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Готові списки джерел за темами / Oxidative stress / Статті в журналах

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Статті в журналах з теми "Oxidative stress"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 23 листопада 2024

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1

Sun, Qi-An, Nageswara Madamanchi, and Marschall Runge. "Oxidative stress, NADPH oxidases, and arteries." Hämostaseologie 36, no. 02 (2016): 77–88. http://dx.doi.org/10.5482/hamo-14-11-0076.

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ZusammenfassungDie Atherosklerose und ihre wichtigsten Komplikationen – Myokardinfarkt und Schlaganfall – sind die Hauptursachen für Tod und Behinderung in den USA und weltweit. Eine dramatische Zunahme bei Adipositas und Diabetes mellitus wird wahrscheinlich auch in Zukunft zu einer hohen Prävalenz kardiovaskulärer Erkrankungen (CVD) und deren Auswirkungen auf das Gesundheitswesen führen. Große Fortschritte gibt es bei der Entwicklung neuer Therapien zur Senkung der Inzidenz von Atherosklerose und CVD, besonders bei der Behandlung der Hypercholesterinämie und Hypertonie. Der gemeinsame mechanistische Nenner bei vielen Risikofaktoren für CVD ist oxidativer Stress. Erst seit kurzem verfügen wir über Methoden, um die Schnittstelle zwischen oxidativem Stress und CVD im Tiermodell zu untersuchen. Die wichtigste Quelle für reaktive Sauerstoffspezies (und damit für oxidativen Stress) in vaskulären Zellen sind die Formen der Nicotin - amidadenindinukleotidphosphat-Oxidase (NADPH-Oxidase). Die jüngsten Studien belegen eindeutig, dass 1. NADPH-Oxidasen im Tiermodell von grundlegender Bedeutung für Atherosklerose und Hypertonie sind und 2. der vaskuläre oxidative Stress, angesichts der gewebespezifischen Expression wichtiger Bestandteile der NADPH-Oxidase, ein Ziel bei der Prävention der CVD sein könnte.

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2

Naziya, Dr Saba. "MITOCHONDRIAL CARBON STRESS AND OXIDATIVE STRESS: IMPLICATIONS FOR HUMAN HEALTH." Era's Journal of Medical Research 11, no. 1 (June 2024): 85–92. http://dx.doi.org/10.24041/ejmr2024.14.

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Avital component of cellular redox equilibrium, mitochondria also play a crucial role in the synthesis of energy within cells. Disturbances in the metabolism of carbon inside the mitochondria may cause malfunction and oxidative stress, which in turn may contribute to the etiology of a number of human diseases. This is supported by newly emerging research. The interaction of oxidative stress and mitochondrial carbon stress is examined in this review, with particular attention on how these effects affect human health. We go over the processes that underlie oxidative stress caused by mitochondrial carbon stress and its consequences for various physiological processes such as aging, cancer, metabolic disorders, and neurodegenerative illnesses. We also highlight prospective therapeutic approaches that focus on redox balance and mitochondrial function in order to lessen the harmful effects of oxidative stress and mitochondrial carbon stress on human health.

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3

Dorovskikh, V. A., N. V. Simonova, E. Yu Yurtaeva, R. A. Anokhina, and M. A. Shtarberg. "PHYTOCORRECTION OF OXIDATIVE STRESS IN EXPERIMENT." Amur Medical Journal, no. 15-16 (2016): 35–37. http://dx.doi.org/10.22448/amj.2016.15-16.35-37.

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4

Nsonwu, Magnus, SJ Ozims, and JK Nnodim. "Perspective of Cataract and Oxidative Stress." Series of Clinical and Biomedical Research 1, no. 1 (March 23, 2024): 1–10. http://dx.doi.org/10.54178/2997-2701.v1i1a1994.

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One of the main causes of blindness is the multifactorial condition known as cataract. It is believed that oxidative stress plays a significant role in starting the cataractogenesis process. Today, it is a well-established fact that oxidative stress plays a role in both diabetes-induced cataract (diabetic) and age-related cataract (senile). The most likely cause of oxidative damage to the lens is a compromised antioxidant defense system brought on by age and diabetes-related increases in reactive oxygen species (ROS) production. The main factor contributing to cataract formation is systemic oxidative stress, which is produced externally to the lens. An imbalance between pro- and antioxidant-oxidants leads to oxidative stress. It is essential to eliminate hazardous free radicals because they are a byproduct of normal metabolism. Globally, cataracts are the primary cause of blindness. Oxidative stress is the direct cause of the lens’s opacity. Although age is the main cause of cataracts, diabetes is also a common cause, as higher superoxide levels in the mitochondria arise from hyperglycemia. This review will look into ultraviolet (UV) light, diabetes, and diet (fat, alcohol, and vitamins) as risk factors for cataracts.

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5

Malenica, Maja, and Neven Meseldžić. "Oxidative stress and obesity." Arhiv za farmaciju 72, no. 2 (2022): 166–83. http://dx.doi.org/10.5937/arhfarm72-36123.

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Obesity is a disease of excessive accumulation of adipose tissue due to an increased energy intake which is disproportionate to the energy expenditure in the body. The visceral adipose tissue in the obese accumulated in that way increases the risk of developing a number of metabolic and cardiovascular diseases. Disorders such as diabetes, dyslipidemia, inflammation, endothelial dysfunction and mitochondria can contribute to the development of oxidative stress, which is especially pronounced in the abdominal type of obesity. Obesity can induce systemic oxidative stress through a variety of biochemical mechanisms. Although ROS is generated in a large number of cells, mitochondria play a significant role in their intracellular production through the process of oxidative phosphorylation of the respiratory chain, and in fatty acid oxidation reactions. Oxidative stress is a unique link between the various molecular disorders present in the development of insulin resistance that plays a key role in the pathogenesis and progression of chronic metabolic, proinflammatory diseases. The progression of insulin resistance is also affected by inflammation. Both of these can be the cause and the consequence of obesity. The synthesis of the inflammatory mediators is induced by oxidative stress, thus bringing the inflammation and the oxidative stress into a very significant relation. This review aims to highlight recent findings on the role of oxidative stress in the pathogenesis of obesity, with special reference to the mechanisms that explain its occurrence.

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6

BÜYÜKOĞLU, Tülay, and Nurcanan ASLAN. "Oxidative Stress and Effects of Oxidative Stress on the Dairy Cattle During Transition Period." Turkiye Klinikleri Journal of Veterinary Sciences 9, no. 2 (2018): 33–41. http://dx.doi.org/10.5336/vetsci.2018-60899.

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7

Kibel, Aleksandar, Ana Marija Lukinac, Vedran Dambic, Iva Juric, and Kristina Selthofer Relatic. "Oxidative Stress in Ischemic Heart Disease." Oxidative Medicine and Cellular Longevity 2020 (December 28, 2020): 1–30. http://dx.doi.org/10.1155/2020/6627144.

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One of the novel interesting topics in the study of cardiovascular disease is the role of the oxidation system, since inflammation and oxidative stress are known to lead to cardiovascular diseases, their progression and complications. During decades of research, many complex interactions between agents of oxidative stress, oxidation, and antioxidant systems have been elucidated, and numerous important pathophysiological links to na number of disorders and diseases have been established. This review article will present the most relevant knowledge linking oxidative stress to vascular dysfunction and disease. The review will focus on the role of oxidative stress in endotheleial dysfunction, atherosclerosis, and other pathogenetic processes and mechanisms that contribute to the development of ischemic heart disease.

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8

LATHA, A. "OXIDATIVE STRESS." NARAYANA NURSING JOURNAL 3, no. 2 (2014): 13. http://dx.doi.org/10.5455/nnj.2014-06-4.

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9

Poncin, Sylvie, Sandrine Van Eeckoudt, Kevin Humblet, Ides M. Colin, and Anne-Catherine Gérard. "Oxidative Stress." American Journal of Pathology 176, no. 3 (March 2010): 1355–63. http://dx.doi.org/10.2353/ajpath.2010.090682.

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10

Dabrowski, Andrzej, and Antoni Gabryelewicz. "Oxidative stress." International Journal of Pancreatology 12, no. 3 (December 1992): 193–99. http://dx.doi.org/10.1007/bf02924357.

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11

Finaud, Julien, G??rard Lac, and Edith Filaire. "Oxidative Stress." Sports Medicine 36, no. 4 (2006): 327–58. http://dx.doi.org/10.2165/00007256-200636040-00004.

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12

RAMASARMA, T. "Oxidative Stress." Biochemical Society Transactions 14, no. 3 (June 1, 1986): 666. http://dx.doi.org/10.1042/bst0140666a.

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13

Faraci, Frank M. "Oxidative Stress." Stroke 36, no. 2 (February 2005): 186–88. http://dx.doi.org/10.1161/01.str.0000153067.27288.8b.

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14

Sies, Helmut, Carsten Berndt, and Dean P. Jones. "Oxidative Stress." Annual Review of Biochemistry 86, no. 1 (June 20, 2017): 715–48. http://dx.doi.org/10.1146/annurev-biochem-061516-045037.

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15

Stevanovic, Jelka, Suncica Borozan, Tatjana Bozic, Slavoljub Jovic, Tatjana Djekic, and Blagoje Dimitrijevic. "Oxidative stress." Veterinarski glasnik 66, no. 3-4 (2012): 273–83. http://dx.doi.org/10.2298/vetgl1204273s.

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The unceasing need for oxygen is in contradiction to the fact that it is in fact toxic to mammals. Namely, its monovalent reduction can have as a consequence the production of short-living, chemically very active free radicals and certain non-radical agents (nitrogen-oxide, superoxide-anion-radicals, hydroxyl radicals, peroxyl radicals, singlet oxygen, peroxynitrite, hydrogen peroxide, hypochlorous acid, and others). There is no doubt that they have numerous positive roles, but when their production is stepped up to such an extent that the organism cannot eliminate them with its antioxidants (superoxide-dismutase, glutathione-peroxidase, catalase, transferrin, ceruloplasmin, reduced glutathion, and others), a series of disorders is developed that are jointly called ?oxidative stress.? The reactive oxygen species which characterize oxidative stress are capable of attacking all main classes of biological macromolecules, actually proteins, DNA and RNA molecules, and in particular lipids. The free radicals influence lipid peroxidation in cellular membranes, oxidative damage to DNA and RNA molecules, the development of genetic mutations, fragmentation, and the altered function of various protein molecules. All of this results in the following consequences: disrupted permeability of cellular membranes, disrupted cellular signalization and ion homeostasis, reduced or loss of function of damaged proteins, and similar. That is why the free radicals that are released during oxidative stress are considered pathogenic agents of numerous diseases and ageing. The type of damage that will occur, and when it will take place, depends on the nature of the free radicals, their site of action and their source.

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16

Preiser, Jean-Charles. "Oxidative Stress." Journal of Parenteral and Enteral Nutrition 36, no. 2 (February 2012): 147–54. http://dx.doi.org/10.1177/0148607111434963.

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17

Nugent, Kenneth. "Oxidative stress." Southwest Respiratory and Critical Care Chronicles 7, no. 27 (January 18, 2019): 1–3. http://dx.doi.org/10.12746/swrccc.v7i27.518.

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18

Storz, Gisela, and James A. Imlayt. "Oxidative stress." Current Opinion in Microbiology 2, no. 2 (April 1999): 188–94. http://dx.doi.org/10.1016/s1369-5274(99)80033-2.

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19

Halliwell, B. "Oxidative stress." FEBS Letters 216, no. 1 (May 25, 1987): 170–71. http://dx.doi.org/10.1016/0014-5793(87)80784-6.

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20

Henry, Yann. "Oxidative stress." Biochimie 69, no. 2 (February 1987): 166. http://dx.doi.org/10.1016/0300-9084(87)90256-2.

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21

Opara, Emmanuel C. "Oxidative Stress." Disease-a-Month 52, no. 5 (May 2006): 183–98. http://dx.doi.org/10.1016/j.disamonth.2006.05.003.

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22

Bast, A., and R. J. A. Goris. "Oxidative stress." Pharmaceutisch Weekblad Scientific Edition 11, no. 6 (December 1989): 199–206. http://dx.doi.org/10.1007/bf01959411.

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23

Soffler, Carl. "Oxidative Stress." Veterinary Clinics of North America: Equine Practice 23, no. 1 (April 2007): 135–57. http://dx.doi.org/10.1016/j.cveq.2006.11.004.

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24

Burton, Graham J., and Eric Jauniaux. "Oxidative stress." Best Practice & Research Clinical Obstetrics & Gynaecology 25, no. 3 (June 2011): 287–99. http://dx.doi.org/10.1016/j.bpobgyn.2010.10.016.

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25

Catanzaro, Orlando. "Diabetic oxidative stress and bone loss complications." Endocrinology and Disorders 5, no. 1 (March 5, 2021): 01–04. http://dx.doi.org/10.31579/2640-1045/056.

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Diabetes mellitus is a group of metabolic disorder characterize by and absolute or partial insulin deficiency. Diabetic hyperglycemia is produce by the effect of homeostasis between proteolytic enzymes, their inhibitors and the antioxidants defense that protect and repair vital tissues and molecular components. Bone consist of both component and trabecular bone tissue. Organic matrix and albumin form part of noncollagenous of bone .Initiation of mineralization and collagen fibrils form the phase of mineral matrix. Calcium flux into and out of bone depend of osteoclastic and osteoblastic activity. The remodeling is initiated by resorption and new bone formation at the resorption site. Diabetic complication is a critical factor for bone pathology and could start early inflammatory stage even before hyperglycemia. Diabetic produces bone loss from reduce osteoblast activity. Partly insulin deficiency produce defective bone remodeling indirect by oxidative stress. The current treatment for defective bone in diabetes state include biophosphonate and cinaciguat. Biphosphonate inhibit bone resorption, but may worsen bone quality. A novel type of activation of sGMP is cinaciguat an NO independent activator of oxidative GC, increase c GMP synthesis on diabetic and restore proliferation and survival of osteoblasts. Chronic hyperglycemia interferes with the oseointegration of implants in diabetics. Both diabetic and aging plays a role in abnormal differentiation of osteroblasts. In diabetic patients may improve the oral health to have a positive impact if optimal glycemic control is emphasized. However with cinaciguat present as a novel paradigm enhancing bone formation under hyperglycemia and protect bone implants.

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26

Tiwari, Supriya. "Oxidative Stress and Antioxidant Defense in Cells." Global Journal For Research Analysis 3, no. 8 (June 15, 2012): 11–14. http://dx.doi.org/10.15373/22778160/august2014/4.

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27

Zayyanu, Tukur. "Antioxidant in Oxidative Stress and Neurodegenerative Diseases." Journal of Medical Science And clinical Research 11, no. 08 (August 30, 2023): 10–22. http://dx.doi.org/10.18535/jmscr/v11i8.02.

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Background: Natural substances have long been used for developing traditional medicines, and the production of innovative drugs is encouraged by the use of these natural ingredients. The key interaction between oxidative stress and inflammation in disease etiology is supported by mounting research. Reactive oxygen species (ROS) generated by inflammatory cells cause oxidative stress, which has been recognized as the key mediator of the relationship between inflammation and the spread for diseases. Curcumin (DFM), demethoxycurcumin (DMC), and bisdemethoxycurcumin (BDMC) are the three main components of the rhizomes of turmeric. That filters the superoxide radicals, nitric oxide, and hydrogen peroxide while inhibiting lipid peroxidation, a successful Nano medicine using a curcumin will result in treatment of age-related neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease. Aims: The goal of this research is to present a new current Nano biotechnological approach to disease treatment and the use of encapsulated Nano cur cumin for treatment of age-related neurodegenerative diseases such as Alzheimer’s and Parkinson’s diseases.

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28

Chen, Chuck T., Marc-Olivier Trépanier, Kathryn E. Hopperton, Anthony F. Domenichiello, Mojgan Masoodi та Richard P. Bazinet. "Inhibiting Mitochondrial β-Oxidation Selectively Reduces Levels of Nonenzymatic Oxidative Polyunsaturated Fatty Acid Metabolites in the Brain". Journal of Cerebral Blood Flow & Metabolism 34, № 3 (11 грудня 2013): 376–79. http://dx.doi.org/10.1038/jcbfm.2013.221.

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Schönfeld and Reiser recently hypothesized that fatty acid β-oxidation is a source of oxidative stress in the brain. To test this hypothesis, we inhibited brain mitochondrial β-oxidation with methyl palmoxirate (MEP) and measured oxidative polyunsaturated fatty acid (PUFA) metabolites in the rat brain. Upon MEP treatment, levels of several nonenzymatic auto-oxidative PUFA metabolites were reduced with few effects on enzymatically derived metabolites. Our finding confirms the hypothesis that reduced fatty acid β-oxidation decreases oxidative stress in the brain and β-oxidation inhibitors may be a novel therapeutic approach for brain disorders associated with oxidative stress.

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29

Ussipbek, B. A., L. C. López, N. T. Ablaikhanova, and M. K. Murzakhmetova. "OXIDATIVE STRESS AND MITOCHONDRIAL DYSFUNCTION." Series of biological and medical 2, no. 338 (April 15, 2020): 31–40. http://dx.doi.org/10.32014/10.32014/2020.2519-1629.10.

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The process of cell damage resulting from the action of free radicals – reactive oxygen species (ROS) – is called oxidative stress. Most ROS are constantly formed in the cell – about 5 % of the oxygen consumed by tissues is converted into free radicals, but their level is normally so small that the cell inactivates them with the help of an antioxidant system. Different organs and tissues are exposed to different degrees of ROS and demonstrate different stability during the implementation of oxidative stress. The mechanisms of ROS formation by mitochondria under oxidative stress are still unclear. At the same time, it was found that mitochondrial dysfunction and the accumulation of mitochondrial mutations in tissues make a significant contribution to the aging process, as well as to the pathogenesis of a number of diseases characterized by neurodegeneration. Mutations lead to increased generation of free radicals, reduced ATP levels, and energy failure of cells. Coenzyme Q10 is a component of the mitochondrial respiratory chain. Violation of the biosynthesis of coenzyme Q10 can lead to a number of mitochondrial diseases. When coenzyme Q10 is deficient, sulfide metabolism plays a critical role. Sulfide metabolism in mammalian cells includes trans-sulfuration (biosynthetic) and hydrogen sulfide oxidation (H2S) (catabolic). Violation of H2S oxidation may contribute to oxidative stress in coenzyme Q deficiency or may play a synergistic role with oxidative stress in the pathogenesis of tissue specificity in coenzyme Q deficiency.

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30

Miglioranza Scavuzzi, Bruna, and Joseph Holoshitz. "Endoplasmic Reticulum Stress, Oxidative Stress, and Rheumatic Diseases." Antioxidants 11, no. 7 (June 29, 2022): 1306. http://dx.doi.org/10.3390/antiox11071306.

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Background: The endoplasmic reticulum (ER) is a multi-functional organelle responsible for cellular homeostasis, protein synthesis, folding and secretion. It has been increasingly recognized that the loss of ER homeostasis plays a central role in the development of autoimmune inflammatory disorders, such as rheumatic diseases. Purpose/Main contents: Here, we review current knowledge of the contribution of ER stress to the pathogenesis of rheumatic diseases, with a focus on rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). We also review the interplay between protein folding and formation of reactive oxygen species (ROS), where ER stress induces oxidative stress (OS), which further aggravates the accumulation of misfolded proteins and oxidation, in a vicious cycle. Intervention studies targeting ER stress and oxidative stress in the context of rheumatic diseases are also reviewed. Conclusions: Loss of ER homeostasis is a significant factor in the pathogeneses of RA and SLE. Targeting ER stress, unfolded protein response (UPR) pathways and oxidative stress in these diseases both in vitro and in animal models have shown promising results and deserve further investigation.

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31

Basu, Samar. "Fatty acid oxidation and isoprostanes: Oxidative strain and oxidative stress." Prostaglandins, Leukotrienes and Essential Fatty Acids (PLEFA) 82, no. 4-6 (April 2010): 219–25. http://dx.doi.org/10.1016/j.plefa.2010.02.031.

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32

Naviaux, Robert K. "Oxidative Shielding or Oxidative Stress?" Journal of Pharmacology and Experimental Therapeutics 342, no. 3 (June 13, 2012): 608–18. http://dx.doi.org/10.1124/jpet.112.192120.

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33

Shang, F., and A. Taylor. "Oxidative stress and recovery from oxidative stress are associated with altered ubiquitin conjugating and proteolytic activities in bovine lens epithelial cells." Biochemical Journal 307, no. 1 (April 1, 1995): 297–303. http://dx.doi.org/10.1042/bj3070297.

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Roles for ubiquitin (an 8.5 kDa polypeptide) involve its conjugation to proteins as a signal to initiate degradation and as a stress protein. We investigated ubiquitin conjugation and ubiquitin-dependent proteolytic activities in cultured bovine lens epithelial cells (BLECs) upon oxidative challenge. A 44% decrease in intracellular glutathione confirmed oxidative stress upon incubation with 1 mM H2O2. After 30 min incubation, endogenous high-molecular-mass ubiquitin conjugates decreased 73%, and intracellular proteolysis decreased about 50%. In the supernatants of the oxidatively treated BLECs, the ability to form high-molecular-mass ubiquitin conjugates with exogenous 125I-labelled ubiquitin decreased 28%, and ATP-dependent degradation of oxidized alpha-crystallin decreased 36%. When the H2O2-treated BLECs were allowed to recover for 60 min, intracellular proteolysis returned to the level of control cells. There was also a subsequent transient enhancement of intracellular proteolysis and a simultaneous recovery of endogenous high-molecular-mass ubiquitin conjugates. In parallel cell-free experiments, conjugating activity with exogenous 125I-labelled ubiquitin and ATP-dependent degradation of oxidized alpha-crystallin increased 35% and 72% respectively compared with non-oxidatively treated BLECs. ATP-independent proteolysis showed little response to exposure or removal of H2O2. These results indicate that (1) the rate of intracellular proteolysis in BLECs is associated with the level of endogenous high-molecular-mass ubiquitin conjugates and (2) oxidative stress may inactivate the ubiquitin conjugation activity with coordinate depression of proteolytic capability. Enhancement in ubiquitin conjugation and proteolytic activities during recovery from oxidative stress may be important in removal of damaged proteins and restoration of normal function of BLECs. The inactivation of ubiquitin-dependent proteolysis by oxidation may be involved in the accumulation of altered proteins and other adverse sequelae in the oxidatively challenged aging lens.

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34

Saha, Atanu. "Assessment of Oxidative Stress and Association of Oxidative Markers among High School Teachers." Indian Journal of Applied Research 4, no. 2 (October 1, 2011): 7–9. http://dx.doi.org/10.15373/2249555x/feb2014/179.

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35

Kiffin, Roberta, Christopher Christian, Erwin Knecht, and Ana Maria Cuervo. "Activation of Chaperone-mediated Autophagy during Oxidative Stress." Molecular Biology of the Cell 15, no. 11 (November 2004): 4829–40. http://dx.doi.org/10.1091/mbc.e04-06-0477.

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Oxidatively damaged proteins accumulate with age in almost all cell types and tissues. The activity of chaperone-mediated autophagy (CMA), a selective pathway for the degradation of cytosolic proteins in lysosomes, decreases with age. We have analyzed the possible participation of CMA in the removal of oxidized proteins in rat liver and cultured mouse fibroblasts. Added to the fact that CMA substrates, when oxidized, are more efficiently internalized into lysosomes, we have found a constitutive activation of CMA during oxidative stress. Oxidation-induced activation of CMA correlates with higher levels of several components of the lysosomal translocation complex, but in particular of the lumenal chaperone, required for substrate uptake, and of the lysosomal membrane protein (lamp) type 2a, previously identified as a receptor for this pathway. In contrast with the well characterized mechanism of CMA activation during nutritional stress, which does not require de novo synthesis of the receptor, oxidation-induced activation of CMA is attained through transcriptional up-regulation of lamp2a. We conclude that CMA is activated during oxidative stress and that the higher activity of this pathway under these conditions, along with the higher susceptibility of the oxidized proteins to be taken up by lysosomes, both contribute to the efficient removal of oxidized proteins.

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36

Singh, Abhishek Kumar, Sandeep Singh, Geetika Garg, and Syed Ibrahim Rizvi. "Rapamycin alleviates oxidative stress-induced damage in rat erythrocytes." Biochemistry and Cell Biology 94, no. 5 (October 2016): 471–79. http://dx.doi.org/10.1139/bcb-2016-0048.

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An imbalanced cellular redox system promotes the production of reactive oxygen species (ROS) that may lead to oxidative stress-mediated cell death. Erythrocytes are the best-studied model of antioxidant defense mechanism. The present study was undertaken to investigate the effect of the immunosuppressant drug rapamycin, an inducer of autophagy, on redox balance of erythrocytes and blood plasma of oxidatively challenged rats. Male Wistar rats were oxidatively challenged with HgCl2 (5 mg/kg body mass (b.m.)). A significant (p < 0.05) induction in ROS production, plasma membrane redox system (PMRS), intracellular Ca2+ influx, lipid peroxidation (LPO), osmotic fragility, plasma protein carbonyl (PCO) content, and plasma advanced oxidation protein products (AOPP) and simultaneously significant reduction in glutathione (GSH) level and ferric reducing ability of plasma (FRAP) were observed in rats exposed to HgCl2. Furthermore, rapamycin (0.5 mg/kg b.m.) provided significant protection against HgCl2-induced alterations in rat erythrocytes and plasma by reducing ROS production, PMRS activity, intracellular Ca2+ influx, LPO, osmotic fragility, PCO content, and AOPP and also restored the level of antioxidant GSH and FRAP. Our observations provide evidence that rapamycin improves redox status and attenuates oxidative stress in oxidatively challenged rats. Our data also demonstrate that rapamycin is a comparatively safe immunosuppressant drug.

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Hao, Yue, Mingjie Xing, and Xianhong Gu. "Research Progress on Oxidative Stress and Its Nutritional Regulation Strategies in Pigs." Animals 11, no. 5 (May 13, 2021): 1384. http://dx.doi.org/10.3390/ani11051384.

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Oxidative stress refers to the dramatic increase in the production of free radicals in human and animal bodies or the decrease in the ability to scavenging free radicals, thus breaking the antioxidation–oxidation balance. Various factors can induce oxidative stress in pig production. Oxidative stress has an important effect on pig performance and healthy growth, and has become one of the important factors restricting pig production. Based on the overview of the generation of oxidative stress, its effects on pigs, and signal transduction pathways, this paper discussed the nutritional measures to alleviate oxidative stress in pigs, in order to provide ideas for the nutritional research of anti-oxidative stress in pigs.

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Wang, Xiaole, Chuqiao Shen, Jie Zhu, Guoming Shen, Zegeng Li, and Jingcheng Dong. "Long Noncoding RNAs in the Regulation of Oxidative Stress." Oxidative Medicine and Cellular Longevity 2019 (February 17, 2019): 1–7. http://dx.doi.org/10.1155/2019/1318795.

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Oxidative stress takes responsibility for various diseases, such as chronic obstructive pulmonary disease (COPD), Alzheimer’s disease (AD), and cardiovascular disease; nevertheless, there is still a lack of specific biomarkers for the guidance of diagnosis and treatment of oxidative stress-related diseases. In recent years, growing studies have documented that oxidative stress has crucial correlations with long noncoding RNAs (lncRNAs), which have been identified as important transcriptions involving the process of oxidative stress, inflammation, etc. and been regarded as the potential specific biomarkers. In this paper, we review links between oxidative stress and lncRNAs, highlight lncRNAs that refer to oxidative stress, and conclude that lncRNAs have played a negative or positive role in the oxidation/antioxidant system, which may be helpful for the further investigation of specific biomarkers of oxidative stress-related diseases.

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Soria-Meneses, Pedro Javier, Alejandro Jurado-Campos, Virgilio Gómez-Rubio, Irene Sánchez-Ajofrín, Ana Josefa Soler, José Julián Garde, and María del Rocío Fernández-Santos. "Determination of Ram (Ovis aries) Sperm DNA Damage Due to Oxidative Stress: 8-OHdG Immunodetection Assay vs. SCSA®." Animals 12, no. 23 (November 25, 2022): 3286. http://dx.doi.org/10.3390/ani12233286.

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Conventional DNA analysis techniques can hardly detect DNA damage in ruminant spermatozoa due to high DNA compaction in these cells. Furthermore, these techniques cannot discriminate whether the damage is due to oxidative stress. The main purpose of this study was to evaluate the efficacy of two techniques for determining DNA damage in ovine sperm when the source of that damage is oxidative stress. Semen samples from twenty Manchega rams (Ovis aries) were collected and cryopreserved. After thawing, the samples were subjected to different levels of oxidative stress, and DNA oxidation was quantified using an 8-hydroxy-2′-deoxyguanosine (8-OHdG) immunodetection assay and Sperm Chromatin Structure Assay (SCSA®). For this purpose, we evaluated five different concentrations of an oxidation solution (H2O2/FeSO4•7H2O) on ram sperm DNA. Our study with the 8-OHdG immunodetection assay shows that there are higher values for DNA oxidation in samples that were subjected to the highest oxidative stress (8 M H2O2/800 µM FeSO4•7H2O) and those that were not exposed to high oxidative stress, but these differences were not significant (p ≥ 0.05). The two SCSA® parameters considered, DNA fragmentation index (DFI %) and high DNA stainability (HDS %), showed significant differences between samples that were subjected to high concentrations of the oxidation agent and those that were not (p < 0.05). We can conclude that the 8-OHdG immunodetection assay and SCSA® detect DNA damage caused by oxidative stress in ovine sperm under high oxidative conditions; SCSA® is a more straightforward method with more accurate results. For these reasons, an oxidative-stress-specific assay such as 8-OHdG immunodetection is not needed to measure DNA damage caused by oxidative stress in ram sperm samples.

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Namıduru, Emine Siber, and Mustafa Namıduru. "Oxidative stress in viral HEPATITIS B and C." Asian Pacific Journal of Health Sciences 6, no. 4 (December 2019): 47–48. http://dx.doi.org/10.21276/apjhs.2019.6.4.10.

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Waghmare, P. A. "Some Oxidative Stress Markers in Pregnant Anemic Woman." Journal of Medical Science And clinical Research 05, no. 06 (June 30, 2017): 24121–24. http://dx.doi.org/10.18535/jmscr/v5i6.213.

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Garrido, Gabino. "Oxidative stress in hemodialysis patients infected with HIV." Clinical Research and Clinical Trials 6, no. 2 (June 27, 2022): 01–09. http://dx.doi.org/10.31579/2693-4779/101.

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Background: HIV-infected population presents the impaired renal function as a risk factor for death, and comorbid conditions are related in some traits to oxidative stress (OS). Objetive: To analyze the influence of OS in Human Immunodeficiency Virus Infection (HIV) and chronic kidney disease (CKD) by comparing the redox status between HIV patients with and without CKD and HIV hemodialysis patients. Methods: A comparative longitudinal study of the hemodialysis process was developed. The study included 96 individuals divided into four groups namely, supposedly healthy volunteers, patients with HIV infection without renal illnesses, patients with HIV infection and chronic renal disease, and HIV(-) with chronic renal disease. Indexes evaluating redox, hematological, hemochemical, immunologic, and virological aspects were determined. These indexes were also assessed before and after hemodialysis. Results: Viral load, uric acid, creatinine, and urea concentration were significantly (p<0.05) lower after hemodialysis. The two HIV infected groups were significantly different (p<0.05) regarding redox indexes of damage and antioxidant status compared to the group of supposedly healthy volunteers. Significantly increased values (p<0.05) of malondialdehyde, advanced oxidation protein product (AOPP), and peroxidation potential (PP) and significantly lower values glutathione (GSH) (p<0.05) were found after hemodialysis in both groups. In the case of HIV patients, increased values of superoxide dismutase were also found. HIV infected patients under HD tretament exhibited significantly (p<0.05) higher values of AOPP and PP and lower values of GSH than HIV(-) hemodialysis patients after hemodialysis. Conclusion: Oxidative stress occurs in both HIV and CKD conditions, and it is also increased after hemodialysis intervention. Otherwise non-viral control could influence on oxidative status in HIV/CKD patients, that´s why ART affectivities should be monitoring using HIV progression markers. Redox indexes should be diagnosed in HIV hemodialysis patients for treatment and management adjustment.

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M V, Sailaja, Sharan B. Singh M, Ch Rajendhra, and N. Mallikarjuna Reddy. "Role of Oxidative Stress on Age and Gender." International Journal of Integrative Medical Sciences 2, no. 2 (February 28, 2015): 61–69. http://dx.doi.org/10.16965/ijims.2015.103.

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Thomas, Megan M., Maricela Haghiac, Catalin Grozav, Judi Minium, Virtu Calabuig-Navarro, and Perrie O’Tierney-Ginn. "Oxidative Stress Impairs Fatty Acid Oxidation and Mitochondrial Function in the Term Placenta." Reproductive Sciences 26, no. 7 (October 10, 2018): 972–78. http://dx.doi.org/10.1177/1933719118802054.

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Placental fatty acid oxidation (FAO) is impaired and lipid storage is increased in pregnancy states associated with chronic oxidative stress. The effect of acute oxidative stress, as seen in pregnancies complicated with asthma, on placental lipid metabolism is unknown. We hypothesized that induction of acute oxidative stress would decrease FAO and increase esterification. We assessed [3H]-palmitate oxidation and esterification in term placental explants from lean women after exposure to hydrogen peroxide (H2O2) for 4 hours. Fatty acid oxidation decreased 16% and 24% in placental explants exposed to 200 ( P = .02) and 400 µM H2O2 ( P = .01), respectively. Esterification was not altered with H2O2 exposure. Neither messenger RNA nor protein expression of key genes involved in FAO (eg, peroxisome proliferator-activated receptor α, carnitine palmitoyl transferase 1b) were altered. Adenosine triphosphate (ATP) levels decreased with induction of oxidative stress, without increasing cytotoxicity. Acute oxidative stress decreased FAO and ATP production in the term placenta without altering fatty acid esterification. As decreases in placental FAO and ATP production are associated with impaired fetal growth, pregnancies exposed to acute oxidative stress may be at risk for fetal growth restriction.

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Karanikas, Evangelos, Nikolaos P. Daskalakis, and Agorastos Agorastos. "Oxidative Dysregulation in Early Life Stress and Posttraumatic Stress Disorder: A Comprehensive Review." Brain Sciences 11, no. 6 (May 29, 2021): 723. http://dx.doi.org/10.3390/brainsci11060723.

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Traumatic stress may chronically affect master homeostatic systems at the crossroads of peripheral and central susceptibility pathways and lead to the biological embedment of trauma-related allostatic trajectories through neurobiological alterations even decades later. Lately, there has been an exponential knowledge growth concerning the effect of traumatic stress on oxidative components and redox-state homeostasis. This extensive review encompasses a detailed description of the oxidative cascade components along with their physiological and pathophysiological functions and a systematic presentation of both preclinical and clinical, genetic and epigenetic human findings on trauma-related oxidative stress (OXS), followed by a substantial synthesis of the involved oxidative cascades into specific and functional, trauma-related pathways. The bulk of the evidence suggests an imbalance of pro-/anti-oxidative mechanisms under conditions of traumatic stress, respectively leading to a systemic oxidative dysregulation accompanied by toxic oxidation byproducts. Yet, there is substantial heterogeneity in findings probably relative to confounding, trauma-related parameters, as well as to the equivocal directionality of not only the involved oxidative mechanisms but other homeostatic ones. Accordingly, we also discuss the trauma-related OXS findings within the broader spectrum of systemic interactions with other major influencing systems, such as inflammation, the hypothalamic-pituitary-adrenal axis, and the circadian system. We intend to demonstrate the inherent complexity of all the systems involved, but also put forth associated caveats in the implementation and interpretation of OXS findings in trauma-related research and promote their comprehension within a broader context.

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Shchulkin, Aleksey V., Yulia V. Abalenikhina, Olga V. Kosmachevskaya, Alexey F. Topunov, and Elena N. Yakusheva. "Regulation of P-Glycoprotein during Oxidative Stress." Antioxidants 13, no. 2 (February 8, 2024): 215. http://dx.doi.org/10.3390/antiox13020215.

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P-glycoprotein (Pgp, ABCB1, MDR1) is an efflux transporter protein that removes molecules from the cells (outflow) into the extracellular space. Pgp plays an important role in pharmacokinetics, ensuring the absorption, distribution, and excretion of drugs and its substrates, as well as in the transport of endogenous molecules (steroid and thyroid hormones). It also contributes to tumor cell resistance to chemotherapy. In this review, we summarize the mechanisms of Pgp regulation during oxidative stress. The currently available data suggest that Pgp has a complex variety of regulatory mechanisms under oxidative stress, involving many transcription factors, the main ones being Nrf2 and Nf-kB. These factors often overlap, and some can be activated under certain conditions, such as the deposition of oxidation products, depending on the severity of oxidative stress. In most cases, the expression of Pgp increases due to increased transcription and translation, but under severe oxidative stress, it can also decrease due to the oxidation of amino acids in its molecule. At the same time, Pgp acts as a protector against oxidative stress, eliminating the causative factors and removing its by-products, as well as participating in signaling pathways.

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Watson, Walter H., and Dean P. Jones. "Oxidation of nuclear thioredoxin during oxidative stress." FEBS Letters 543, no. 1-3 (April 29, 2003): 144–47. http://dx.doi.org/10.1016/s0014-5793(03)00430-7.

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Gasparovic, Ana Cipak, Neven Zarkovic, and Serge P. Bottari. "Biomarkers of nitro-oxidation and oxidative stress." Current Opinion in Toxicology 7 (February 2018): 73–80. http://dx.doi.org/10.1016/j.cotox.2017.10.002.

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Mazumdar, Pinku, Jadab Kishore Phukan, and Vidhya Srinivasan. "OXIDATIVE STRESS MARKERS IN TYPE 2 DIABETES MELLITUS." International Journal of Advanced Research 12, no. 06 (June 30, 2024): 1225–32. http://dx.doi.org/10.21474/ijar01/18987.

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Insulin resistance and high blood glucose are hallmarks of type 2 diabetes mellitus (T2DM), a serious global health concern. In the pathogenesis of T2DM, oxidative stress-a mismatch between antioxidant defenses and reactive oxygen species (ROS)-is a major factor. The mechanisms causing oxidative stress and its clinical consequences are highlighted in this review, which offers a thorough overview of oxidative stress markers in T2DM. We classify oxidative stress according to its origins, pathways, impacted biomolecules, and related illnesses. We stress the significance of keeping an eye on indicators of oxidative stress, including glutathione (GSH), catalase, advanced oxidation protein products (AOPPs), protein carbonyls, malondialdehyde (MDA), and superoxide dismutase (SOD). Comprehending these indicators is crucial for formulating focused treatment approaches to reduce oxidative stress and enhance clinical results in individuals with T2DM.

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Lozano-Picazo, Carmen María, and Francisco Fernández-Belda. "Especies reactivas de oxígeno y su implicación en Biomedicina." Anales de Veterinaria de Murcia 34 (December 16, 2020): 17–26. http://dx.doi.org/10.6018/analesvet.332621.

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Las especies reactivas de oxígeno (ROS) actúan como regulador intracelular cuando se generan de forma controlada en puntos concretos de la célula. Modifican la función de proteínas mediante la oxidación reversible de cisteínas. Hay quinasas y fosfatasas de proteínas, factores de transcripción y canales iónicos que están regulados por ROS. Estrés oxidativo y daño celular aparecen cuando los mecanismos antioxidantes de protección son incapaces de mantener bajo el nivel intracelular de ROS. En estas condiciones, ROS inducen pérdida de viabilidad celular en patologías degenerativas de corazón y cerebro y promueven proliferación celular ilimitada en procesos tumorales. La alteración de la función mitocondrial juega un papel clave en la generación del estrés oxidativo y por tanto es una diana terapéutica preferente para evitar o aminorar los daños oxidativos producidos por ROS. Reactive oxygen species (ROS) act as intracellular regulator when they are generated under control in specific cell spots. They modify proteins function by cysteine reversible oxidation. There are protein kinases and phosphatases, transcription factors and ionic channels that are regulated by ROS. Oxidative stress and cell damage arise when the protection antioxidant mechanisms are unable to keep low the intracellular ROS level. Under these conditions, ROS induce cell viability loss in heart and brain degenerative pathologies and promote unlimited cell proliferation in tumor processes. Alteration of the mitochondrial function is a key player in the oxidative stress generation and therefore it is preferential therapeutic target for prevention or attenuation of the ROS-induced oxidative damage.

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