[Transamination in the mechanism of protection of mitochondria from Ca2+ overload].

A high sensitivity of the succinate-dependent uptake of Ca2+ by mitochondria to (1) the transamination (TA) substrates glutamate (GLU) and alpha-ketoglutarate (KGL) and (2) the inhibitor of TA aminooxyacetate (AOA) was revealed. The effect of the TA substrates on Ca2+ uptake depends on the ratio (1:10 mM) of their concentrations: 1 mM GLU activates and 10 mM KGL decreases this activation by 35-46%, whereas AOA suppresses the Ca2+ capacity by 60% and the inhibitor of succinate oxidation malonate, by 80-90%. A similarity in the limiting action of KGL and phosphoenolpyruvate (PEP), two sources of oxaloacetate (OAA) and GTP, on Ca2+ capacity was revealed. The differences in the effects of KGL and GLU and the similarity in the effects of KGL and PEP on succinate oxidation are explained by the effect of OAA and GTP on this oxidation. The alternating inflow of OAA in coupled processes of TA, pyruvate cycle, and tricarboxylic acids cycle provides the reciprocal activation and cyclic recurrence of Ca2+ uptake, i. e., protection from the chronic exhausting activation of Ca2+-regulated dehydrogenases, the overload of Ca2+-outgoing channels, and the excessive production of free radicals in mitochondria. The reciprocal regulation of Ca2+ uptake by TA is considered as a mechanism of the maintenance of Ca2+ homeostasis and protection of mitochondria against Ca2+ overload.

[Correlation between succinate-dependent Ca2+ accumulation and transamination in the heart and the liver mitochondria of experimental animals].

Glutamate (GLU) and alpha-ketoglutarate (KGL), the substrates involved in transamination, have reciprocal effects on succinate-dependent respiration, NADH reduction, as well as on the accumulation and stable retention of Ca2+ in heart and liver mitochondria and homogenates from experimental animals. The succinate-dependent Ca2+ accumulation was shown to be highly sensitive to changes of the concentration ratios of GLU and KGL within the range 1:10 mM. GLU activated this process by transamination of oxalacetate (OAA) to aspartate. The predomination of KGL blocked the activating effect of GLU. The predomination of GLU eliminated the block produced by KGL or phosphoenolpyruvate (sources of OAA and GTP) but did not eliminate the Ca2+ accumulation-suppressing effect of aminoacetate, inhibitor of transaminases.

[Assessment of energy-dependent Ca2+ transport in myocardial mitochondria in the ventricular fibrillation: potential diagnostic implication]. / Otsenka énergozavisimogo transporta Ca+ v mitokhondriiakh serdechnoi myshtsy pri fibrilliatsii zheludochkov: diagnosticheskie vozmozhnosti metoda.

The method of evaluation of ATP synthesis from ADP and Ca2+ transport in myocardial mitochondria has been developed. The addition of glutamate to the homogenisation media improved the parameters studied. It was shown that the Ca2+ transport test is highly informative and sensitive for the estimation of heart muscle energetic state.

[Liver mitochondria in antigenic stress in rats]. / Mitokhondrii pecheni v realizatsii antigennogo napriazheniia organizma u krys.

The penomenon of reciprocal regulation of succinate dehidrogenase activity in rat liver mitochondria was elicited in antigenic strain induced by the administration of activated lymphocytes from animals with allotransplated heart. Two coupled but opposite changes (simultaneous activation and inhibition) in succinate depended ATP synthesis and calcium transport occur. The inhibition was correlated with the activation of synthetic processes in hepatocytes. Similar changes were provoked by epinephrine (either administered i.p. or released endogenously under immobilization stress and in myocardium infarction) as well as in patients with stomach tumor. The physiological significance of the reciprocal regulation of succinate dehydrogenase is discussed.