[Effect of menadione and vicasol on mitochondrial energy during inhibition of initiation sites of the respiration chain].

Menadione and vicasol completely restore the respiration rate of rat liver mitochondria after its inhibition by rotenone. Under the same conditions these compounds stimulate oxygen consumption by rabbit heart mitochondria up to 40% of the maximal uncoupled respiration rate in the presence of 5 mM glutamate and up to 30% of the maximal uncoupled respiration rate in a lymphocyte suspension containing glucose. Cyanide and dicumarol, specific inhibitors of DT-diaforase, completely suppress the stimulating effect of menadione and vicasol in isolated mitochondria and by 50% in lymphocyte suspensions. The DiS-C3-(5) fluorescence in lymphocyte suspensions suggests that the menadione and vicasol-induced respiration is capable of supporting the mitochondrial transmembrane potential in lymphocytes. Thus, in different tissues menadione and vicasol can restore oxygen consumption in mitochondria, in which the first and second energy coupling sites are inhibited.