Tag Archives: toxic injury
Indexes of citrulline metabolism in rat liver under the toxic injury against the background of alimentary protein deficiency
H. P. Kopylchuk, I. M. Nykolaichuk, I. S. Lylyk
Yuriy Fedkovych Chernivtsi National University, Ukraine;
Institute of Biology, Chemistry and Bioresources, Chernivtsi, Ukraine;
e-mail: g.kopilchuk@chnu.edu.ua
Received: 29 May 2019; Accepted: 29 November 2019
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.
Rat liver arginase system under acetaminophen-induced toxic injury and protein deprivation
H. P. Kopylchuk, I. M. Nykolaichuk, O. M. Zhuretska
Yuriy Fedkovych Chernivtsi National University, Ukraine;
Institute of Biology, Chemistry and Bioresourses, Chernivtsi, Ukraine;
e-mail: kopilchuk@gmail.com
Arginase activity and L-arginine content in both cytosolic and mitochondrial fractions of rat liver cells under the conditions of toxic injury on the background of protein deprivation was studied. The most significant reduction of arginase activity in liver cells and depletion of L-arginine pool was found in rats with toxic acetaminophen-induced liver injury maintained on the ration balanced by all nutrients as well as in protein deficiency rats. It was concluded that reduction of the arginase activity in the cytosolic fraction of rat liver cells, combined with simultaneous decrease of L-arginine content, may be considered as one of the mechanisms of ornithine cycle disturbance. The decline of activity of mitochondrial isoform of arginase II, for certain, is related with activation of NO-synthase system.