REACTIVE OXYGEN SPECIES: TRAINING, FUNCTION AND OXIDATIVE STRESS
Keywords:
Estrés oxidativo, antioxidantes, especies reactivas del oxígeno, control redox, radicales libres.Abstract
Reactive oxigen species (ROS) are produced as the consequence of the normal aerobic physiological metabolism. The electron transport chain in mitochondrial, peroxisomes, NADPH oxidases, uncoupled nitric oxide synthase (NOS) and cytochrome P450 system are the most important sources of ROS production. The imbalance of the ROS production and antioxidants defense system in the living systems causes oxidative stress brings to cellular function disruption and damage. This imbalance occurs due to over production of ROS and reduction of the antioxidant defense mechanism. Protective actions against ROS are performed by several enzymes (superoxide dismutase, catalase and glutation peroxidase) as well as nonenzimatic compounds (vitamin E, ascorbate, glutathione, transferrin, ceruloplasmin, etc). ROS are crucial modulators of cellular functions. At low concentrations, ROS are essential participants in cell signaling, induction of mitogenic response, involvement in defense against infectious agents, whereas excess ROS can disrupt normal cellular function and promote irreversible damage to cellular lipids, nucleic acids, and proteins. ROS, especially H2O2, serve as a signal molecule through oxidative modification of signaling proteins. Thus, a balance between ROS production and their removal allows for normal cellular function, whereas an imbalance causes oxidative stress with pathological consequences.
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9. Lay, S. L., Simard, G., Martinez, M. C. & Andriantsitohaina, R. (2014). Oxidative stress and metabolic pathologies: from an adipocentric point of view. Oxidative Medicine and Cellular Longevity, 2014, 1-18.
10. Di Meo, S. Reed, T. T., Venditti, P. & Victor, V. M. (2016). Role of ROS and RNS sources in physiological and pathological conditions. Oxidative Medicine and Cellular Longevity, 2016, 1-44.
11. Sainz, R., Lombo, F. & Mayo, J. C. (2012). Radical decisions in cancer: redox control of cell growth and death. Cancers, 4, 442-474.
12. González, J., Valls, N., Brito, R. & Rodrigo, R. (2014). Essential hypertension and oxidative stress: new insights. World J Cardiology, 6(6), 353-366.
13. Aroor, A., Mandavia, C., Ren, J., Sowers, J. & Pulakat, L. (2012). Mitochondrial and oxidative stress in the cardiorenal metabolic syndrome. CardioRenal Medicine, 2, 87-109.
14. Mudau, M., Genis, A., Lochner, A. & Strijdom, H. (2012). Endothelial dysfunction: the
early predictor of atherosclerosis. Cardiovasc JAfr, 23(4), 222-231.
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25. Handy, D. & Loscalzo, J. (2012). Redox regulation of mitochondrial function. Antioxidants & Redox Signaling, 16(11), 1323-1367.
26. Biswas, S. K. (2016). Does the interdependence between oxidative stress and inflammation explain the antioxidant paradox? Oxidative Medicine and Cellular Longevity, 2016, 1-9.
27. Mudau, M., Genis, A., Lochner, A. & Strijdom, H. (2012). Endothelial dysfunction: the early predictor of atherosclerosis. Cardiovasc J Afr, 23(4), 222-231.
28. Muniyappa, R. & Sowers, J. (2013). Role of insulin resistance in endothelial dysfunction. Rev Endocr Metab Disord, 14, 1, 5-12.
29. Matsuzawa, Y. & Lerman, A. (2014). Endothelial dysfunction and coronary artery disease: assessment, prognosis and treatment. Coron Artery Dis, 25(8), 713-724.
30. Hadi, H., Carr, C. & Suwaidi, J. (2005). Endothelial dysfunction: cardiovascular risk factors, therapy, and outcome. Vascular Health and Risk Management, 1(3), 183-198.
31. Widlansky, M. E. & Gutterman, D. (2011). Regulation of endothelial function by mitochondrial reactive oxygen species. Antioxidants & Redox Signaling, 15(6), 1517-1530.
32. Zuo, L. & Pannell, B. (2015). Redox characterization of functioning skeletal muscle. Frontiers Physiology, 6, 1-9.
33. Chiarugi, P., Pani, G., Giannoni, E., Taddei, L., Colavitti, R., Raugei, G., et al. (2003). Reactive oxygen species as essential mediators of cell adhesion: the oxidative inhibition of a FAK tyrosine phosphatase is required for cell adhesion. J Cell Biology, 161(5), 933-944.
34. Gulati, P., Klohn P.C., Krug, H., Gottlicher, M., Markova, B., F.D. Bohmer, F. D., & Herrlich. P. (2001). Redox regulation in mammalian signal transduction. IUBMB Life. 52, 25–28.
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38. Li, S., Tan, H-Y., Wang, N., Zhang, Z-J., Lao, L., Wong, C-W. & Feng, Y. (2015). The role of oxidative stress and Antioxidants in liver diseases. Int J Molecular Sciences, 16, 26087-26124.
39. Crowley, S. (2014). The cooperative roles of inflammation and oxidative stress in the pathogenesis of hypertension. Antioxidants & Redox Signaling, 20(1), 102-120.
40. Fischer R. & Maier, O. (2015). Interrelation of oxidative stress and inflammation in neurodegenerative disease: role of TNF. Oxidative Medicine and Cellular Longevity, 2015, 1-18.
41. Spuch, C., Ortolano, S. & Navarro, C. (2012). New insights in the amyloid-beta interaction with mitochondria. J Aging Research, 2012, 1-9.
42. Bonda, D., Wang, X., Lee, H-g., Smith, M. A., Perry, G. & Zhu, X. (2014). Neuronal failure in Alzheimer disease: a view through the oxidative stress looking-glass. Neurosci Bull, 30(2), 243-252.
43. Dai, D-F., Chiao, Y. A., Marcinel, D., Szeto, H. & Rabinovitch, P. (2014). Mitochondrial oxidative stress in aging and healthspan. Longevity & Healthspan, 3, 1-22.
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2020-11-16
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REACTIVE OXYGEN SPECIES: TRAINING, FUNCTION AND OXIDATIVE STRESS. (2020). Medicina Legal De Costa Rica, 36(1). https://www.binasss.sa.cr/ojssalud/index.php/mlcr/article/view/116
