[Energy metabolism in the kidneys after hypokinesia of varying duration]. / Energeticheskii obmen v pochkakh pri deistvii na organizm gipokinezii razlichnoi dlitel'nosti.

This paper presents data suggesting that tissue homogenates can be used to assess mitochondrial oxidation. The effect of hypokinesia of various duration on tissue respiration and oxidative phosphorylation of rat kidneys was investigated for the first time. It was found that 3-day hypokinesia led to a decrease of tissue respiration due to a lower contribution of endogenous fatty acids; 10-day hypokinesia caused activation of tissue respiration on endogenous and exogenous pyridine and flavoprotein-dependent substrates; 30-, 70- and 140-day hypokinesia brought about changes in energy formation at the expense of inhibition of respiratory activity of preparations and uncoupling of oxidative phosphorylation. Mechanisms of the above disturbances in energy metabolism reactions of kidneys are discussed.

[Energy metabolism in muscle tissue during hypokinesia of various durations]. / Sostoianie énergeticheskogo obmena myshechnoi tkani pri gipokinezii razlichnoi dlitel'nosti.

The state of energy metabolism in skeletal muscles and myocardium of albino rats was studied under long hypokinesia. It is established that on the 30th-70th days of hypokinesia endogenic fatty acids, whose oxidation promotes the uncoupling of oxidative phosphorylation and inhibition of the creatine phosphokinase reaction, are the main substrate of energy metabolism. In blood there occurs hyperlipemia and a decrease in the glucose content. A further immobilization results in predominance of succinate-dependent respiration, in blood there occurs a certain decrease in lipemia, normalization of the glucose level and an increase in the urea content.

[Energy metabolism disorders in the myocardium due to alcoholic intoxication]. / Narushenie énergeticheskogo obmena v miokarde pod vliianiem alkogol'noi intoksikatsii.

Energy metabolism was studied in rat myocardial mitochondria by estimation of respiratory enzymes activity and content of the Krebs cycle substrates under conditions of acute and chronic intoxication with ethyl alcohol. In the acute intoxication mitochondrial redox enzymes were inhibited (glutamate- and malate dehydrogenases, NADH cytochrome C oxidoreductase and cytochrome C oxidase), succinate- and lactate dehydrogenases were activated; at the same time, contents of pyruvate, succinate, and alpha-ketoglutarate were elevated and the content of oxalacetic acid was decreased. Prolonged administration of alcohol (within 2 months) caused an intensification of glycolysis and an increase in NADH cytochrome C oxidoreductase pathway with preferable oxidation of succinate and activation of cytochrome C oxidase; the phenomenon appears to be an adaptation to chronic "alcohol hypoxia". Discontinuation of alcohol administration led to deficiency of native substrates in myocardium (primarily, oxalacetic and succinic acids) due to decrease in NAD reduction via alcohol dehydrogenase reaction and to increase in oxidation of NAD-dependent endogenous substrates.

[Effect of glutamate on the trace element content in the mitochondria of the liver, heart and kidneys of rats with acute and chronic hypoxia]. / Vliianie glutamata na soderzhanie mikroélementov v mitokhondriiakh pecheni, serdtsa i pochek krys pri ostroi i khronicheskoi gipoksii

Acute hypoxia ("height" 8000 metres, 60 minutes) decreases concentration of copper, zinc and magnesium in mitochondria of the liver, kidney, that of copper and magnesium decreases in the heart. Chronic hypoxia ("height" 6000 metres, 6 hours a day for 2 weeks) also causes a decrease in the concentration of copper, zinc and magnesium in mitochondria of the liver, kidney and that of copper and magnesium--in the heart. Glutamic acid (acute and chronic hypoxia) increases the level of copper, zinc and magnesium in mitochondria of the liver, heart and kidney of albino rats which is close to its values in the normal animals.