Park J R, Tappel A L
Department of Food Science and Technology, University of California, Davis 95616.
Toxicol Lett. 1991 Sep;58(1):29-36. doi: 10.1016/0378-4274(91)90187-b.
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.
研究了氨和尿素的变化，将其作为体内蛋白质自由基损伤及受损蛋白质后续代谢的潜在标志物。通过硫代巴比妥酸反应性物质（TBARS）测定，给大鼠喂食维生素E缺乏饮食会增加血清和肝脏脂质过氧化产物。急性注射马来酸二乙酯和溴三氯甲烷（DEM/BrCCl3）会增加喂食维生素E缺乏饮食大鼠肝脏中的TBARS。血清和肝脏中氨和尿素的浓度与脂质过氧化无关。在喂食维生素E缺乏饮食的大鼠中，DEM/BrCCl3处理会降低肝脏谷氨酰胺酶和精氨酸酶的活性。维生素E缺乏饮食会降低谷氨酸-氨连接酶的活性，但DEM/BrCCl3处理不会。鸟氨酸氨甲酰转移酶、精氨琥珀酸合成酶、精氨琥珀酸裂解酶和谷氨酸脱氢酶（NAD(P)+）不受饮食维生素E或DEM/BrCCl3的影响。数据表明，氮代谢的主要副产物氨和尿素的浓度不会因氧化损伤和脂质过氧化而改变，并且它们在体内的调控是各种代谢途径的动态平衡。
