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It is known that citrulline is converted into arginine in the series of metabolic transformations. Results of our previous studies showed that acetaminophen-induced toxic injury on the background of the alimentary deprivation of protein is accompanied by a decrease in arginine level in rat hepatocytes, but citrulline liver metabolism at these conditions remains incompletely clear. In this work, the content of citrulline in the rat liver mitochondrial and cytosolic fractions and the activity of citrulline-degrading enzymes -argininosuccinate synthase and argininosuccinate lyase were investigated. It was found that in the mitochondrial fraction a maximal reduction of the citrulline levels occurred after administration of acetaminophen toxic doses regardless of the protein amount in the ration, while in the cytosolic fraction the alimentary protein deficiency was a key factor in decreasing the activity of argininosuccinate synthase and arginino-succinate lyase. The data obtained indicated the disturbances of the urea cycle functioning and explained the decrease of l-arginine level in hepatocytes in conditions of acetaminophen-induced toxic injury against the background alimentary protein deficiency. K e y w o r d s: L-сitrulline, аrgininosuccinate synthetase, argininosuccinate lyase, acetaminophen, toxic injury, alimentary deprivation of protein.

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The work is devoted to the study of the fractional distribution of sialic acids in the blood plasma of rats under the conditions of toxic damage with acetaminophen after alimentary protein deprivation. The content of free, protein-bound and oligo-bound sialic acids in the blood plasma of animals was investigated under experimental conditions. The animals consumed a semi-synthetic diet during the experiment according to the recommendations of the American Institute of Nutrition. In order to simulate alimentary protein deprivation, rats received a low-protein diet containing 1/3 of the standard daily protein requirement daily for 28 days. The animals were modeled acute toxic damage with acetaminophen after four weeks of experimental diet. The administration of the toxin was carried out at doses of 1250 mg/kg animal body weight in suspension in 2 % starch gel solution once a day for 2 days by gavage. The concentration of free, protein- and oligo-bound sialic acids was determined spectrophotometrically at 549 nm by color reaction with thiobarbituric acid. Removal of non-sialic acid specific chromogens were performed by the addition of n-butanol. It has been shown that the increase of total sialic acids in the blood plasma of protein-deficient rats (by 40% compared to control) is due only to the increase in the level of the oligo-bound fraction. Thus, protein deficiency is a key factor in the established changes, which probably indicates the intensification of catabolism processes of intracellular easily mobilized proteins under the conditions of protein deficiency in the diet. At the same time, toxin (acetaminophen) intake, leads to an increase in the concentration of total sialic acids, mainly due to the increase of free and protein-bound fractions, which indicates the development of inflammatory processes in the tissues of the body, regardless of the amount of exogenous protein consumed.

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