Acta Medica Medianae
UPON THE LIVER ARGINASE ACTIVITY IN THE ACUTE KIDNEY DAMAGE
Jelenka Nikolic, Tatjana Cvetkovic, Dusan
Sokolovic, Tatjana Jevtovic, Gordana Bjelakovic and Jelena Dordevic
Biochemistry Institute of the Faculty of Medicine, Nis
The acute damage of the kidney function leads to an outstanding disbalance of many homeostatic mechanisms in the organism that emerges as a consequence of the reduced glomerulic filtration and the accompanying oliguria. This conditions the emergence ofasothemia, that is, the state caracterized by an increase of the level of urea, creatinine and other ureic toxins in the blood. The results of the previous examinations show that the acute renal insufficiency is a disturbance accompanied with accelerated protein catabolism. The urea is a terminal product of the protein catabolism whose synthesis is mainly taking place in the liver; that is why the research aimed at examining the liver arginase activity, terminal enzyme in the urea synthesis cycle in various experimental models of the acute renal insufficiency. The acute asothemia is experimentally caused upon the male Spraque Dawlly rats by means of two models, namely, the model of bilateral binding of the urethra (BPU) and the clycerolic model. The arginase activity in the liver tissue homogenate is measured by the Porembsky and Cedra method on the basis of the liberated omithine liberation. In the plasma of the experimental animals the level of urea and creatinine was measured for the sake of estimating the renal function. In both the models of the acute kidney damage there was a considerable increase of the urea and creatinine concentration in the plasma (p<0,001) which is followed by a significant increase of the hepatic arginase activity with respect to the control group of the animals. On the basis of the obtained results it can be conclude that asothemia in the acute renal insufficiency is followed by an increase in the liver arginase activity.