Аннотация:The literature review reflects the present view of pathological mechanisms for mitochondrial dysfunction in hypoxia during critical conditions. It notes the role of succinates in the development of mitochondrial dysfunction, further organdisorders, and multiple organ dysfunctions in different diseases during emergency hypoxia adaptation only due to the mobilization of energy resources: their centralization, intensified carbohydrate, fat, and protein catabolism, as well as to suppressed anabolic processes in tissues. The mechanism of emergency adaptation to hypoxia during critical conditions develops with a characteristic decrease in the amount of succinate (as a substrate for the enzyme), which enables the correction of its deficiency with the promising increase of oxygen consumption, the activation of aerobic oxygenation processes, and the reduction of intracellular aerobic metabolic processes.
