (AL), an antioxidant substance that improves glycemic control associated with diabetes mellitus, on metabolic disorders and plasma oxidative stress induced by fructose intake, in rats. Sprague-Dawley rats (48 animals) were randomized into two series (n = 24): rats fed with standard chow or with standard chow supplemented with 60% fructose. In each of the two series, for 2 weeks/month over 12 weeks, a group of rats (n = 12) was intraperitoneally injected with NaCl 0.9%, and a second group (n = 12) received AL 50 mg/kg/day. Body weight, glycemia, and systolic blood pressure were monitored throughout the study. After 12 weeks, IR, plasma lipoproteins, uric acid, transaminase activities, and oxidative stress markers were assessed. The high fructose-enriched diet induced cardiometabolic disorders (hypertension, hyperglycemia, IR and dyslipidemia), an increase in uric acid concentration, transaminase activities and C-reactive protein level. This diet also enhanced plasma products of lipid and protein oxidation, homocysteine level, and decreased GSH/GSSG ratio. In this field, there is evidence to indicate that oxidative stress plays an important role in the etiology of diabetic complications. AL discontinuous treatment prevents the metabolic disorders induced by fructose intake, reduced plasma lipid and protein oxidation-products, and restored the GHS/GSSG ratio. Our study proves a promising potential of the chronic-discontinuous treatment of AL and highlights the pleiotropic effects of this antioxidant substance in metabolic disorders such as diabetes.
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Dunford, H. Brian, e Yuchiong Hsuanyu. "Kinetics of oxidation of serotonin by myeloperoxidase compounds I and II". Biochemistry and Cell Biology 77, n.º 5 (1 de outubro de 1999): 449–57. http://dx.doi.org/10.1139/o99-052.
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The oxidation of serotonin (5-hydroxytryptamine) by the myeloperoxidase intermediates compounds I and II was investigated by using transient-state spectral and kinetic measurements at 25.0 ± 0.1°C. Rapid scan spectra demonstrated that both compound I and compound II oxidize serotonin via one-electron processes. Rate constants for these reactions were determined using both sequential-mixing and single-mixing stopped-flow techniques. The second order rate constant obtained for the one-electron reduction of compound I to compound II by serotonin is (1.7 ± 0.1) × 107 M-1·s-1, and that for compound II reduction to native enzyme is (1.4 ± 0.1) × 106 M-1·s-1 at pH 7.0. The maximum pH of the compound I reaction with serotonin occurs in the pH range 7.0-7.5. At neutral pH, the rate constant for myeloperoxidase compound I reacting with serotonin is an order of magnitude larger than for its reaction with chloride, (2.2 ± 0.2) × 106 M-1·s-1. A direct competition of serotonin with chloride for myeloperoxidase compound I oxidation was observed. Our results suggest that serotonin may have a role to protect lipoproteins from oxidation and to prevent enzymes from inactivation caused by the potent oxidants HOCl and active oxygen species.Key words: serotonin oxidation, myeloperoxidase, chloride, competition of serotonin, blood platelets, neutrophils.
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KHAN, Jamshad, M. David BRENNAN, Nicholas BRADLEY, Beirong GAO, Richard BRUCKDORFER e Michael JACOBS. "3-Nitrotyrosine in the proteins of human plasma determined by an ELISA method". Biochemical Journal 330, n.º 2 (1 de março de 1998): 795–801. http://dx.doi.org/10.1042/bj3300795.
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The modification of tyrosine residues in proteins to 3-nitrotyrosine by peroxynitrite or other potential nitrating agents has been detected in biological systems that are subject to oxidative stress. A convenient semi-quantitative method has been developed to assay nitrated proteins in biological fluids and homogenates using a competitive ELISA developed in our laboratory. This assay selectivity detected 3-nitro-L-tyrosine residues in a variety of peroxynitrite-treated proteins (BSA, human serum albumin (HSA), α1-antiprotease inhibitor, pepsinogen and fibrinogen) and also in a nitrated peptide, but had a low affinity for free 3-nitro-L-tyrosine and 3-chloro-L-tyrosine. The IC50 values for the inhibition of antibody binding by different nitrated proteins were in the range 5-100 nM, suggesting that the antibody discriminated between nitrotyrosine residues in different environments. The presence of nitrotyrosine in plasma proteins was detected by Western blot analysis and quantified by the ELISA. A concentration of 0.12±0.01 μM nitro-BSA equivalents was measured in the proteins of normal plasma which was increased in peroxynitrite-treated plasma and was elevated in inflammatory conditions. HSA and low-density lipoprotein (LDL) isolated from plasma contained 0.085±0.04 and 0.03±0.006 nmol nitro-BSA equivalents/mg protein, respectively. Comparison of the level of nitration in peroxynitrite-treated HSA and LDL in the presence and absence of plasma indicates that nitration and presumably oxidation is inhibited by plasma antioxidants. The presence of nitrotyrosine in LDL is consistent with previous reports implicating peroxynitrite in the oxidative modification of lipoproteins and the presence of a low concentration of oxidized LDL in the blood.
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Constantinescu, Alina A., Hans Vink e Jos A. E. Spaan. "Elevated capillary tube hematocrit reflects degradation of endothelial cell glycocalyx by oxidized LDL". American Journal of Physiology-Heart and Circulatory Physiology 280, n.º 3 (1 de março de 2001): H1051—H1057. http://dx.doi.org/10.1152/ajpheart.2001.280.3.h1051.
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Proteoglycans and plasma proteins bound to the endothelial cell glycocalyx are essential for vascular function, but at the same time, they lower capillary tube hematocrit by reducing capillary volume available to flowing blood. Because oxidized low-density lipoproteins (oxLDL) reduce the effective thickness of the glycocalyx (Vink H, Constantinescu AA, and Spaan JAE. Circulation 101: 1500–1502, 2000), we designed the present study to determine whether this is caused by pathological degradation of glycocalyx constituents or increased glycocalyx deformation by elevated shear forces of flowing blood. Capillaries from the right cremaster muscle of 24 hamsters were examined by using intravital microscopy after systemic administration of normal LDL ( n = 4), moderate oxLDL (6-h oxidation with CuSO4, n = 7), severe oxLDL (18-h oxidation, n = 5), and moderate oxLDL plus superoxide dismutase (SOD) and catalase ( n = 8). Capillary tube hematocrit increased from 0.16 ± 0.03 to 0.37 ± 0.05 and from 0.15 ± 0.01 to 0.31 ± 0.03 after moderate oxLDL and severe oxLDL, respectively. These changes were paralleled by increases in red blood cell flux from 8.7 ± 1.9 to 13.8 ± 3 and from 10.7 ± 2.1 to 16.3 ± 3.2 cells/s after moderate oxLDL and severe oxLDL, respectively, in the absence of changes in anatomic capillary diameter. Red blood cell velocity, as a measure for the shear forces on the glycocalyx, was not affected by oxLDL, whereas tissue pretreatment with SOD and catalase completely abolished the effects of oxLDL on glycocalyx thickness, capillary hematocrit, and red blood cell flux. We conclude that elevation of capillary tube hematocrit by oxLDL reflects degradation of the endothelial glycocalyx by oxygen-derived free radicals.
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Cannon, Richard O. "Role of nitric oxide in cardiovascular disease: focus on the endothelium". Clinical Chemistry 44, n.º 8 (1 de agosto de 1998): 1809–19. http://dx.doi.org/10.1093/clinchem/44.8.1809.
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Abstract Nitric oxide is a soluble gas continuously synthesized by the endothelium. This substance has a wide range of biological properties that maintain vascular homeostasis, including modulation of vascular dilator tone, regulation of local cell growth, and protection of the vessel from injurious consequences of platelets and cells circulating in blood. A growing list of conditions, including those commonly associated as risk factors for atherosclerosis such as hypertension and hypercholesterolemia, are associated with diminished release of nitric oxide into the arterial wall either because of impaired synthesis or excessive oxidative degradation. Diminished nitric oxide bioactivity may cause constriction of coronary arteries during exercise or during mental stress and contribute to provocation of myocardial ischemia in patients with coronary artery disease. Additionally, diminished nitric oxide bioactivity may facilitate vascular inflammation that could lead to oxidation of lipoproteins and foam cell formation, the precursor of the atherosclerotic plaque. Numerous therapies have been investigated to assess the possibility of reversing endothelial dysfunction by enhancing the release of nitric oxide from the endothelium, either through stimulation of nitric oxide synthesis or protection of nitric oxide from oxidative inactivation and conversion to toxic molecules such as peroxynitrite. Accordingly, causal relationships between improved endothelial function and reduction in myocardial ischemia and acute coronary events can now be investigated.
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Getz, Godfrey S. "An Overview of Atherosclerosis: A Look to the Future*". Toxicologic Pathology 18, n.º 4a (janeiro de 1990): 623–35. http://dx.doi.org/10.1177/019262339001804a12.
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This overview briefly summarizes the cellular pathobiology of experimental atherosclerosis and is then followed by a consideration of how 3 major risk factors interact with the hypothesized pathogenetic process. First, since hemodynamics and blood flow influence the localization of atherosclerotic plaques, possible mechanisms and directions of research are considered. Secondly, the recent hypothesis relating the oxidation of LDL to several of the early processes of atherogenesis is briefly discussed in view of the fact that hyperlipidemia is a major risk factor. The possibility that subsets of LDL and lipoproteins other than LDL might be involved is also discussed. Family history is the last of the 3 contributors to atherosclerosis reviewed and some prototypes of gene abnormalities are considered. Finally, the needs and prospects of future research are summarized.
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Urquiaga, Inés, Danitza Troncoso, Maria Mackenna, Catalina Urzúa, Druso Pérez, Sara Dicenta, Paula de la Cerda et al. "The Consumption of Beef Burgers Prepared with Wine Grape Pomace Flour Improves Fasting Glucose, Plasma Antioxidant Levels, and Oxidative Damage Markers in Humans: A Controlled Trial". Nutrients 10, n.º 10 (1 de outubro de 2018): 1388. http://dx.doi.org/10.3390/nu10101388.
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Wine grape pomace flour (WGPF) is a fruit byproduct that is high in fiber and antioxidants. We tested whether WGPF consumption could affect blood biochemical parameters, including oxidative stress biomarkers. In a three-month intervention study, 27 male volunteers, each with some components of metabolic syndrome, consumed a beef burger supplemented with 7% WGPF containing 3.5% of fiber and 1.2 mg gallic equivalents (GE)/g of polyphenols (WGPF-burger), daily, during the first month. The volunteers consumed no burgers in the second month, and one control-burger daily in the third month. At baseline and after these periods, we evaluated the metabolic syndrome components, plasma antioxidant status (i.e., 2,2-diphenyl-1-picrylhydrazyl radical scavenging capacity (DPPH), vitamin E, vitamin C), and oxidative damage markers (i.e., advanced oxidation protein products (AOPPs), oxidized low-density lipoproteins (oxLDLs), malondialdehyde (MDA)). The WGPF-burger intake significantly reduced glycemia and homeostatic model assessment-based measurement of insulin resistance. Vitamin C increased and decreased during the consumption of the WGPF-burger and control-burger, respectively. The WGPF-burger intake significantly decreased AOPP and oxLDL levels. Vitamin E and MDA levels showed no significant changes. In conclusion, the consumption of beef burgers prepared with WGPF improved fasting glucose and insulin resistance, plasma antioxidant levels, and oxidative damage markers. Therefore, this functional ingredient has potential as a dietary supplement to manage chronic disease risk in humans.
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Richards, S. E., S. Hicklin, T. Lord, A. Nickson, J. Long, J. Brackenbury e J. R. Newbold. "Effects of B vitamins and methyl group donors on milk production, milk composition and blood biochemistry in dairy cows". Proceedings of the British Society of Animal Science 2002 (2002): 196. http://dx.doi.org/10.1017/s1752756200008528.
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Recent reviews highlight the importance of the liver in the coordination of nutrient fluxes in support of pregnancy and lactation (e.g. Drackley et al., 2001). Mobilisation of body fat reserves in the late dry period and early lactation leads to an increase in uptake of non-esterified fatty acids (NEFA) by the liver. Their metabolic fate is either oxidation or esterification into triacylglycerides (TAG) that are either exported in very low density lipoproteins (VLDL) or accumulated within liver cells. Recent evidence indicates that TAG accumulation impairs ureagenic and gluconeogenic capacity of the liver, with consequent reductions in feed intake and milk yield, increased incidence of disease and decreased reproductive performance (Overton and Piepenbrink, 1999).LiFTTM (NuTec Ltd.) is a proprietary mixture of B-group vitamins and methyl group donors (rumen protected choline, niacin, vitamin B12, biotin, folic acid and thiamine) designed to reduce the accumulation of TAG in the liver and accelerate VLDL export. The objective of this experiment was to evaluate the effect of LiFT on milk yield and composition and concentrations of metabolites in blood.
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Stancu, Camelia, Elena Constantinescu e Anca Sima. "Ceruloplasmin and oxidized LDL colocalize in atherosclerotic lesions of hamster". Open Life Sciences 6, n.º 1 (1 de fevereiro de 2011): 23–31. http://dx.doi.org/10.2478/s11535-010-0076-3.
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AbstractEpidemiological studies show that the risk for cardiovascular diseases increases with increasing levels of free-copper in plasma. It is known that intact ceruloplasmin (CP), the major protein transporter of copper in human plasma, oxidizes low density lipoproteins (LDL) in vitro. Our aim was to study the interaction between LDL and CP in vitro and in vivo, in an animal model of diet-induced atherosclerosis. In order to visualize the pathway of LDL into the arterial wall, human native LDL was labeled with fluorescent DiI and injected into male, Golden Syrian hyperlipemic hamsters. In vitro results demonstrated that slightly degraded CP has a significant oxidation potential against LDL at neutral pH. In vivo, after 24 hours circulation, LDL-DiI was taken up by the enlarged intima and fatty streaks of the arterial wall. Immunohistochemical localization of oxidized LDL and CP revealed their presence in the same areas of the arteries that take up LDL-DiI. Co-localization of LDL and CP in the enlarged intima of pro-atherosclerotic areas might explain the possible copper-induced oxidation process that might occur after native LDL is taken-up from the blood, transcytosed through the endothelium and accumulated in focalized deposits.
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Shen, Yixiao, Jing Han, Xiaoyan Zheng, Binling Ai, Yang Yang, Dao Xiao, Lili Zheng e Zhanwu Sheng. "Rosemary Leaf Extract Inhibits Glycation, Breast Cancer Proliferation, and Diabetes Risks". Applied Sciences 10, n.º 7 (26 de março de 2020): 2249. http://dx.doi.org/10.3390/app10072249.
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Advanced glycation end products (AGEs) generated from glycation can cause inflammation-related diseases such as diabetes and cancer. The bioactive compounds of rosemary extract (RE) were extracted and incubated with sugar-protein rich food and breast cancer cell MCF-7 to investigate its inhibitory effect on glycation and cancer cell proliferation, respectively. The diabetic rat was dosed with RE to investigate its effect on blood glucose, serum malondialdehyde (MDA), cholesterol (CHO), triglycerides (TG), low-density lipoproteins (LDLs), anti-oxidation capacity (T-AOC), superoxide dismutase (SOD) activity, anti-oxidation capacity alkaline phosphatase (ALP), glutamate pyruvate transaminase (GPT), and glutamate oxaloacetate transaminase (GOT). The results show that RE contained seven major phenolics ranging from 17.82 mg/g for rosemarinic acid to 0.01 mg/g for ferulic acid on dry weight basis. It significantly lowered AGEs, carboxymethyl lysine (CML), and protein glycation in a sugar-protein rich intermediate-moisture-food (IMF) model. Furthermore, the survival rates of MCF-7 cells decreased to 6.02 and 2.16% after 96 h of incubation with 1.0 and 2.0 mg/mL of RE, respectively. The blood glucose, MDA, CHO, TG, and LDLs in diabetic rats of RE treatment were decreased. The RE treatment also enhanced the T-AOC and SOD activity. Furthermore, the RE treatment improved liver function through improving ALP, GPT, and GOT activities in diabetic rats. The results provide important information for the nutriaceutical and pharmaceutical application of rosemary extract.
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SALONEN, J. T., H. KORPELA, K. NYYSSÖNEN, E. PORKKALA, T. P. TUOMAINEN, J. D. BELCHER, D. R. JACOBS e R. SALONEN. "Lowering of body iron stores by blood letting and oxidation resistance of serum lipoproteins: a randomized cross-over trial in male smokers". Journal of Internal Medicine 237, n.º 2 (fevereiro de 1995): 161–68. http://dx.doi.org/10.1111/j.1365-2796.1995.tb01156.x.
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Saptaningtyas, Ragil, Regitha Wahyuhendra e Joko Teguh Isworo. "CORRELATION BETWEEN FASTING BLOOD SUGAR AND LDL CHOLESTEROL OF TYPE 2 DM PATIENTS ON WILLIAM BOOTH HOSPITAL SEMARANG". Jambura Journal of Health Sciences and Research 4, n.º 3 (10 de fevereiro de 2022): 604–8. http://dx.doi.org/10.35971/jjhsr.v4i3.12161.
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Type 2 diabetes mellitus is a metabolic disorder characterized by hyperglycemia as a result of reducing insulin secretion of pancreas beta cells or insulin function disorder. Type 2 DM can cause lipid metabolism disorder (dyslipidemia) such as increasing total cholesterol, triglyceride, and decreasing HDL levels. The small and dense , Rafparticle of LDL is susceptible to oxidation, so it makes LDL more atherogenic than other lipoproteins. A high level of LDL is a factor in atherosclerosis. It can be affected by patients’ lifestyles. The aim of this study is to figure out the relation between fasting blood sugar and LDL Cholesterol of Type 2 DM Patients on William Booth Hospital Semarang. This study used secondary data taken from 85 patients from the medical report and laboratory test results of William Booth Hospital Semarang from January to May 2021 that fit inclusion and exclusion criteria. Result data were analyzed by a statistical test with Spearman’s correlation test. The result of this study showed that 96,5% of patients had high levels of fasting blood sugar and 76,4% of high levels of LDL cholesterol, with Spearman's correlation p-value was 0,977. The study concluded that there is no meaningful correlation between fasting blood sugar and LDL cholesterol of type 2 DM patients on William Booth Hospital Semarang.
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Farinazzi-Machado, Flavia Maria Vasques. "Can the consumption of Seeds, Leaves and Fruit Peels avoid the risk factors for Cardiovascular Disorders?" International Journal of Nutrology 10, n.º 02 (abril de 2017): 037–45. http://dx.doi.org/10.1055/s-0040-1705287.
Texto completo da fonteResumo:
ABSTRACTChanges in the feeding pattern of the population have recently led to a greater occurrence of cardiovascular risk factors that contribute to a high rate of morbidity and mortality worldwide. The presence of beneficial bioactive compounds in fruits and processed sub-products have proven to have a negative association with risk factors, such as blood pressure reduction, plasmatic lipoproteins control and increased resistance of LDL-c to oxidation, in addition to glycemic control and antioxidant effects. The aim of this review is to show that several studies have demonstrated many different chemical compounds in seeds, leaves and fruit peels, including their metabolic and physiologic effects on the risk factors of cardiovascular diseases. We reviewed the relevant literature by searching English-language publications in Pubmed, Google Scholar, Scielo and Lilacs, and references from relevant articles published since 2010, especially in the last five years. Eighty-seven relevant articles were included.
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Efimenko, Natalia V., e A. V. Abramtsova. "The specific changes in the activity of the antioxidative system of blood under the influence of courses of treatment with the use of mineral water from the Pyatigorsk source modified by nano-scale particles of selenium (an experimental study)". Russian Journal of Physiotherapy, Balneology and Rehabilitation 15, n.º 3 (15 de junho de 2016): 116–20. http://dx.doi.org/10.18821/1681-3456-2016-15-3-116-120.
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The objective of the present study was to evaluate the influence of the courses of intake of Pyatigorsk spring water characterized by the level of mineralization up to 5.01 g / l (weakly acidic, containing sulfates, bicarbonates, chlorides, calcium, and sodium) modified by nano-scale particles of selenium. The experiments were carried out on 46 male Wistar rats allocated into 6 groups of 8 animals each (1 control group and 5 experimental groups). The animals of the former group were given native drinking mineral water during 21 days while those of the latter ones drank the same water modified by nano-scale particles of selenium added at two doses, either 40 mg / kg or 20 mg / kg. Some animals received water containing dissolved nanoparticles of selenium at the same doses. The parameters measured included the leukocyte blood profile, the level of glutathione peroxidase, and indicators of metabolic stress (aminotransferase and malone dialdehyde levels, i.e. modified oxidized low-density lipoproteins, total protein and glucose levels in blood). It was shown that the levels of malone dialdehyde and modified oxidized low-density lipoproteins did not change in the animals of experimental groups compared with those in the control group. It suggested resistance of lipids to free radical oxidation under the conditions of the course drinking of natural water and the water modified by nano-scale particles of selenium. Native mineral water proved to increase the level of glutathione in blood to above the control values in 50% of the test animals whereas mineral water modified by selenium nanoparticles caused a similar increase in 75% of the experimental animals regardless of the selenium concentration. It is concluded that the enhancement of the activity of the antioxidative system under effect of addition of the selenium nanoparticles into mineral water at the doses of 20mg/kg and 40mg/kg limits the production of organic hydroperoxides. The data obtained can be used to choose the optimal amount of selenium nanoparticles for the introduction into mineral water for the purpose of increasing its biological potential.
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Mason, R. Preston, Peter Libby e Deepak L. Bhatt. "Emerging Mechanisms of Cardiovascular Protection for the Omega-3 Fatty Acid Eicosapentaenoic Acid". Arteriosclerosis, Thrombosis, and Vascular Biology 40, n.º 5 (maio de 2020): 1135–47. http://dx.doi.org/10.1161/atvbaha.119.313286.
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Patients with well-controlled LDL (low-density lipoprotein) levels still have residual cardiovascular risk associated with elevated triglycerides. Epidemiological studies have shown that elevated fasting triglyceride levels associate independently with incident cardiovascular events, and abundant recent human genetic data support the causality of TGRLs (triglyceride-rich lipoproteins) in atherothrombosis. Omega-3 fatty acids, such as eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), lower blood triglyceride concentrations but likely exert additional atheroprotective properties at higher doses. Omega-3 fatty acids modulate T-cell differentiation and give rise to various prostaglandins and specialized proresolving lipid mediators that promote resolution of tissue injury and inflammation. The REDUCE-IT (Reduction of Cardiovascular Events with Icosapent Ethyl–Intervention Trial) with an EPA-only formulation lowered a composite of cardiovascular events by 25% in patients with established cardiovascular disease or diabetes mellitus and other cardiovascular risk factors. This clinical benefit likely arises from multiple molecular mechanisms discussed in this review. Indeed, human plaques readily incorporate EPA, which may render them less likely to trigger clinical events. EPA and DHA differ in their effects on membrane structure, rates of lipid oxidation, inflammatory biomarkers, and endothelial function as well as tissue distributions. Trials that have evaluated DHA-containing high-dose omega-3 fatty acids have thus far not shown the benefits of EPA alone demonstrated in REDUCE-IT. This review will consider the mechanistic evidence that helps to understand the potential mechanisms of benefit of EPA.
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Serebryakova, L. I., I. M. Studneva, O. M. Veselova, I. V. Dobrokhotov, G. G. Konovalova, A. A. Timoshin, A. A. Abramov et al. "The anti-ischemic and antioxidant activity of the pharmacological agonist of galanin receptor GalR2 and carnosine in in vitro and in vivo model systems". Biomeditsinskaya Khimiya 68, n.º 3 (2022): 190–200. http://dx.doi.org/10.18097/pbmc20226803190.
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Antioxidant and anti-ischemic properties of the pharmacological agonist of galanin receptor GalR2 WTLNSAGYLLGPβAH (Gal) and its C-terminal fragment, dipeptide carnosine (βAH), were studied in the model of regional ischemia and reperfusion of the rat heart in vivo in the dose range of 0.5-5.0 mg/kg and Cu²⁺-induced free radical oxidation of low density lipoproteins (LDL) of human plasma in vitro for peptide concentrations of 0.01 mM and 0.1 mM. Gal was obtained by automatic solid phase synthesis using the Fmoc methodology; its structure was characterized by 1H-NMR spectroscopy and MALDI-TOF mass spectrometry. Intravenous administration of the optimal dose of Gal (1 mg/kg) to rats after ischemia was more effective than carnosine in reducing of the myocardial infarct size and the activity of creatine kinase-MB and lactate dehydrogenase in blood plasma at the end of reperfusion. It also improved the metabolic state of the reperfused myocardium and reduced the formation of peroxidation products during reperfusion. Gal reduced more effectively the formation of adducts of hydroxyl radicals in the interstitium of the area at risk (AAR) of the rat heart than carnosine. Carnosine at a dose of 1 mg/kg more effectively increased the activity of catalase and glutathione peroxidase in the AAR by the end of reperfusion compared to Gal. In a model of Cu²⁺-initiated oxidation of human plasma LDL 0.1 mM carnosine demonstrated a significantly more pronounced reduction in the formation of lipid radicals compared to Gal. The results show that Gal can be considered as a promising agent that reduces myocardial injury during reperfusion and oxidative stress.
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Vendrame, Felipe, Leticia Marani, Sara T. Olalla Saad, Fernando F. Costa e Kleber Yotsumoto Fertrin. "Elevated Levels of Hepatokine Angiopoietin-like 3 Correlate Paradoxically with Hypocholesterolemia and Hemolysis in Sickle Cell Anemia". Blood 132, Supplement 1 (29 de novembro de 2018): 1069. http://dx.doi.org/10.1182/blood-2018-99-113851.
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Abstract Sickle cell disease (SCD) is characterized by chronic hemolytic anemia and vaso-occlusion. Hypocholesterolemia has been long recognized in SCD patients, and while it has been postulated that it is secondary to increased erythropoiesis, these mechanisms are not fully understood. Despite their name, angiopoietin-like proteins (ANGPTLs) are family of regulators of angiogenesis unable to bind to receptors classically targeted by angiopoetins. ANGPTL3 and ANGPTL4 are also inhibitors of lipoprotein lipase (LPL), and have become pharmacological targets in the treatment of dyslipidemia. We hypothesized that ANGPTL levels would be abnormal in SCD and could contribute to the understanding of lipid dysregulation. We aimed to determine, compare and correlate the circulating concentrations of ANGPTL3 and ANGPTL4 with hemolysis, lipid metabolism and endothelial dysfunction biomarkers in patients with sickle cell anemia (HbSS), hemoglobin SC disease (HbSC), and healthy individuals (HbAA). Thirty-six HbSS patients (age range 18-55, 21 men), 19 HbSC patients (HbSC) (age range 29-68, 8 men), and 31 HbAA controls (age range 18-66, 23 men) were enrolled in this study. Exclusion criteria were pregnancy, history of blood transfusion or sickle cell pain crisis in the past 3 months. Peripheral blood samples were collected for complete blood counts, biochemistry tests (lactate dehydrogenase [LDH], bilirubin, cholesterol and low and high density fractions, oxidized LDL [oxLDL], hemopexin), and determination of ANGPTL3, ANGPTL4, and soluble vascular cell adhesion molecule-1 (sVCAM-1) levels as marker of endothelial dysfunction. Differences in the intensity of hemolytic anemia between the two groups of SCD were confirmed, as well as decrease in total cholesterol (AA 176±32, SC 141±28 and SS 124±33mg/dL, p<0.0001), HDL (AA 46±11, SC 45±9, SS 37±11mg/dL, p<0.001) and LDL (AA 97±30, SC 76±34 or SS 63±27mg/dL, p<0.0001), as expected. Levels of both ANGPTL3 and ANGPTL4 were significantly higher in both SCD groups than in controls (ANGPTL3: AA 106±30, SC 147±37 and SS 155±58ng/mL, p<0.0001; ANGPTL4: AA 29±23ng/mL, SC 49±52ng/mL, SS 52±39ng/mL, p=0.04). While ANGPTL4 correlated only with LDH and HDL, ANGPTL3 correlated positively with reticulocyte count, LDH, total bilirubin, sVCAM-1, and the degree of LDL oxidation as estimated by oxLDL/LDL ratio, and negatively with hemoglobin, hemopexin, total cholesterol, and LDL levels. Our findings are surprising because the increase in AGPTLs should enhance inhibition of lipoprotein lipase, which is expected to cause hypercholesterolemia. It is therefore possible that hemolytic stimulus is able to override a feedback controlled by the liver between the amount of circulating lipoproteins and the need for LPL inhibition. This may also at least partially support the assumption that the plasma cholesterol pool is consumed for the synthesis of new red blood cells, so inhibition of LPL in this setting could be a compensatory mechanism. Nevertheless, the lack of significant differences between HbSS and HbSC suggests that erythropoietic drive is not the only determining factor. ANGPTL3 has been reported to be elevated in atherosclerosis and in rheumatic disease, so low grade chronic inflammation affecting the endothelium, along with a tendency towards more LDL oxidation could explain the positive correlation between sVCAM-1 and ANGPTL3. It is most remarkable that only ANGPTL3 correlated with hemolysis. ANGPTL3 is exclusively produced by the liver, while ANGPTL4 can be synthesized by adipose tissue, muscle, kidney, heart and thyroid, suggesting the stimulus for its overproduction generated by hemolysis is mostly sensed by hepatocytes. Considering the negative correlation with hemopexin, one possibility is that heme-hemopexin complexes taken up by liver cells and subsequent heme oxygenase induction may be involved in upregulation of ANGPTL3. Our data reveal that the production of lipoprotein lipase inhibitors is dysregulated in SCD-associated hypocholesterolemia, with a paradoxical increase in ANGPTLs which is most likely due to a liver response to hemolysis. Further studies should determine whether this mechanism is compensatory or driven by excessive heme production. Disclosures Fertrin: Alexion Pharmaceuticals Brasil: Speakers Bureau; Apopharma Inc.: Honoraria.
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Varela, Lourdes M., Elena Meseguer, Bertrand Lapergue, David Couret, Pierre Amarenco e Olivier Meilhac. "Changes in High-Density Lipoproteins Related to Outcomes in Patients with Acute Stroke". Journal of Clinical Medicine 9, n.º 7 (17 de julho de 2020): 2269. http://dx.doi.org/10.3390/jcm9072269.
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Modifications in high-density lipoprotein (HDL) particle sizes and HDL-binding proteins have been reported in stroke patients. We evaluated whether the lipoprotein profile, HDL composition and functionality were altered in stroke patients according to their clinical outcome using the modified Rankin Score at 3 months. Plasma samples were obtained from stroke patients treated with intravenous thrombolysis. Levels of cardiovascular and inflammatory markers in plasma were measured using the Human CVD Panel 1 (Milliplex® MAP). Lipoprotein subfractions from plasma were quantified by non-denaturing acrylamide gel electrophoresis, using the Lipoprint®-System (Quantimetrix®), and HDLs were isolated by ultracentrifugation. Relative amounts of paraoxonase-1 (PON1) and alpha-1 anti-trypsin (AAT) in the isolated HDLs were determined by Western blot. HDL anti-inflammatory function was evaluated in human blood–brain barrier endothelial cells stimulated with 100 ng/mL TNFα, and HDL antioxidant function was evaluated via their capacity to limit copper-induced low-density lipoprotein oxidation. Stroke patients with unfavorable outcomes had a lower proportion of small-sized HDLs and increased plasma levels of E-selectin (SELE) and the intercellular adhesion molecule 1 (ICAM1). HDLs from patients with unfavorable outcomes had lower levels of PON1 and displayed a blunted capacity to reduce the expression of SELE, interleukin 8 (IL8) and the monocyte chemoattractant protein-1 (MCP1) mRNA induced by TNFα in endothelial cells. These HDLs also had a reduced antioxidant capacity relative to HDLs from healthy donors. In conclusion, an increased ratio of large/small HDLs with impaired anti-inflammatory and antioxidant capacities was associated with unfavorable outcomes in stroke patients. Alteration of HDL functionality was mainly associated with a low amount of PON1 and high amount of AAT.
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Puga, Guilherme M., Christian Meyer, Sarah Everman, Lawrence J. Mandarino e Christos S. Katsanos. "Postprandial lipemia in the elderly involves increased incorporation of ingested fat in plasma free fatty acids and small (Sf 20–400) triglyceride-rich lipoproteins". American Journal of Physiology-Endocrinology and Metabolism 301, n.º 2 (agosto de 2011): E356—E361. http://dx.doi.org/10.1152/ajpendo.00670.2010.
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In the elderly, the rise in postprandial plasma triglyceride (TG) concentrations is increased, contributing to their increased risk of cardiovascular disease. We sought to determine the incorporation of ingested fat (whipping cream enriched with [1,1,1-13C]triolein) into plasma lipids during the postprandial period in six healthy elderly (67 ± 1 yr old) and six healthy young (23 ± 2 yr old) subjects. Blood and expired air samples were taken before and at 2-h intervals during the 8-h postprandial period. As expected, the area under the curve of postprandial plasma TG concentrations was larger in the elderly compared with the young subjects (152 ± 38 vs. 66 ± 27 mg·dl−1·h, P < 0.05). The incorporation of [13C]oleate in plasma free fatty acids (FFAs) and TG of the small (Sf = 20–400) triglyceride-rich lipoprotein (TRL) fraction was significantly higher in the elderly compared with the young subjects, resulting in increased postprandial contributions of the ingested lipid to plasma FFAs (41 ± 3 vs. 26 ± 6%, P < 0.05) and the small TRL fraction (36 ± 5 vs. 21 ± 3%, P < 0.05) in elderly. Plasma apoB-100 concentration was higher, whereas the rate of oxidation of the ingested lipid was lower ( P < 0.05) in the elderly. We conclude that increased postprandial lipemia in the elderly involves increased contribution of ingested lipid to the plasma small TRLs. This appears to be driven at least in part by increased appearance of the ingested fat as plasma FFA and increased availability of apo B-100 lipoproteins in the elderly.
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Lamuela-Raventós, R. M., A. I. Romero-Pérez, C. Andrés-Lacueva e A. Tornero. "Review: Health Effects of Cocoa Flavonoids". Food Science and Technology International 11, n.º 3 (junho de 2005): 159–76. http://dx.doi.org/10.1177/1082013205054498.
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Flavonoids are phenolic substances widely found in fruits and vegetables. Many epidemiological studies associate the ingestion of flavonoids with a reduced risk of cardiovascular disease and certain types of cancer. These effects are due to the physiological activity of flavonoids in the reduction of oxidative stress, inhibiting low-density lipoproteins (LDL) oxidation and platelet aggregation, acting as vasodilators in blood vessels, inhibiting the adherence of monocytes to the vascular endothelium, promoting fibrinolysis, acting as immunomodulators and anti-inflammatory agents and as inhibitors in the different phases of tumour process. Cocoa is an important source of polyphenols, which comprise 12-18% of its total weight on dry basis; the major phenolic compounds are epicatechin, proanthocyanidins and cate-chin. The levels of flavonoids contained are higher than the ones founds in apples, onions or wine, foods known for their high amount of phenolic compounds. Cocoa and cocoa products are important sources of flavonoids in our diet. In the Dutch population chocolate contributes up to 20% of the total flavonoid intake in adults, and in children the percentage is even higher. The bioavailability of these compounds depends on other food constituents, and their interaction with the food matrix. This article reviews current evidence on the health effects of cocoa flavonoids in our diet. The compiled data supports the premise that the consumption of cocoa flavonoids is beneficial to human health.
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Gross, Myron, Michael Steffes, David R. Jacobs, Xinhua Yu, Linda Lewis, Cora E. Lewis e Catherine M. Loria. "Plasma F2-Isoprostanes and Coronary Artery Calcification: The CARDIA Study". Clinical Chemistry 51, n.º 1 (1 de janeiro de 2005): 125–31. http://dx.doi.org/10.1373/clinchem.2004.037630.
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Abstract Background: Oxidation of lipids in lipoproteins and cells may initiate and enhance the early development of cardiovascular disease. Method and Results: We assayed F2-isoprostanes, oxidation products of arachidonic acid, by gas chromatography–mass spectrometry in a biracial cohort of 2850 young healthy adult men and women. Coronary artery calcification (CAC), a component of coronary artery atherosclerosis, was detectable in 10% of the cohort and appeared to be in its initial stages (Agatston scores <20 in 47% and <100 in 83% of CAC-positive participants). After adjusting for sex, clinical site, age, and race, the presence of any CAC was 24% more likely among those with high vs low concentrations of F2-isoprostanes [odds ratio (OR) = 1.24 per 92.2 pmol/L (32.7 ng/L; 1 SD of F2-isoprostanes); 95% confidence interval (CI), 1.09–1.41]. The OR was only slightly attenuated [1.18 per 92.2 pmol/L (32.7 ng/L); CI, 1.02–1.38] after further adjustment for body mass index, smoking, serum lipids, C-reactive protein, antioxidant supplementation use, diabetes, and blood pressure. As a continuous variable, the Agatston score increased by 6.9% per 92.2 pmol/L (32.7 ng/L) of F2-isoprostane concentration (P <0.01). Whereas CAC prevalence was lower in women than men, mean (SD), F2-isoprostanes were higher in women {190 (108.9) pmol/L [67.4 (38.6) ng/L]} than in men {140.4 (55.6) pmol/L [49.8 (19.7) ng/L]}. Nevertheless, F2-isoprostanes were associated with an increased risk of CAC in both sexes. Conclusion: This association between increased concentrations of circulating F2-isoprostanes and CAC in young healthy adults supports the hypothesis that oxidative damage is involved in the early development of atherosclerosis.
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Jandrić-Kočić, Marijana. "The importance of polyphenols in the prevention of chronic non-communicable diseases". Zdravstvena zastita 50, n.º 3 (2021): 91–106. http://dx.doi.org/10.5937/zdravzast50-33638.
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Polyphenols are compounds that contain in their structure one or more hydroxyl groups attached directly to one or more aromatic hydrocarbons. They represent one of the most numerous and widespread groups of secondary plant metabolites with more than 8000 polyphenolic structures. Polyphenols are antioxidants that reduce endothelial dysfunction and blood pressure, improve the immune defense, alleviate the inflammatory response, block platelet aggregation and oxidation of low-density lipoproteins. Some studies suggest that there is an indirect link between flavonoid intake and myocardial infarction and coronary heart disease. Dark chocolate, nuts, grapes, red wine and the Mediterranean diet (based on fruits and vegetables, fish and olive oil) are rich in polyphenols and are key in preventing cardiovascular disease. Polyphenols prevent neurodegenerative changes associated with cerebral ischemia. Blueberry anthocyanins have antiatherogenic and anti-inflammatory properties so they have a neuroprotective effect. Red wine extract, rich in anthocyanin, reduces injuries caused by cerebral ischemia. Food intake of polyphenols can reduce hypertension, anti-inflammatory and antioxidant effects, as well as increased production of nitric oxide. The importance of black and green tea in lowering blood pressure is especially pointed out. Further research on polyphenols is needed in order to make as clear recommendations as possible for their general preventive use.
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Holvoet, Paul, Jan Donck, Michèle Landeloos, Els Brouwers, Kristel Luijtens, Jozef Arnout, Emmanuel Lesaffre, Yves Vanrenterghem e Désiré Collen. "Correlation between Oxidized Low Density Lipoproteins and von Willebrand Factor in Chronic Renal Failure". Thrombosis and Haemostasis 76, n.º 05 (1996): 663–69. http://dx.doi.org/10.1055/s-0038-1650639.
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SummaryAn ELISA specific for a wide spectrum of oxidized apo B-100 in OxLDL was developed and applied to blood samples from 27 control subjects, 20 mild chronic renal failure (MCRF) patients, 21 severe chronic renal failure patients on conservative treatment (SCRF) and 56 severe chronic renal failure patients on maintenance hemodialysis (HEMO). Mean levels of OxLDL were 0.59 mg/dl in controls (95% Cl, 0.52-0.66 mg/dl), and were 2.7-fold (p <0.01), 3.1-fold (p <0.001) and 5.4-fold (p <0.001) higher in MCRF, SCRF and HEMO patients, respectively. Levels of von Willebrand factor, a marker of endothelial injury, were 100 percent in controls (95% Cl, 90-110 percent), and were 1.5-fold (p = NS), 1.6-fold (p <0.01) and 2.1-fold (p <0.001) higher in MCRF, SCRF and HEMO patients, respectively. Multiple regression analysis revealed that the extent of renal failure (F = 14; p = 0.0004) accounted for a significant fraction of the variation in OxLDL levels, also after exclusion of patients with evidence of ischemic atherosclerotic disease (F = 21; p = 0.0001). After adjustment for the extent of renal failure, hemodialysis (F = 5.6; p = 0.021) and LDL cholesterol levels (F = 7.1, p = 0.0095) contributed significantly to the variation in OxLDL levels. Whereas the extent of renal failure contributed only marginally to the individual variations in vWF levels (F = 4.1; p = 0.048), these levels correlated significantly with plasma levels of OxLDL (F=26; p=0.0001). In conclusion, atherogenic OxLDL increase progressively during the development of renal failure suggesting that the oxidation of LDL may be associated with endothelial injury and atherogenesis in these patients.
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Farinazzi-Machado, Flavia Maria Vasques. "Can the consumption of Seeds, Leaves and Fruit Peels avoid the risk factors for Cardiovascular Disorders?" International Journal of Nutrology 10, n.º 2 (12 de abril de 2017): 37. http://dx.doi.org/10.22565/ijn.v10i2.270.
Texto completo da fonteResumo:
Changes in the feeding pattern of the population have recently led to a greater occurrence of<br />cardiovascular risk factors that contribute to a high rate of morbidity and mortality worldwide. The<br />presence of beneficial bioactive compounds in fruits and processed sub-products have proven to have<br />a negative association with risk factors, such as blood pressure reduction, plasmatic lipoproteins control<br />and increased resistance of LDL-c to oxidation, in addition to glycemic control and antioxidant effects.<br />The aim of this review is to show that several studies have demonstrated many different chemical<br />compounds in seeds, leaves and fruit peels, including their metabolic and physiologic effects on the risk<br />factors of cardiovascular diseases. We reviewed the relevant literature by searching English-language<br />publications in Pubmed, Google Scholar, Scielo and Lilacs, and references from relevant articles<br />published since 2010, especially in the last five years. Eighty-seven relevant articles were included.
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Vendrame, Felipe, Sara T. O. Saad, Fernando F. Costa e Kleber Yotsumoto Fertrin. "Circulating Lipoprotein Concentrations Correlate with Total but Not Free Heme in Different Sickle Cell Disease Genotypes". Blood 126, n.º 23 (3 de dezembro de 2015): 4580. http://dx.doi.org/10.1182/blood.v126.23.4580.4580.
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Abstract In chronic hemolytic states, hemoglobin is released in the bloodstream and free heme is formed upon hemoglobin oxidation. Free heme has been shown to trigger vaso-occlusion in animal models of sickle cell disease (SCD) by activating endothelial cells through toll-like receptor 4 (TLR4). Serum levels of glycoproteins specialized in clearing hemoglobin and heme, such as haptoglobin and hemopexin, are typically depleted in SCD plasma. High-density (HDL) and low-density lipoproteins (LDL) can also bind heme and work as the first line of defense against heme toxicity. Heme can react with LDL and generate oxidized LDL (ox-LDL), another TLR4 ligand.We aimed to investigate the importance of lipoproteins as heme scavengers by comparing SCD patients with homozygous sickle cell anemia (SS) patients and double heterozygous hemoglobin SC disease (SC) patients, who present with higher and lower hemolytic rates, respectively. Eighty-three patients (aged 18-68 years old, 44 female) participated in this study: 43 SS (12 receiving hydroxyurea - HU) and 40 SC. Exclusion criteria were pregnancy, blood transfusion, pain crisis, or use of lipid lowering drugs in the past 3 months. Peripheral venous blood samples were collected in tubes with EDTA for complete blood counts and without antiocoagulant for serum separation after centrifugation at 500g for 20 min. Serum lactate dehydrogenase, total cholesterol and HDL were measured by conventional enzymatic-colorimetric methods on a Roche Hitachi Modular automation system (Roche, Germany). LDL was calculated by Friedewald equation. Serum oxidized LDL (ox-LDL), total and free heme were determined with commercially available ELISA assays (Mercodia Oxidized LDL ELISA, Heme QuantiChrom Assay, Bioassay Systems, USA). Statistical analysis was performed with SPSS v.22.0. LDH and reticulocyte count were significantly higher in SS patients than SC, and hemoglobin was significantly lower (P=0.001). Total heme was significantly higher in SS patients taking HU (SSHU) (90 ± 59 mM) compared with SC patients (66 ± 18 mM), P=0.01. Total cholesterol was higher in SC than in SS patients, 141 ± 28 vs. 107 ± 20 mg/dL, respectively, P =0.01). We found no significant differences between groups regarding LDL (P=0.08), HDL (P=0.10), ox-LDL (P=0.52). Total heme correlated negatively with total cholesterol (r=-0.33, P=0.037) and HDL (r=-0.49, P=0.001) in the whole population, regardless of genotype or treatment with HU. Surprisingly, free heme did not differ between SS, SSHU, or SC groups of patients (P=0.19), and did not correlate with cholesterol levels. The negative correlation between total heme and total cholesterol supports that lipoproteins contribute to defend the body against heme toxicity. Despite HDL, LDL, and ox-LDL not being significantly different among the groups, the stronger negative correlation between total heme and HDL suggests that this cholesterol fraction may be more important in heme scavenging. We hypothesize that more intense hemolysis may lead to the production of heme capable of oxidizing lipoproteins, which can then be rapidly cleared by macrophages, explaining hypocholesterolemia in SS patients. Similar concentrations of free heme and ox-LDL in all groups suggests that, in steady state, their concentrations are kept relatively constant regardless of hemolytic rate. Since circulating concentrations of these TLR4 ligands did not differ between SC and SS patients in our study, this might indicate that the contribution of hemolysis to endothelial dysfunction and to differences in severity and in the variety of complications between these genotypes may be better explained by TLR4 activation by bound heme rather than by activation by free heme or ox-LDL. Financial support: FAPESP/CAPES/CNPq Disclosures No relevant conflicts of interest to declare.