Nishihata T, Ikawa C, Saitoh Y, Sakai K
Pharmaceutical Chemistry Department, University of Kansas, Lawerence 66046.
J Pharm Pharmacol. 1988 May;40(5):333-6. doi: 10.1111/j.2042-7158.1988.tb05262.x.
The relationship between chemically induced glycogenolysis and decreased thiol content in the rat isolated, perfused liver has been examined. Chemicals such as 2,4-dinitrophenol (DNP), diethyl maleate, alcohols and anti-inflammatory agents (except for sodium salicylate) accelerated glycogenolysis. Protein thiol loss correlated well with a marked increased rate of glucose release. Non-protein thiol loss, without significant loss of protein thiol, caused by a slight increase in the rate of glycogenolysis compared with controls. Since it has been reported that protein thiol loss rather than non-protein thiol loss is correlated to liver cell injury, a marked glucose release from the perfused liver may be a convenient measure of hepatic toxicity for a variety of chemicals.
已对化学诱导的糖原分解与大鼠离体灌注肝脏中硫醇含量降低之间的关系进行了研究。2,4-二硝基苯酚（DNP）、马来酸二乙酯、醇类和抗炎剂（除水杨酸钠外）等化学物质可加速糖原分解。蛋白质硫醇的损失与葡萄糖释放速率的显著增加密切相关。与对照组相比，糖原分解速率略有增加导致非蛋白质硫醇损失，而蛋白质硫醇无明显损失。由于据报道蛋白质硫醇损失而非非蛋白质硫醇损失与肝细胞损伤相关，因此灌注肝脏中显著的葡萄糖释放可能是衡量多种化学物质肝毒性的便捷指标。
