DOI: https://doi.org/10.22141/2224-0586.16.1.2020.196926

Oxidative stress as a non-specific factor of organ damage pathogenesis (review of literature and own data)

V.I. Lysenko

Abstract


The review highlights current literature and our own researches in the field of clinical medicine and biology of the molecular mechanisms of oxidative stress, its role in the pathogenesis of many diseases and organ damages. New data on general bio­logical patterns of cell, organ, or organism death as a whole are presented. One of the central non-specific mechanisms of stress injury has been found to be the stimulation of free-radical processes as a result of the frequent concomitant hypoxemia/hypo­xia and the prooxidant effects of catecholamines. The causes and mechanisms of disturbances of redox reactions in the respiratory chain of mitochondria are revealed. It has been found that redox reactions in mitochondrial membranes are clearly regulated by genes locally. Respiratory unbundling is associated not only with mechanical damage to the membrane, but also with the action of a number of poisonous substances, bacterial toxins and drugs on this process. The dependence of the total respiratory rate and the limit of aerobic performance are considered. An important role is played by the self-regulating, so-called quasi-closed system of the body, which works against entropy. In clinical studies, the pathways of catastrophic accumulation of free radicals and cytotoxic metabolites of their catabolism, the triggering mechanisms of oxidative stress and its role in the development of apoptosis and severe postoperative complications have been established. A decrease in the activity of endogenous aldehyde catabolism enzymes in tissues and subcellular fractions reduces the adaptive capacity of the body. Determination of the level of catabolism enzymes of endogenous aldehydes can serve as one of the criteria for the severity of stress and mitochondrial dyshomeostasis in critical conditions. The role of oxidase and oxygenase oxidation in microsomes during hypoxemia/hypoxia and exposure to xenobiotics is indicated. Data on the regulatory and adaptive effect of free radical products (reactive oxygen species and nitrogen) on the regulation of gene expression and increased production of antistress proteins, stimulation of mitochondrial biogenesis and normalization of energy metabolism are presented. Attention is drawn to the causes of the insufficient clinical effectiveness of the antioxidants used and the pathways of metabolic adaptation in critical conditions.


Keywords


free radicals; hypoxia; mitochondria; oxidative stress; apoptosis; organ damages; review

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