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[Oxidative phosphorylation activity, F0F1-ATPase and level of liver mitochondrial cytochromes in rats with congenitally increased ability for free radical formation].

The rates of oxygen consumption in liver mitochondria of strain S rats (2-3- and 10-12-months-old) with inherited free radical hyperproduction during oxidation of three types of substrates (glutamate+maleate, succinate+rotenone and ascorbate+TMPD) as well as cytochrome a level in the respiratory chain are lowered in comparison with Wistar controls. In liver mitochondria of 10-12-months-old rats these changes are more pronounced and manifest themselves as decreased ADP/O, phosphorylation rates and F0F1-ATPase activity. The phosphorylation potential, ATP content and adenine nucleotide pool in rat liver are also reduced. The experimental results give a better insight into the pathogenetic mechanisms of morbid states (e.g., degenerative diseases) in human beings and shed additional light on the origin of short lifespan and premature in strain S rats.