Journal articles: 'Advanced lipoxidation end product'

1

Pamplona, Reinald. "Advanced lipoxidation end-products." Chemico-Biological Interactions 192, no. 1-2 (June 2011): 14–20. http://dx.doi.org/10.1016/j.cbi.2011.01.007.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

Ghodsi, Ramin, Sorayya Kheirouri, and Rahmat Nosrati. "Carnosine supplementation does not affect serum concentrations of advanced glycation and precursors of lipoxidation end products in autism: a randomized controlled clinical trial." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 56, no. 1 (September 6, 2018): 148–54. http://dx.doi.org/10.1177/0004563218796860.

Full text

Abstract:

Background Abundant evidence indicate the increased levels of oxidative stress in patients with autism. Advanced glycation end products and advanced lipoxidation end products and their precursors play a major role in increased oxidative stress in numerous metabolic and neurologic diseases. Carnosine is a natural dipeptide with antiglycation effects. The aim of this trial was to examine the effects of carnosine supplementation on the advanced glycation end products and the precursors of advanced lipoxidation end products in patients with autism. Method This randomized double-blind, placebo-controlled clinical trial was conducted on 36 autistic children, 18 in the carnosine group and 18 in the placebo group. The groups received a daily supplement of 500 mg carnosine or placebo for two months, respectively. Plasma concentrations of glycation and precursors of lipoxidation markers were evaluated by enzyme-linked immunosorbent assay method. Results In all, 63.9% of the autistic children had normal nutritional status. Carnosine supplementation did not significantly alter plasma concentrations of advanced glycation end products and precursors of advanced lipoxidation end products in autistic children. Conclusion The findings indicate that supplementation of carnosine could not change advanced glycation end products and precursor of advanced lipoxidation end products in autistic children.

APA, Harvard, Vancouver, ISO, and other styles

3

MIYATA, TOSHIO, KIYOSHI KUROKAWA, and CHARLES VAN YPERSELE DE STRIHOU. "Advanced Glycation and Lipoxidation End Products." Journal of the American Society of Nephrology 11, no. 9 (September 2000): 1744–52. http://dx.doi.org/10.1681/asn.v1191744.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Jové, Mariona, Natàlia Mota-Martorell, Irene Pradas, Meritxell Martín-Gari, Victoria Ayala, and Reinald Pamplona. "The Advanced Lipoxidation End-Product Malondialdehyde-Lysine in Aging and Longevity." Antioxidants 9, no. 11 (November 15, 2020): 1132. http://dx.doi.org/10.3390/antiox9111132.

Full text

Abstract:

The nonenzymatic adduction of malondialdehyde (MDA) to the protein amino groups leads to the formation of malondialdehyde-lysine (MDALys). The degree of unsaturation of biological membranes and the intracellular oxidative conditions are the main factors that modulate MDALys formation. The low concentration of this modification in the different cellular components, found in a wide diversity of tissues and animal species, is indicative of the presence of a complex network of cellular protection mechanisms that avoid its cytotoxic effects. In this review, we will focus on the chemistry of this lipoxidation-derived protein modification, the specificity of MDALys formation in proteins, the methodology used for its detection and quantification, the MDA-lipoxidized proteome, the metabolism of MDA-modified proteins, and the detrimental effects of this protein modification. We also propose that MDALys is an indicator of the rate of aging based on findings which demonstrate that (i) MDALys accumulates in tissues with age, (ii) the lower the concentration of MDALys the greater the longevity of the animal species, and (iii) its concentration is attenuated by anti-aging nutritional and pharmacological interventions.

APA, Harvard, Vancouver, ISO, and other styles

5

MIYATA, TOSHIO, YASUHIKO UEDA, KOICHI ASAHI, YUKO IZUHARA, REIKO INAGI, AKIRA SAITO, CHARLES VAN YPERSELE DE STRIHOU, and KIYOSHI KUROKAWA. "Mechanism of the Inhibitory Effect of OPB-9195 [(±)-2-Isopropylidenehydrazono-4-oxo-thiazolidin-5-ylacetanilide] on Advanced Glycation End Product and Advanced Lipoxidation End Product Formation." Journal of the American Society of Nephrology 11, no. 9 (September 2000): 1719–25. http://dx.doi.org/10.1681/asn.v1191719.

Full text

Abstract:

Abstract.The accumulation in uremic plasma of reactive carbonyl compounds (RCO) derived from both carbohydrates and lipids (“carbonyl stress”) contributes to uremic toxicity by accelerating the advanced glycation and lipoxidation of proteins. It was previously demonstrated that OPB-9195 [(±)-2-isopropylidenehydrazono-4-oxo-thiazolidin-5-ylacetanilide] inhibited thein vitroformation of advanced glycation end products (AGE) in uremic plasma. This study was designed to elucidate the mechanism of action of OPB-9195 by further delineating the AGE and advanced lipoxidation end product (ALE) precursors targeted by this drug. The inhibitory effects of OPB-9195 on the formation of two AGE (Nϵ-carboxymethyllysine and pentosidine) on bovine serum albumin incubated with various AGE precursors were examined. Inhibition ofNϵ-carboxymethyllysine and pentosidine formation with OPB-9195 was more efficient than with aminoguanidine. OPB-9195 also proved effective in blocking the carbonyl amine chemical processes involved in the formation of two ALE (malondial-dehyde-lysine and 4-hydroxynonenal-protein adduct). The efficiency of OPB-9195 was similar to that of aminoguanidine. When glucose-based peritoneal dialysis fluid was incubated in the presence of OPB-9195, a similar inhibition of AGE formation was observed. The direct effect of OPB-9195 on major glucose-derived RCO in peritoneal dialysis fluids was then evaluated. The effects of OPB-9195 could be accounted for by its ability to trap RCO. The concentrations of three major glucose-derived RCO (glyoxal, methylglyoxal, and 3-deoxy-glucosone) were significantly lower in the presence of OPB-9195 than in its absence. Aminoguanidine had a similar effect. In conclusion, OPB-9195 inhibits both AGE and ALE formation, probably through its ability to trap RCO. OPB-9195 might prove to be a useful tool to inhibit some of the effects of RCO-related uremic toxicity.

APA, Harvard, Vancouver, ISO, and other styles

6

Shanmugam, N., J. L. Figarola, Y. Li, P. M. Swiderski, S. Rahbar, and R. Natarajan. "Proinflammatory Effects of Advanced Lipoxidation End Products in Monocytes." Diabetes 57, no. 4 (November 14, 2007): 879–88. http://dx.doi.org/10.2337/db07-1204.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

STROMAN, M. L., T. O. METZ, S. R. THORPE, and J. W. BAYNES. "Cleavage of Dicarbonyl Compounds by the Advanced Glycation/Lipoxidation End Product Inhibitor Pyridoxamine." Annals of the New York Academy of Sciences 1043, no. 1 (June 2005): 946. http://dx.doi.org/10.1196/annals.1333.160.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Spickett, Corinne M., and Andrew R. Pitt. "Modification of proteins by reactive lipid oxidation products and biochemical effects of lipoxidation." Essays in Biochemistry 64, no. 1 (December 23, 2019): 19–31. http://dx.doi.org/10.1042/ebc20190058.

Full text

Abstract:

Abstract Lipid oxidation results in the formation of many reactive products, such as small aldehydes, substituted alkenals, and cyclopentenone prostaglandins, which are all able to form covalent adducts with nucleophilic residues of proteins. This process is called lipoxidation, and the resulting adducts are called advanced lipoxidation end products (ALEs), by analogy with the formation of advanced glycoxidation end products from oxidized sugars. Modification of proteins by reactive oxidized lipids leads to structural changes such as increased β-sheet conformation, which tends to result in amyloid-like structures and oligomerization, or unfolding and aggregation. Reaction with catalytic cysteines is often responsible for the loss of enzymatic activity in lipoxidized proteins, although inhibition may also occur through conformational changes at more distant sites affecting substrate binding or regulation. On the other hand, a few proteins are activated by lipoxidation-induced oligomerization or interactions, leading to increased downstream signalling. At the cellular level, it is clear that some proteins are much more susceptible to lipoxidation than others. ALEs affect cell metabolism, protein–protein interactions, protein turnover via the proteasome, and cell viability. Evidence is building that they play roles in both physiological and pathological situations, and inhibiting ALE formation can have beneficial effects.

APA, Harvard, Vancouver, ISO, and other styles

9

Aldini, Giancarlo, Giulio Vistoli, Milan Stefek, N. Chondrogianni, Tilman Grune, Jolanta Sereikaite, Izabela Sadowska-Bartosz, and Grzegorz Bartosz. "Molecular strategies to prevent, inhibit, and degrade advanced glycoxidation and advanced lipoxidation end products." Free Radical Research 47, sup1 (May 7, 2013): 93–137. http://dx.doi.org/10.3109/10715762.2013.792926.

Full text

APA, Harvard, Vancouver, ISO, and other styles

10

Miyata, Toshio, Akira Saito, Kiyoshi Kurokawa, and Charles van Ypersele de Strihou. "Advanced glycation and lipoxidation end products: reactive carbonyl compounds‐related uraemic toxicity." Nephrology Dialysis Transplantation 16, suppl_4 (June 2, 2001): 8–11. http://dx.doi.org/10.1093/ndt/16.suppl_4.8.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Ghodsi, Ramin. "Carnosine Effect on Advanced Lipoxidation End-Products: a Brief Review on Tissues." Current Pharmacology Reports 5, no. 4 (June 6, 2019): 214–18. http://dx.doi.org/10.1007/s40495-019-00188-3.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Ames, Jennifer M. "Mass spectrometry to detect the site specificity of advanced glycation/lipoxidation end-product formation on protein: some challenges and solutions." Biochemical Society Transactions 36, no. 5 (September 19, 2008): 1051–54. http://dx.doi.org/10.1042/bst0361051.

Full text

Abstract:

Formation of AGEs (advanced glycation end-products) and ALEs (advanced lipoxidation end-products) on proteins is associated with aging and various diseases of oxidative stress, notably diabetes and its complications. Modification of protein to AGE/ALEs is known to be site-directed and this has potential implications for protein functionality and design of AGE/ALE inhibitors. Determination of the site-specificity of modification is achieved most efficiently by MS. The present paper summarizes some of the challenges that need to be addressed when determining the site-specificity of AGE/ALE formation on protein by MS, using the protein RNase as an example. The following topics are discussed: formation and significance of AGE/ALEs, location of glycated peptides, enzymic digestion of glycated peptides and selection of mass spectrometric settings of analysis for glycated peptides.

APA, Harvard, Vancouver, ISO, and other styles

13

Bayarsaikhan, Govigerel, Delger Bayarsaikhan, Jaewon Lee, and Bonghee Lee. "Targeting Scavenger Receptors in Inflammatory Disorders and Oxidative Stress." Antioxidants 11, no. 5 (May 9, 2022): 936. http://dx.doi.org/10.3390/antiox11050936.

Full text

Abstract:

Oxidative stress and inflammation cannot be considered as diseases themselves; however, they are major risk factors for the development and progression of the pathogenesis underlying many illnesses, such as cancer, neurological disorders (including Alzheimer’s disease and Parkinson’s disease), autoimmune and metabolic disorders, etc. According to the results obtained from extensive studies, oxidative stress–induced biomolecules, such as advanced oxidation protein products, advanced glycation end products, and advanced lipoxidation end products, are critical for an accelerated level of inflammation and oxidative stress–induced cellular damage, as reflected in their strong affinity to a wide range of scavenger receptors. Based on the limitations of antioxidative and anti-inflammatory molecules in practical applications, targeting such interactions between harmful molecules and their cellular receptors/signaling with advances in gene engineering technology, such as CRISPR or TALEN, may prove to be a safe and effective alternative. In this review, we summarize the findings of recent studies focused on the deletion of scavenger receptors under oxidative stress as a development in the therapeutic approaches against the diseases linked to inflammation and the contribution of advanced glycation end products (AGEs), advanced lipid peroxidation products (ALEs), and advanced oxidation protein products (AOPPs).

APA, Harvard, Vancouver, ISO, and other styles

14

Bengmark, Stig. "Advanced Glycation and Lipoxidation End Products–Amplifiers of Inflammation: The Role of Food." Journal of Parenteral and Enteral Nutrition 31, no. 5 (September 2007): 430–40. http://dx.doi.org/10.1177/0148607107031005430.

Full text

APA, Harvard, Vancouver, ISO, and other styles

15

Sarkar, Pinaki, Kaushik Kar, Mohan Chandra Mondal, Indrani Chakraborty, and Manoj Kar. "Elevated Level of Carbonyl Compounds Correlates with Insulin Resistance in Type 2 Diabetes." Annals of the Academy of Medicine, Singapore 39, no. 12 (December 15, 2010): 909–12. http://dx.doi.org/10.47102/annals-acadmedsg.v39n12p909.

Full text

Abstract:

Introduction: Recent periodicals direct that reactive carbonyl compounds are formed due to existing oxidative stress in type 2 diabetes mellitus, which further nonenzymatically react with proteins and lipids to form irreversible advanced glycation end products (AGE) and advanced lipoxidation end products (ALE). In type 2 diabetes mellitus, insulin resistance plays a pivotal role in hyperglycaemia. In this study, we tried to find the relation between insulin resistance and carbonyl stress. Materials and Methods: Forty-seven patients of type 2 diabetes mellitus (age 51 ± 5.06 years) were selected and fasting plasma glucose, serum insulin, total carbonyl compounds, HbA1c, thiobarbituric acid reacting substances (TBARS) and Trolox equivalent antioxidant capacity (TEAC) were estimated using standard protocols. Homeostatic model assessment of insulin resistance (HOMA-IR) was evaluated from fasting plasma glucose and serum insulin levels. Results: We found highly significant correlations of carbonyl compounds with HOMA-IR, fasting plasma glucose and glycated haemoglobin (HbA1c). Correlations of lipid peroxidation end product, TBARS were not so significant. Conclusion: Findings from this study indicate that the level of carbonyl compounds can be a biomarker of insulin resistance in type 2 diabetes mellitus. Keywords: Carbonyl stress, HOMA-IR, Oxidative stress

APA, Harvard, Vancouver, ISO, and other styles

16

Curtis, T. M., R. Hamilton, P. H. Yong, C. M. McVicar, A. Berner, R. Pringle, K. Uchida, R. Nagai, S. Brockbank, and A. W. Stitt. "Müller glial dysfunction during diabetic retinopathy in rats is linked to accumulation of advanced glycation end-products and advanced lipoxidation end-products." Diabetologia 54, no. 3 (November 30, 2010): 690–98. http://dx.doi.org/10.1007/s00125-010-1971-x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

17

Faruqui, Tabrez, Mohd Sajid Khan, Yusuf Akhter, Salman Khan, Zeeshan Rafi, Mohd Saeed, Ihn Han, Eun-Ha Choi, and Dharmendra Kumar Yadav. "RAGE Inhibitors for Targeted Therapy of Cancer: A Comprehensive Review." International Journal of Molecular Sciences 24, no. 1 (December 23, 2022): 266. http://dx.doi.org/10.3390/ijms24010266.

Full text

Abstract:

The receptor for advanced glycation end products (RAGE) is a member of the immunoglobulin family that is overexpressed in several cancers. RAGE is highly expressed in the lung, and its expression increases proportionally at the site of inflammation. This receptor can bind a variety of ligands, including advanced glycation end products, high mobility group box 1, S100 proteins, adhesion molecules, complement components, advanced lipoxidation end products, lipopolysaccharides, and other molecules that mediate cellular responses related to acute and chronic inflammation. RAGE serves as an important node for the initiation and stimulation of cell stress and growth signaling mechanisms that promote carcinogenesis, tumor propagation, and metastatic potential. In this review, we discuss different aspects of RAGE and its prominent ligands implicated in cancer pathogenesis and describe current findings that provide insights into the significant role played by RAGE in cancer. Cancer development can be hindered by inhibiting the interaction of RAGE with its ligands, and this could provide an effective strategy for cancer treatment.

APA, Harvard, Vancouver, ISO, and other styles

18

Kang, Z., H. Li, G. Li, and D. Yin. "Reaction of pyridoxamine with malondialdehyde: Mechanism of inhibition of formation of advanced lipoxidation end-products." Amino Acids 30, no. 1 (July 5, 2005): 55–61. http://dx.doi.org/10.1007/s00726-005-0209-6.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Pereira, Evelyn Nunes Goulart da Silva, Beatriz Peres de Araujo, Karine Lino Rodrigues, Raquel Rangel Silvares, Carolina Souza Machado Martins, Edgar Eduardo Ilaquita Flores, Caroline Fernandes-Santos, and Anissa Daliry. "Simvastatin Improves Microcirculatory Function in Nonalcoholic Fatty Liver Disease and Downregulates Oxidative and ALE-RAGE Stress." Nutrients 14, no. 3 (February 8, 2022): 716. http://dx.doi.org/10.3390/nu14030716.

Full text

Abstract:

Increased reactive oxidative stress, lipid peroxidation, inflammation, and fibrosis, which contribute to tissue damage and development and progression of nonalcoholic liver disease (NAFLD), play important roles in microcirculatory disorders. We investigated the effect of the modulatory properties of simvastatin (SV) on the liver and adipose tissue microcirculation as well as metabolic and oxidative stress parameters, including the advanced lipoxidation end product–receptors of advanced glycation end products (ALE-RAGE) pathway. SV was administered to an NAFLD model constructed using a high-fat–high-carbohydrate diet (HFHC). HFHC caused metabolic changes indicative of nonalcoholic steatohepatitis; treatment with SV protected the mice from developing NAFLD. SV prevented microcirculatory dysfunction in HFHC-fed mice, as evidenced by decreased leukocyte recruitment to hepatic and fat microcirculation, decreased hepatic stellate cell activation, and improved hepatic capillary network architecture and density. SV restored basal microvascular blood flow in the liver and adipose tissue and restored the endothelium-dependent vasodilatory response of adipose tissue to acetylcholine. SV treatment restored antioxidant enzyme activity and decreased lipid peroxidation, ALE-RAGE pathway activation, steatosis, fibrosis, and inflammatory parameters. Thus, SV may improve microcirculatory function in NAFLD by downregulating oxidative and ALE-RAGE stress and improving steatosis, fibrosis, and inflammatory parameters.

APA, Harvard, Vancouver, ISO, and other styles

20

Vistoli, G., D. De Maddis, A. Cipak, N. Zarkovic, M. Carini, and G. Aldini. "Advanced glycoxidation and lipoxidation end products (AGEs and ALEs): an overview of their mechanisms of formation." Free Radical Research 47, sup1 (June 17, 2013): 3–27. http://dx.doi.org/10.3109/10715762.2013.815348.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Januszewski, A. S., N. L. Alderson, T. O. Metz, S. R. Thorpe, and J. W. Baynes. "Role of lipids in chemical modification of proteins and development of complications in diabetes." Biochemical Society Transactions 31, no. 6 (December 1, 2003): 1413–16. http://dx.doi.org/10.1042/bst0311413.

Full text

Abstract:

Hyperglycaemia is the major risk factor for the development of complications in both Type I and Type II diabetes; however, there is growing evidence from several clinical trials that dyslipidaemia, including hypertriglyceridaemia, is a significant and independent risk factor for diabetic complications. In this paper, we propose that chemical modification of proteins by lipids may be a underlying pathogenic mechanism linking dyslipidaemia to diabetic complications. Thus the major AGEs (advanced glycation end-products) in tissues, such as carboxymethyl-lysine, carboxyethyl-lysine and hydroimidazolones, may, in fact, be ALEs (advanced lipoxidation end-products), derived from lipids. Increased lipid peroxidation and accelerated ALE formation, possibly catalysed by hyperglycaemia and oxidative stress, may be the mechanistic link between dyslipidaemia and diabetic complications. If correct, this proposal would suggest that inhibition or reversal of glycation, which is a central theme of this symposium, may not be sufficient for protection against diabetic complications.

APA, Harvard, Vancouver, ISO, and other styles

22

Iacobini, Carla, Stefano Menini, Carlo Ricci, Angela Scipioni, Viola Sansoni, Giulia Mazzitelli, Samantha Cordone, et al. "Advanced lipoxidation end‐products mediate lipid‐induced glomerular injury: role of receptor‐mediated mechanisms." Journal of Pathology 218, no. 3 (July 2009): 360–69. http://dx.doi.org/10.1002/path.2536.

Full text

APA, Harvard, Vancouver, ISO, and other styles

23

Deng, Yan, Lijian Xu, Xin Zeng, Zhiyang Li, Binbing Qin, and Nongyue He. "New Perspective of GABA as an Inhibitor of Formation of Advanced Lipoxidation End-Products: It's Interaction with Malondiadehyde." Journal of Biomedical Nanotechnology 6, no. 4 (August 1, 2010): 318–24. http://dx.doi.org/10.1166/jbn.2010.1130.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Mol, Marco, Genny Degani, Crescenzo Coppa, Giovanna Baron, Laura Popolo, Marina Carini, Giancarlo Aldini, Giulio Vistoli, and Alessandra Altomare. "Advanced lipoxidation end products (ALEs) as RAGE binders: Mass spectrometric and computational studies to explain the reasons why." Redox Biology 23 (May 2019): 101083. http://dx.doi.org/10.1016/j.redox.2018.101083.

Full text

APA, Harvard, Vancouver, ISO, and other styles

25

Moldogazieva, Nurbubu T., Innokenty M. Mokhosoev, Tatiana I. Mel’nikova, Yuri B. Porozov, and Alexander A. Terentiev. "Oxidative Stress and Advanced Lipoxidation and Glycation End Products (ALEs and AGEs) in Aging and Age-Related Diseases." Oxidative Medicine and Cellular Longevity 2019 (August 14, 2019): 1–14. http://dx.doi.org/10.1155/2019/3085756.

Full text

Abstract:

Oxidative stress is a consequence of the use of oxygen in aerobic respiration by living organisms and is denoted as a persistent condition of an imbalance between the generation of reactive oxygen species (ROS) and the ability of the endogenous antioxidant system (AOS) to detoxify them. The oxidative stress theory has been confirmed in many animal studies, which demonstrated that the maintenance of cellular homeostasis and biomolecular stability and integrity is crucial for cellular longevity and successful aging. Mitochondrial dysfunction, impaired protein homeostasis (proteostasis) network, alteration in the activities of transcription factors such as Nrf2 and NF-κB, and disturbances in the protein quality control machinery that includes molecular chaperones, ubiquitin-proteasome system (UPS), and autophagy/lysosome pathway have been observed during aging and age-related chronic diseases. The accumulation of ROS under oxidative stress conditions results in the induction of lipid peroxidation and glycoxidation reactions, which leads to the elevated endogenous production of reactive aldehydes and their derivatives such as glyoxal, methylglyoxal (MG), malonic dialdehyde (MDA), and 4-hydroxy-2-nonenal (HNE) giving rise to advanced lipoxidation and glycation end products (ALEs and AGEs, respectively). Both ALEs and AGEs play key roles in cellular response to oxidative stress stimuli through the regulation of a variety of cell signaling pathways. However, elevated ALE and AGE production leads to protein cross-linking and aggregation resulting in an alteration in cell signaling and functioning which causes cell damage and death. This is implicated in aging and various age-related chronic pathologies such as inflammation, neurodegenerative diseases, atherosclerosis, and vascular complications of diabetes mellitus. In the present review, we discuss experimental data evidencing the impairment in cellular functions caused by AGE/ALE accumulation under oxidative stress conditions. We focused on the implications of ALEs/AGEs in aging and age-related diseases to demonstrate that the identification of cellular dysfunctions involved in disease initiation and progression can serve as a basis for the discovery of relevant therapeutic agents.

APA, Harvard, Vancouver, ISO, and other styles

26

Li, Wenjuan, Haiyan Gao, Honglei Mu, Hangjun Chen, Xiangjun Fang, Yongjun Zhou, and Fei Tao. "Three different active aldehydes induce the production of advanced lipoxidation end products upon incubation with bovine serum albumin." European Journal of Lipid Science and Technology 117, no. 9 (March 19, 2015): 1432–43. http://dx.doi.org/10.1002/ejlt.201400339.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

Hörl, Walter H. "Hemodialysis Membranes: Interleukins, Biocompatibility, and Middle Molecules." Journal of the American Society of Nephrology 13, suppl 1 (January 2002): S62—S71. http://dx.doi.org/10.1681/asn.v13suppl_1s62.

Full text

Abstract:

ABSTRACT. Maintenance hemodialysis patients display evidence of elevated interleukin-1 (IL-1) and tumor necrosis factor alpha release after stimulation either by contaminated dialysate, bioincompatible membrane material, or both. This release is followed by the stimulated secretion of a large number of other interleukins, particularly IL-6, the cytokine principally responsible for acute-phase protein synthesis. It has been shown that high levels of the circulating proinflammatory cytokines IL-1, tumor necrosis factor alpha, IL-6, and IL-13 are associated with mortality in hemodialysis patients. Essential functions of polymorphonuclear leukocytes—that is, phagocytosis, oxygen species production, upregulation of specific cell surface receptor proteins, or apoptosis—are disturbed in patients with end-stage renal disease. These are further altered as a result of complement activation by the hemodialysis procedure, particularly if bioincompatible dialyzers are used. Polymorphonuclear leukocyte degranulation occurring during extracorporeal circulation does not depend on complement activation but rather on intracellular calcium and the presence or absence of the degranulation inhibitory proteins angiogenin and complement factor D. Clinical signs and symptoms of end-stage renal disease patients are at least in part related to the accumulation of middle molecules such as β2-microglobulin, parathyroid hormone, advanced glycation end products, advanced lipoxidation end products, advanced oxidation protein products (formed as a result of oxidative stress, carbonyl stress, or both), granulocyte inhibitory proteins, or leptin. Currently available membrane materials do not provide long-lasting, effective reduction of middle molecules in patients who require maintenance hemodialysis.

APA, Harvard, Vancouver, ISO, and other styles

28

Pejnovic, Nada. "Galectin-3 In Obesity And Type 2 Diabetes." Serbian Journal of Experimental and Clinical Research 16, no. 4 (December 1, 2015): 273–80. http://dx.doi.org/10.1515/sjecr-2015-0057.

Full text

Abstract:

AbstractGalectin-3 is an important regulator of inflammation and acts as a receptor for advanced-glycation (AGE) and lipoxidation end-products (ALE). Evidence indicates a significant upregulation in circulating levels and visceral adipose tissue production of Galectin-3 in obesity and type 2 diabetes. Recent studies demonstrate development of obesity and dysregulation of glucose metabolism in Galectin-3 “knockout” (KO) mice, which also develop accelerated and more severe pathology in models of atherosclerosis and metabolically-induced kidney damage. Thus, evidence that Galectin-3 is an important player in metabolic disease is accumulating. This review discusses current evidence on the connection between Galectin-3 and metabolic disease, focusing on mechanisms by which this galectin modulates adiposity, glucose metabolism and obesity-associated inflammatory responses.

APA, Harvard, Vancouver, ISO, and other styles

29

Solís-Calero, Christian, Joaquín Ortega-Castro, Juan Frau, and Francisco Muñoz. "Nonenzymatic Reactions above Phospholipid Surfaces of Biological Membranes: Reactivity of Phospholipids and Their Oxidation Derivatives." Oxidative Medicine and Cellular Longevity 2015 (2015): 1–22. http://dx.doi.org/10.1155/2015/319505.

Full text

Abstract:

Phospholipids play multiple and essential roles in cells, as components of biological membranes. Although phospholipid bilayers provide the supporting matrix and surface for many enzymatic reactions, their inherent reactivity and possible catalytic role have not been highlighted. As other biomolecules, phospholipids are frequent targets of nonenzymatic modifications by reactive substances including oxidants and glycating agents which conduct to the formation of advanced lipoxidation end products (ALEs) and advanced glycation end products (AGEs). There are some theoretical studies about the mechanisms of reactions related to these processes on phosphatidylethanolamine surfaces, which hypothesize that cell membrane phospholipids surface environment could enhance some reactions through a catalyst effect. On the other hand, the phospholipid bilayers are susceptible to oxidative damage by oxidant agents as reactive oxygen species (ROS). Molecular dynamics simulations performed on phospholipid bilayers models, which include modified phospholipids by these reactions and subsequent reactions that conduct to formation of ALEs and AGEs, have revealed changes in the molecular interactions and biophysical properties of these bilayers as consequence of these reactions. Then, more studies are desirable which could correlate the biophysics of modified phospholipids with metabolism in processes such as aging and diseases such as diabetes, atherosclerosis, and Alzheimer’s disease.

APA, Harvard, Vancouver, ISO, and other styles

30

Ghodsi, Ramin, and Sorayya Kheirouri. "Positive Association Between Plasma Levels of Advanced Glycation and Precursor of Lipoxidation end Products with Gastrointestinal Problems in Children with Autism." Current Pediatric Reviews 15, no. 3 (December 9, 2019): 184–90. http://dx.doi.org/10.2174/1573396315666190628141333.

Full text

Abstract:

Background: Increased oxidative stress has been reported in autistic patients besides, evidence linking oxidative stress to enhancement of advanced glycation and lipoxidation end products (AGEs and ALEs) and their precursors. Objective: This study aimed to compare the plasma levels of the AGEs and precursors of ALEs in autistic and healthy children and to evaluate their relationship with autism comorbidities. Methods: In this descriptive study, 54 children, 36 autistic and 18 healthy participated. Plasma levels of AGEs and precursors of ALEs were measured by ELISA method. Severity of autism and Gastrointestinal (GI) disorders were measured by GARSII questionnaire and QPGS-ROME III questionnaire, respectively. Results: Plasma levels of AGEs and precursors of ALEs in autistic children were comparable with healthy children. Plasma levels of AGEs and precursor of ALEs were correlated with physical activity and GI disorders in autistic children. A strong association was also found between AGEs and precursors of ALEs. Conclusions: The results indicate that AGEs and ALEs have a strong correlation together but the AGEs and precursor of ALEs in autistic children are not different from healthy children.

APA, Harvard, Vancouver, ISO, and other styles

31

Pérez-Ruiz, Irantzu, Susana Meijide, María-Luisa Hérnandez, Rosaura Navarro, Zaloa Larreategui, Marcos Ferrando, María-Begoña Ruiz-Larrea, and José-Ignacio Ruiz-Sanz. "Analysis of Protein Oxidative Modifications in Follicular Fluid from Fertile Women: Natural Versus Stimulated Cycles." Antioxidants 7, no. 12 (November 27, 2018): 176. http://dx.doi.org/10.3390/antiox7120176.

Full text

Abstract:

Oxidative stress is associated with obstetric complications during ovarian hyperstimulation in women undergoing in vitro fertilization. The follicular fluid contains high levels of proteins, which are the main targets of free radicals. The aim of this work was to determine specific biomarkers of non-enzymatic oxidative modifications of proteins from follicular fluid in vivo, and the effect of ovarian stimulation with gonadotropins on these biomarkers. For this purpose, 27 fertile women underwent both a natural and a stimulated cycle. The biomarkers, glutamic semialdehyde (GSA), aminoadipic semialdehyde (AASA), Nε-(carboxymethyl)lysine (CML), and Nε-(carboxyethyl)lysine (CEL), were measured by gas-liquid chromatography coupled to mass spectrometry. Results showed that follicular fluid contained products of protein modifications by direct metal-catalyzed oxidation (GSA and AASA), glycoxidation (CML and CEL), and lipoxidation (CML). GSA was the most abundant biomarker (91.5%). The levels of CML amounted to 6% of the total lesions and were higher than AASA (1.3%) and CEL (1.2%). In the natural cycle, CEL was significantly lower (p < 0.05) than in the stimulated cycle, suggesting that natural cycles are more protected against protein glycoxidation. These findings are the basis for further research to elucidate the possible relevance of this follicular biomarker of advanced glycation end product in fertility programs.

APA, Harvard, Vancouver, ISO, and other styles

32

Altomare, Alessandra, Giovanna Baron, Marta Balbinot, Alessandro Pedretti, Beatrice Zoanni, Maura Brioschi, Piergiuseppe Agostoni, Marina Carini, Cristina Banfi, and Giancarlo Aldini. "In-Depth AGE and ALE Profiling of Human Albumin in Heart Failure: Ex Vivo Studies." Antioxidants 10, no. 3 (February 27, 2021): 358. http://dx.doi.org/10.3390/antiox10030358.

Full text

Abstract:

Advanced glycation end-products (AGEs) and advanced lipoxidation end-products (ALEs), particularly carboxymethyl-lysine (CML), have been largely proposed as factors involved in the establishment and progression of heart failure (HF). Despite this evidence, the current literature lacks the comprehensive identification and characterization of the plasma AGEs/ALEs involved in HF (untargeted approach). This work provides the first ex vivo high-resolution mass spectrometry (HR-MS) profiling of AGEs/ALEs occurring in human serum albumin (HSA), the most abundant protein in plasma, characterized by several nucleophilic sites and thus representing the main protein substrate for AGE/ALE formation. A set of AGE/ALE adducts in pooled HF-HSA samples was defined, and a semi-quantitative analysis was carried out in order to finally select those presenting in increased amounts in the HF samples with respect to the control condition. These adducts were statistically confirmed by monitoring their content in individual HF samples by applying a targeted approach. Selected AGEs/ALEs proved to be mostly CML derivatives on Lys residues (i.e., CML-Lys12, CML-Lys378, CML-Lys402), and one deoxy-fructosyl derivative on the Lys 389 (DFK-Lys 389). The nature of CML adducts was finally confirmed using immunological methods and in vitro production of such adducts further confirmed by mass spectrometry.

APA, Harvard, Vancouver, ISO, and other styles

33

Iacobini, Carla, Martina Vitale, Jonida Haxhi, Carlo Pesce, Giuseppe Pugliese, and Stefano Menini. "Food-Related Carbonyl Stress in Cardiometabolic and Cancer Risk Linked to Unhealthy Modern Diet." Nutrients 14, no. 5 (March 3, 2022): 1061. http://dx.doi.org/10.3390/nu14051061.

Full text

Abstract:

Carbonyl stress is a condition characterized by an increase in the steady-state levels of reactive carbonyl species (RCS) that leads to accumulation of their irreversible covalent adducts with biological molecules. RCS are generated by the oxidative cleavage and cellular metabolism of lipids and sugars. In addition to causing damage directly, the RCS adducts, advanced glycation end-products (AGEs) and advanced lipoxidation end-products (ALEs), cause additional harm by eliciting chronic inflammation through receptor-mediated mechanisms. Hyperglycemia- and dyslipidemia-induced carbonyl stress plays a role in diabetic cardiovascular complications and diabetes-related cancer risk. Moreover, the increased dietary exposure to AGEs/ALEs could mediate the impact of the modern, highly processed diet on cardiometabolic and cancer risk. Finally, the transient carbonyl stress resulting from supraphysiological postprandial spikes in blood glucose and lipid levels may play a role in acute proinflammatory and proatherogenic changes occurring after a calorie dense meal. These findings underline the potential importance of carbonyl stress as a mediator of the cardiometabolic and cancer risk linked to today’s unhealthy diet. In this review, current knowledge in this field is discussed along with future research courses to offer new insights and open new avenues for therapeutic interventions to prevent diet-associated cardiometabolic disorders and cancer.

APA, Harvard, Vancouver, ISO, and other styles

34

Menini, Stefano, Carla Iacobini, Claudia Blasetti Fantauzzi, and Giuseppe Pugliese. "L-carnosine and its Derivatives as New Therapeutic Agents for the Prevention and Treatment of Vascular Complications of Diabetes." Current Medicinal Chemistry 27, no. 11 (April 23, 2020): 1744–63. http://dx.doi.org/10.2174/0929867326666190711102718.

Full text

Abstract:

Vascular complications are among the most serious manifestations of diabetes. Atherosclerosis is the main cause of reduced life quality and expectancy in diabetics, whereas diabetic nephropathy and retinopathy are the most common causes of end-stage renal disease and blindness. An effective therapeutic approach to prevent vascular complications should counteract the mechanisms of injury. Among them, the toxic effects of Advanced Glycation (AGEs) and Lipoxidation (ALEs) end-products are well-recognized contributors to these sequelae. L-carnosine (β-alanyl-Lhistidine) acts as a quencher of the AGE/ALE precursors Reactive Carbonyl Species (RCS), which are highly reactive aldehydes derived from oxidative and non-oxidative modifications of sugars and lipids. Consistently, L-carnosine was found to be effective in several disease models in which glyco/lipoxidation plays a central pathogenic role. Unfortunately, in humans, L-carnosine is rapidly inactivated by serum carnosinase. Therefore, the search for carnosinase-resistant derivatives of Lcarnosine represents a suitable strategy against carbonyl stress-dependent disorders, particularly diabetic vascular complications. In this review, we present and discuss available data on the efficacy of L-carnosine and its derivatives in preventing vascular complications in rodent models of diabetes and metabolic syndrome. We also discuss genetic findings providing evidence for the involvement of the carnosinase/L-carnosine system in the risk of developing diabetic nephropathy and for preferring the use of carnosinase-resistant compounds in human disease. The availability of therapeutic strategies capable to prevent both long-term glucose toxicity, resulting from insufficient glucoselowering therapy, and lipotoxicity may help reduce the clinical and economic burden of vascular complications of diabetes and related metabolic disorders.

APA, Harvard, Vancouver, ISO, and other styles

35

SUZUKI, DAISUKE, TOSHIO MIYATA, NOBORU SAOTOME, KATSUNORI HORIE, REIKO INAGI, YOSHINARI YASUDA, KOJI UCHIDA, et al. "Immunohistochemical Evidence for an Increased Oxidative Stress and Carbonyl Modification of Proteins in Diabetic Glomerular Lesions." Journal of the American Society of Nephrology 10, no. 4 (April 1999): 822–32. http://dx.doi.org/10.1681/asn.v104822.

Full text

Abstract:

Abstract. Advanced glycation end products (AGE) include a variety of protein adducts whose accumulation has been implicated in tissue damage associated with diabetic nephropathy (DN). It was recently demonstrated that among AGE, glycoxidation products, whose formation is closely linked to oxidation, such as carboxymethyllysine (CML) and pentosidine, accumulate in expanded mesangial matrix and nodular lesions in DN, in colocalization with malondialdehyde-lysine (MDA-lysine), a lipoxidation product, whereas pyrraline, another AGE structure whose deposition is rather independent from oxidative stress, was not found within diabetic glomeruli. Because CML, pentosidine, and MDA-lysine are all formed under oxidative stress by carbonyl amine chemistry between protein amino group and carbonyl compounds, their colocalization suggests a local oxidative stress and increased protein carbonyl modification in diabetic glomerular lesions. To address this hypothesis, human renal tissues from patients with DN or IgA nephropathy were examined with specific antibodies to characterize most, if not all, carbonyl modifications of proteins by autoxidation products of carbohydrates, lipids, and amino acids: CML (derived from carbohydrates, lipids, and amino acid), pentosidine (derived from carbohydrates), MDA-lysine (derived from lipids), 4-hydroxynonenal-protein adduct (derived from lipids), and acrolein-protein adduct (derived from lipids and amino acid). All of the protein adducts were identified in expanded mesangial matrix and nodular lesions in DN. In IgA nephropathy, another primary glomerular disease leading to end-stage renal failure, despite positive staining for MDA-lysine and 4-hydroxynonenal-protein adduct in the expanded mesangial area, CML, pentosidine, and acrolein-protein adduct immunoreactivities were only faint in glomeruli. These data suggest a broad derangement in nonenzymatic biochemistry in diabetic glomerular lesions, and implicate an increased local oxidative stress and carbonyl modification of proteins in diabetic glomerular tissue damage (“carbonyl stress”).

APA, Harvard, Vancouver, ISO, and other styles

36

Wybranowski, Tomasz, Marta Napiórkowska, Maciej Bosek, Jerzy Pyskir, Blanka Ziomkowska, Michał Cyrankiewicz, Małgorzata Pyskir, et al. "Study of Albumin Oxidation in COVID-19 Pneumonia Patients: Possible Mechanisms and Consequences." International Journal of Molecular Sciences 23, no. 17 (September 3, 2022): 10103. http://dx.doi.org/10.3390/ijms231710103.

Full text

Abstract:

Oxidative stress induced by neutrophils and hypoxia in COVID-19 pneumonia leads to albumin modification. This may result in elevated levels of advanced oxidation protein products (AOPPs) and advanced lipoxidation end-products (ALEs) that trigger oxidative bursts of neutrophils and thus participate in cytokine storms, accelerating endothelial lung cell injury, leading to respiratory distress. In this study, sixty-six hospitalized COVID-19 patients with respiratory symptoms were studied. AOPPs-HSA was produced in vitro by treating human serum albumin (HSA) with chloramine T. The interaction of malondialdehyde with HSA was studied using time-resolved fluorescence spectroscopy. The findings revealed a significantly elevated level of AOPPs in COVID-19 pneumonia patients on admission to the hospital and one week later as long as they were in the acute phase of infection when compared with values recorded for the same patients 6- and 12-months post-infection. Significant negative correlations of albumin and positive correlations of AOPPs with, e.g., procalcitonin, D-dimers, lactate dehydrogenase, aspartate transaminase, and radiological scores of computed tomography (HRCT), were observed. The AOPPs/albumin ratio was found to be strongly correlated with D-dimers. We suggest that oxidized albumin could be involved in COVID-19 pathophysiology. Some possible clinical consequences of the modification of albumin are also discussed.

APA, Harvard, Vancouver, ISO, and other styles

37

Didangelos, Triantafyllos, and Aristidis Veves. "Treatment of Diabetic Cardiovascular Autonomic, Peripheral and Painful Neuropathy. Focus on the Treatment of Cardiovascular Autonomic Neuropathy with ACE Inhibitors." Current Vascular Pharmacology 18, no. 2 (January 27, 2020): 158–71. http://dx.doi.org/10.2174/1570161117666190521101342.

Full text

Abstract:

Neuropathies of the peripheral and autonomic nervous systems affect up to half of all people with diabetes mellitus, and are major risk factors for foot ulceration, amputation and cardiovascular dysfunction. Peripheral neuropathies manifest with either painful or painless symptoms, but many patients experience both. Once diagnosed appropriately, painful diabetic neuropathy management presents a unique challenge for physicians and should be considered as a syndrome, clinically distinct from diabetic peripheral neuropathy. The aetiology is multifactorial: metabolic changes in diabetes may directly affect neural tissue and neurodegenerative changes are precipitated by compromised nerve vascular supply. Metabolic changes include the elevated polyol pathway activity, the increased oxidative stress, the formation of advanced glycation and lipoxidation end products, and various pro-inflammatory changes. These mechanisms work in combination and interact in a mutually facilitatory fashion. This review focuses on the current therapies for the management of peripheral and cardiovascular autonomic neuropathy and of painful neuropathy as a distinct entity, based on the current knowledge of diabetic neuropathy. Moreover, the role of ACE inhibition has been explored in the treatment of Cardiovascular Autonomic Neuropathy.

APA, Harvard, Vancouver, ISO, and other styles

38

Ono, Y., K. Mizuno, M. Takahashi, and Y. Miura. "SUPPRESSION OF ADVANCED GLYCATION AND LIPOXIDATION END PRODUCTS BY AN ANGIOTENSIN II TYPE-1 RECEPTOR BLOCKER IN ESSENTIAL HYPERTENSION WITH TYPE-2 DIABETES MELLITUS." Journal of Hypertension 22, Suppl. 1 (February 2004): S185. http://dx.doi.org/10.1097/00004872-200402001-00789.

Full text

APA, Harvard, Vancouver, ISO, and other styles

39

ONO, YOSHIAKI, KENJI MIZUNO, MICHIHIKO TAKAHASHI, YUKIO MIURA, and TSUYOSHI WATANABE. "SUPPRESSION OF ADVANCED GLYCATION AND LIPOXIDATION END PRODUCTS BY ANGIOTENSIN II TYPE-1 RECEPTOR BLOCKER CANDESARTAN IN TYPE 2 DIABETIC PATIENTS WITH ESSENTIAL HYPERTENSION." FUKUSHIMA JOURNAL OF MEDICAL SCIENCE 59, no. 2 (2013): 69–75. http://dx.doi.org/10.5387/fms.59.69.

Full text

APA, Harvard, Vancouver, ISO, and other styles

40

Popkov, Vasily A., Denis N. Silachev, Arthur O. Zalevsky, Dmitry B. Zorov, and Egor Y. Plotnikov. "Mitochondria as a Source and a Target for Uremic Toxins." International Journal of Molecular Sciences 20, no. 12 (June 25, 2019): 3094. http://dx.doi.org/10.3390/ijms20123094.

Full text

Abstract:

Elucidation of molecular and cellular mechanisms of the uremic syndrome is a very challenging task. More than 130 substances are now considered to be “uremic toxins” and represent a very diverse group of molecules. The toxicity of these molecules affects many cellular processes, and expectably, some of them are able to disrupt mitochondrial functioning. However, mitochondria can be the source of uremic toxins as well, as the mitochondrion can be the site of complete synthesis of the toxin, whereas in some scenarios only some enzymes of the pathway of toxin synthesis are localized here. In this review, we discuss the role of mitochondria as both the target and source of pathological processes and toxic compounds during uremia. Our analysis revealed about 30 toxins closely related to mitochondria. Moreover, since mitochondria are key regulators of cellular redox homeostasis, their functioning might directly affect the production of uremic toxins, especially those that are products of oxidation or peroxidation of cellular components, such as aldehydes, advanced glycation end-products, advanced lipoxidation end-products, and reactive carbonyl species. Additionally, as a number of metabolic products can be degraded in the mitochondria, mitochondrial dysfunction would therefore be expected to cause accumulation of such toxins in the organism. Alternatively, many uremic toxins (both made with the participation of mitochondria, and originated from other sources including exogenous) are damaging to mitochondrial components, especially respiratory complexes. As a result, a positive feedback loop emerges, leading to the amplification of the accumulation of uremic solutes. Therefore, uremia leads to the appearance of mitochondria-damaging compounds, and consecutive mitochondrial damage causes a further rise of uremic toxins, whose synthesis is associated with mitochondria. All this makes mitochondrion an important player in the pathogenesis of uremia and draws attention to the possibility of reducing the pathological consequences of uremia by protecting mitochondria and reducing their role in the production of uremic toxins.

APA, Harvard, Vancouver, ISO, and other styles

41

Choudhuri, Subhadip, Pijush Kanti Roy, Bhaskar Mitra, Susruta Sen, Rajarshi Sarkar, Mandrita Das, Debashree Biswas, et al. "Hyperlipidemia-Mediated Increased Advanced Lipoxidation End Products Formation, an Important Factor Associated with Decreased Erythrocyte Glucose-6-Phosphate Dehydrogenase Activity in Mild Nonproliferative Diabetic Retinopathy." Canadian Journal of Diabetes 41, no. 1 (February 2017): 82–89. http://dx.doi.org/10.1016/j.jcjd.2016.07.007.

Full text

APA, Harvard, Vancouver, ISO, and other styles

42

Culbertson, Sean M., Gary D. Enright, and K. U. Ingold. "Synthesis of a Novel Radical Trapping and Carbonyl Group Trapping Anti-AGE Agent: A Pyridoxamine Analogue for Inhibiting Advanced Glycation (AGE) and Lipoxidation (ALE) End Products." Organic Letters 5, no. 15 (July 2003): 2659–62. http://dx.doi.org/10.1021/ol0348147.

Full text

APA, Harvard, Vancouver, ISO, and other styles

43

Miyata, Toshio, Yuko Izuhara, Hideto Sakai, and Kiyoshi Kurokawa. "Carbonyl Stress: Increased Carbonyl Modification of Tissue and Cellular Proteins in Uremia." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 19, no. 2_suppl (February 1999): 58–61. http://dx.doi.org/10.1177/089686089901902s10.

Full text

Abstract:

Advanced glycation end-products (AGEs) are formed during non enzymatic glycation and oxidation (glycoxidation) reactions. This process is accelerated in diabetics owing to hyperglycemia, and it has been implicated in the pathogenesis of diabetic complications. Surprisingly, AGEs increase in normoglycemic uremic patients to a much greater extent than in diabetics. AGE accumulation in uremia cannot be attributed to hyperglycemia nor simply to a decreased removal by glomerular filtration. Recently gathered evidence has suggested that, in uremia, the increased carbonyl compounds derived from carbohydrates and lipids modify proteins not only by glycoxidation reaction but also by lipoxidation reaction (“carbonyl stress”). Carbonyl stress has been implicated in the pathogenesis of long-term uremic complications such as dialysisrelated amyloidosis. With regard to continuous ambulatory peritoneal dialysis (CAPD), the peritoneal cavity appears to be in a state of severe overload of carbonyl compounds derived from CAPD solution containing high glucose, from heat sterilization of the solution, and from uremic circulation. Carbonyl stress might modify not only peritoneal matrix proteins and alter their structures, but also react with mesothelial and endothelial cell surface proteins and initiate a range of inflammatory responses. Carbonyl stress might therefore contribute to the development of peritoneal sclerosis in patients with long-term CAPD.

APA, Harvard, Vancouver, ISO, and other styles

44

Menini, Stefano, Carla Iacobini, Claudia Blasetti Fantauzzi, Carlo M. Pesce, and Giuseppe Pugliese. "Role of Galectin-3 in Obesity and Impaired Glucose Homeostasis." Oxidative Medicine and Cellular Longevity 2016 (2016): 1–7. http://dx.doi.org/10.1155/2016/9618092.

Full text

Abstract:

Galectin-3 is an important modulator of several biological functions. It has been implicated in numerous disease conditions, particularly in the long-term complications of diabetes because of its ability to bind the advanced glycation/lipoxidation end products that accumulate in target organs and exert their toxic effects by triggering proinflammatory and prooxidant pathways. Recent evidence suggests that galectin-3 may also participate in the development of obesity and type 2 diabetes. It has been shown that galectin-3 levels are higher in obese and diabetic individuals and parallel deterioration of glucose homeostasis. Two studies in galectin-3 knockout mice fed a high-fat diet (HFD) have shown increased adiposity and adipose tissue and systemic inflammation associated with altered glucose homeostasis, suggesting that galectin-3 negatively modulates the responsiveness of innate and adaptive immunity to overnutrition. However, these studies have also shown that impaired glucose homeostasis occurs in galectin-3 knockout animals independently of obesity. Moreover, another study reported decreased weight and fat mass in HFD-fed galectin-3 knockout mice.In vitro, galectin-3 was found to stimulate differentiation of preadipocytes into mature adipocytes. Altogether, these data indicate that galectin-3 deserves further attention in order to clarify its role as a potential player and therapeutic target in obesity and type 2 diabetes.

APA, Harvard, Vancouver, ISO, and other styles

45

Deepika, R. Sai, Shashidhar KN, Raveesha A, and Muninarayana C. "Serum Carboxy Methyl Lysine, Insulin Resistance and Sensitivity in Type 2 Diabetes Mellitus and Diabetic Nephropathy Cases; an Observational Study." Biomedical and Pharmacology Journal 13, no. 4 (December 30, 2020): 1987–92. http://dx.doi.org/10.13005/bpj/2077.

Full text

Abstract:

Objective: Diabetes Mellitus (DM) and one of its types; type 2 diabetes mellitus (T2DM) is more prevalent from adolescent across the globe, invariable of heredity and age. Diet restriction shall cope up and help body metabolism to absorb the required nutrition and eliminate the junk out of body under healthy diet. Masking of insulin action on target cells leads to insulin resistance (IR) and decreased insulin sensitivity (IS) resulting in increased glycated products such, glycated hemoglobin, glycated albumin and other glycated macromolecules called Advanced Glycation End products. Along with AGE and diabetic profiling, BMI, insulin and lipid profiling may help elucidate the correlation between CML and glucose metabolism in diabetics and diabetic nephropathy cases. CML is formed by Glycoxidation and lipoxidation. Thereby, main objective of this study includes basic renal profiling was also performed to assess kidney functioning and finding its relation with CML. Results: Correlation of CML with important diabetic and metabolic syndrome parameters were performed, giving a supportive evidence for labeling CML as harmful molecule. CML positively correlated with HbA1c, TG and HOMA IR and negatively correlated with QUICKI in group 2 signifying increased damage to tissues due to collective action of glucose, lipid and insulin resistance. Monitoring plasma CML regularly during follow up along with HbA1c may help keep track on plasma glucose status and its deleterious effects on tissues thereby preventing erosion of tissue and vascular lining.

APA, Harvard, Vancouver, ISO, and other styles

46

Bender, Cecilia, Sarah Straßmann, and Pola Heidrich. "Cellular Antioxidant Effects and Bioavailability of Food Supplements Rich in Hydroxytyrosol." Applied Sciences 11, no. 11 (May 22, 2021): 4763. http://dx.doi.org/10.3390/app11114763.

Full text

Abstract:

The present study evaluates the effect of olive (Olea europaea L.) vegetation water on human cells regarding its antioxidant properties and radical scavenger bioactivities. To this aim, two food supplements containing concentrated olive water in combination with 6% lemon juice or 70% grape juice, respectively, were assessed in different oxidation assays. From the investigated polyphenols, hydroxytyrosol, present in olives and in a lesser extent in grapes, was found to be the most abundant in both formulations, followed by tyrosol and oleuropein for the olive-derived concentrate with lemon juice, and by proanthocyanidins and tyrosol for the olive concentrate with grape juice. Cellular studies suggest that both formulations are effective antioxidants. In particular, the combination of olive and grape extracts showed a remarkable superoxides-, hydroxyl radicals-, and hydrogen peroxides-scavenging activity, while the formulation containing 94% olive concentrate wasmore potent in protecting the cells against lipoxidation. Both products showed a significant and similar effect in preventing advanced glycation end products’ (AGEs) formation. In addition, preliminary data indicate that hydroxytyrosol is absorbed into the human body when administered via these hydrophilic matrices, as confirmed by the urinary excretion of free hydroxytyrosol. Since the availability of phytochemicals largely depends on the vehicle in which they are solved, these findings are of relevance and contribute to supporting the healthful effects here assessed in a cellular environment.

APA, Harvard, Vancouver, ISO, and other styles

47

Iacobini, Carla, Giovanna Oddi, Stefano Menini, Lorena Amadio, Carlo Ricci, Clelia Di Pippo, Mariella Sorcini, Flavia Pricci, Francesco Pugliese, and Giuseppe Pugliese. "Development of age-dependent glomerular lesions in galectin-3/AGE-receptor-3 knockout mice." American Journal of Physiology-Renal Physiology 289, no. 3 (September 2005): F611—F621. http://dx.doi.org/10.1152/ajprenal.00435.2004.

Full text

Abstract:

Aging is characterized by renal functional and structural abnormalities resembling those observed in diabetes. These changes have been related to the progressive accumulation of advanced glycation end-products (AGEs) and cumulative oxidative stress occurring in both conditions. We previously reported that galectin-3 ablation is associated with increased susceptibility to diabetes- and AGE-induced glomerulopathy, thus indicating a protective role of galectin-3 as an AGE receptor. To investigate the role of the AGE/AGE receptor pathway in the pathogenesis of age-related renal disease, we evaluated the development of glomerular lesions in aging galectin-3 knockout (KO) vs. wild-type (WT) mice and their relation to the increased AGE levels and oxidative stress characterizing the aging process. KO mice showed significantly more pronounced age-dependent increases in proteinuria, albuminuria, glomerular sclerosis, and glomerular and mesangial areas, starting at 18 mo, as well as renal extracellular matrix mRNA and protein expression, starting at 12 mo vs. age-matched WT mice. Circulating and renal AGEs, plasma isoprostane 8-epi-PGF2α levels, glomerular content of the glycoxidation and lipoxidation products Nε-carboxymethyllysine and 4-hydroxy-2-nonenal, and renal nuclear factor-κB activity also increased more markedly with age in KO than WT mice. AGE levels correlated significantly with renal functional and structural parameters. These data indicate that aging galectin-3 KO mice develop more pronounced changes in renal function and structure than coeval WT mice, in parallel with a more marked degree of AGE accumulation, oxidative stress, and associated low-grade inflammation, thus supporting the concept that the AGE/AGE receptor pathway is implicated in age-related renal disease.

APA, Harvard, Vancouver, ISO, and other styles

48

Boldyrev, Alexander A., Giancarlo Aldini, and Wim Derave. "Physiology and Pathophysiology of Carnosine." Physiological Reviews 93, no. 4 (October 2013): 1803–45. http://dx.doi.org/10.1152/physrev.00039.2012.

Full text

Abstract:

Carnosine (β-alanyl-l-histidine) was discovered in 1900 as an abundant non-protein nitrogen-containing compound of meat. The dipeptide is not only found in skeletal muscle, but also in other excitable tissues. Most animals, except humans, also possess a methylated variant of carnosine, either anserine or ophidine/balenine, collectively called the histidine-containing dipeptides. This review aims to decipher the physiological roles of carnosine, based on its biochemical properties. The latter include pH-buffering, metal-ion chelation, and antioxidant capacity as well as the capacity to protect against formation of advanced glycation and lipoxidation end-products. For these reasons, the therapeutic potential of carnosine supplementation has been tested in numerous diseases in which ischemic or oxidative stress are involved. For several pathologies, such as diabetes and its complications, ocular disease, aging, and neurological disorders, promising preclinical and clinical results have been obtained. Also the pathophysiological relevance of serum carnosinase, the enzyme actively degrading carnosine into l-histidine and β-alanine, is discussed. The carnosine system has evolved as a pluripotent solution to a number of homeostatic challenges. l-Histidine, and more specifically its imidazole moiety, appears to be the prime bioactive component, whereas β-alanine is mainly regulating the synthesis of the dipeptide. This paper summarizes a century of scientific exploration on the (patho)physiological role of carnosine and related compounds. However, far more experiments in the fields of physiology and related disciplines (biology, pharmacology, genetics, molecular biology, etc.) are required to gain a full understanding of the function and applications of this intriguing molecule.

APA, Harvard, Vancouver, ISO, and other styles

49

Mallipattu, Sandeep K., and Jaime Uribarri. "Advanced glycation end product accumulation." Current Opinion in Nephrology and Hypertension 23, no. 6 (November 2014): 547–54. http://dx.doi.org/10.1097/mnh.0000000000000062.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Vlassara, Helen, Jaime Uribarri, Weijing Cai, and Gary Striker. "Advanced Glycation End Product Homeostasis." Annals of the New York Academy of Sciences 1126, no. 1 (April 2008): 46–52. http://dx.doi.org/10.1196/annals.1433.055.

Full text

APA, Harvard, Vancouver, ISO, and other styles

Journal articles on the topic 'Advanced lipoxidation end product'

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles