Babu G R, Reddy G R, Chetty C S
Department of Zoology, Sri Venkateswara University, Tirupati, Andhra Pradesh, India.
Biochem Int. 1989 Jun;18(6):1253-68.
Effects of repeated administration of benthiocarb on the nitrogen metabolism of hepatic and neuronal systems have been studied. Repeated benthiocarb treatment was associated with significant decrease in proteins with a concomitant increase in free amino acids (FAA) and specific activity levels of proteases suggesting impaired protein synthesis or elevated proteolysis. The glycogenic aminotransferases showed a significant elevation in both the tissues indicating high feeding of ketoacids into oxidative pathway for efficient operation of TCA cycle to combat energy crisis during induced benthiocarb stress. However, the activity levels of branched-chain aminotransferases decreased suggesting their reduced contribution of intermediates to TCA cycle. A comparative evaluation of the activity levels of ammonogenic enzymes, AMP deaminase, adenosine deaminase and glutamate dehydrogenase (GDH) indicated that ammonia was mostly contributed by nucleotide deamination rather than by oxidative deamination. GDH exhibited reduced activity due to low availability of glutamate. In accordance with increased levels of urea, the activity levels of arginase, a terminal enzyme of urea cycle was increased suggesting increased urea cycle operation in order to combat the increased ammonia content. As the presence of urea cycle in the brain is rather doubtful, the conversion of ammonia to glutamine for the synthesis of GABA is envisaged in brain whereas in liver, excess ammonia was converted to urea through ornithine-arginine reacting system. The increased glutaminase activity observed during benthiocarb intoxication is accounted for counteracting acidosis or maintenance of metabolic homeostasis. Arginase, a terminal enzyme of ornithine cycle showed increased activity denoting the efficient potentiality of tissues to avert ammonia toxicity. The changes observed in tissues of rat administered with benthiocarb reflects a shift in nitrogen metabolism for efficient mobilization of end products of protein catabolism.
研究了反复施用杀草丹对肝脏和神经系统氮代谢的影响。反复施用杀草丹与蛋白质显著减少有关，同时游离氨基酸（FAA）增加，蛋白酶的比活性水平升高，提示蛋白质合成受损或蛋白水解增加。糖原氨基转移酶在两种组织中均显著升高，表明在杀草丹诱导的应激期间，为有效运行三羧酸循环以应对能量危机，大量酮酸进入氧化途径。然而，支链氨基转移酶的活性水平降低，表明它们对三羧酸循环中间产物的贡献减少。对产氨酶、AMP脱氨酶、腺苷脱氨酶和谷氨酸脱氢酶（GDH）活性水平的比较评估表明，氨主要由核苷酸脱氨而非氧化脱氨产生。由于谷氨酸可用性低，GDH活性降低。与尿素水平升高一致，尿素循环的终末酶精氨酸酶的活性水平增加，表明尿素循环运行增加以应对氨含量的增加。由于脑中尿素循环的存在相当可疑，设想脑中氨转化为谷氨酰胺以合成GABA，而在肝脏中，过量的氨通过鸟氨酸 - 精氨酸反应系统转化为尿素。在杀草丹中毒期间观察到的谷氨酰胺酶活性增加是为了抵消酸中毒或维持代谢稳态。鸟氨酸循环的终末酶精氨酸酶活性增加，表明组织有效避免氨毒性的潜力。在施用杀草丹的大鼠组织中观察到的变化反映了氮代谢的转变，以有效动员蛋白质分解代谢的终产物。
