Bìol. Tvarin, 2019, volume 21, issue 3, pp. 14–20

ACTIVITY OF THE LIVER MITOCHONDRIAL ASPARTATE AMINOTRANSFERASE AND MALATE DEHYDROGENASE IN RATS WITH TOXIC HEPATITIS UNDER CONDITIONS OF ALIMENTARY PROTEIN DEFICIENCY

O. M. Voloshchuk, G. P. Kopylchuk

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Chernivtsi national university named by Yurii Fedkovych, Institute of Biology, Chemistry and Bioresources,
2 Kotsyubinskogo str., Chernivtsi 58012, Ukraine

Nutritional demands in proteins depend on the life stage and health status of organisms. Both humans and experimental animals under stress conditions and especially drug processing become to be more sensitive to the protein deficit in the food. In this study, we examined some acetaminophen-induced metabolic effects potentiated by alimentary protein deprivation (APD) in rat liver. In particular, activities of the liver mitochondrial aspartate aminotransferase and malate dehydrogenase in rat liver were studied in conditions of balanced and imbalanced by protein diets of isocaloric content. It has been found that acute acetaminophen-induced hepatitis in comparison to control does not change the activity of mitochondrial malate dehydrogenase causing simultaneous 4-fold reduction in activity of mitochondrial aspartate aminotransferase and 2.5-fold reduction of mitochondrial oxaloacetate content. Interestingly, alimentary protein deprivation enhances the effects of acetaminophen on the described parameters. Finally, in order to confirm these associations between amount of the protein in the rat diet and physiological measures in their liver with toxic injury, principal component analysis (PCA) was performed. Two principal components characterize changes in physiological measures in our study. Principal component 1 explains about 86 % of the variation among whole dataset mainly related to control group and group subjected to acetaminophen treatment with simultaneous APD. It reveals the tight association of scores for AST activity and oxaloacetate level with control group, which might indicate the high efficiency in the oxaloacetate conversion by AST lacked in both groups with hepatitis. Similarly, principal component 1 explaining the variance in MDH activity shows its linkage to the control group, indicating the importance of MDH for the health status of control animals. On the other side, principal component 2 reveals close association between lactate and pyruvate levels as well as cytosolic NAD+/NADH ratio with acetaminophen-treated group of animals subjected to APD, confirming that toxic liver injury associated with low protein consumption leads to increased lactate-pyruvate turnover in cytosol affecting. This potentially might be associated with energy-generating dysfunction in liver under toxic hepatitis on the background of dietary protein deficiency.

Keywords: ACETAMINOPHEN, LIVER, INJURY, ASPARTATE AMINOTRANSFERASE, MALATE DEHYDROGENASE

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