[Disruption of the structural organization of brain mitochondrial membranes during deprivation of the paradoxal sleep phase and correction for it using lithonite].

A course of lithonite administration exerts a selective membrane-protecting effect stabilizing structure-functional state of the brain mitochondria by non-specific protection of their lipid component and stimulation of the antioxidant system.

Abstract

Interrelation between the structure-functional state of membranes of the brain mitochondria and intensity of metabolic processes in their lipid matrix has been studied during long-term deprivation of the paradoxic sleep and against a background of preventive administration of atypical tranquillizer, lithonite, a derivative of nicotinic acid. It is shown that sleep deprivation for four days is accompanied by expressed activation of lipids' oxidation by free radicals, inhibition of anti-oxidant system and inactivation of the marker enzymes of mitochondrial membranes. The character of binding and distribution of fluorescent probes 1-anilinonaphthalene-8-sulphonate (ANS) and N-phenyl-1-naphthalamine (PNA) in different layers of mitochondrial membranes is broken, which evidences for deep rearrangement of the lipid matrix. Sleep deprivation causes an increase in the relative volume and swelling of mitochondria but a decrease in the inner membrane area and the number of crusts. A course of lithonite administration exerts a selective membrane-protecting effect stabilizing structure-functional state of the brain mitochondria by non-specific protection of their lipid component and stimulation of the antioxidant system. An expediency to use lithonite for correction of other deadaptive processes induced by the membrane destruction is substantiated.