[The molecular-cellular regulation of the mitochondrial respiratory chain]

We propose a new concept of molecular-cellular regulation of the mitochondrial respiratory chain. According to this concept, the cell uses acetaldehyde (AcA) as a main regulator of the respiratory chain. AcA expresses its action by changing the structural-functional state of ubiquinone, the key component of the respiratory chain. Studies were made on white random bred rats using the Langendorff's model of isolated perfused heart. We comparatively estimated the mechanometabolic state of myocardium under the conditions of simulated hypoxia of various degree, as well as in the presence of exogenous ethyl alcohol. Both hypoxia and ethyl alcohol induced severe disturbances of energy metabolism in the myocardium, cells at the level of respiratory chain due, apparently, to the increased content of free AcA. Hydroxyquinone and glycine, capable of binding free AcA, were used for pharmacological protection of the cells. Application of these drugs markedly improved the functional-metabolic state of the cell. We propose that AcA exerts both regulatory (in low doses) and inhibitory (in high doses) effect on the respiratory chain. The results obtained allow a novel insight in the processes of alcoholic and hypoxic damage and their pharmacological correction. It is evident that prophylactic and therapeutic measures in case of hypoxia or alcoholic intoxication should be first directed at decreasing the level of free AcA in the cell.