glutaminase and diethyl-maleate

Changes in ammonia and urea were investigated as potential marker products of free radical damage to protein and subsequent metabolism of those damaged proteins in vivo. Both serum and liver lipid peroxidation products as measured by thiobarbituric-acid-reactive substances (TBARS) were increased by feeding rats a vitamin-E-deficient diet. The acute injection of diethyl maleate and bromotrichloromethane (DEM/BrCCl3) increased TBARS in liver of rats fed a vitamin-E-deficient diet. The concentrations of ammonia and urea in the serum and liver did not correlate with lipid peroxidation. The activities of liver glutaminase and arginase were decreased by DEM/BrCCl3 treatment in rats fed vitamin-E-deficient diet. Glutamate-ammonia ligase activity was decreased by vitamin-E-deficient diet but not by DEM/BrCCl3 treatment. Ornithine carbamoyltransferase, arginosuccinate synthase, argininosuccinate lyase and glutamate dehydrogenase (NAD(P)+) were not affected by dietary vitamin E or by DEM/BrCCl3. The data suggest that the concentrations of ammonia and urea, major by-products of nitrogen metabolism, are unchanged by the oxidant damage and lipid peroxidation, and that their control in vivo is a dynamic equilibrium of various metabolic pathways.

Topics: Ammonia; Animals; Arginase; Argininosuccinate Lyase; Argininosuccinate Synthase; Bromotrichloromethane; Carbamoyl-Phosphate Synthase (Ammonia); gamma-Glutamyltransferase; Glutamate Dehydrogenase; Glutaminase; Lipid Peroxidation; Liver; Male; Maleates; Mitochondria, Liver; Ornithine Carbamoyltransferase; Proteins; Rats; Rats, Inbred Strains; Urea; Vitamin E