Wang D, Verney E, Sidransky H
Exp Mol Pathol. 1985 Dec;43(3):364-74. doi: 10.1016/0014-4800(85)90073-5.
The effects of the administration of tryptophan and/or cysteine on carbon tetrachloride (CCl4)-induced hepatic injury were investigated. Rats received CCl4 (1 ml/kg ip) followed 6 hr later by tryptophan (300 mg/kg) and/or cysteine (950 mg/kg) via stomach tube and rats were killed after 24 hr. Treatment with tryptophan, cysteine, or both reduced the degree of hepatic necrosis observed histologically. While CCl4 caused polyribosomal disaggregation and decreased [14C]leucine incorporation into liver proteins in vitro and in vivo, treatment with tryptophan, cysteine, or both caused a shift in polyribosomes toward heavier aggregation and protein synthesis was increased. Serum activities of lactic dehydrogenase (LDH), glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, and gamma-glutamyl-transpeptidase were markedly increased after CCl4 alone but after subsequent treatment with cysteine or with tryptophan and cysteine appreciable decreases occurred. Glutathione concentration decreased but total amount remained constant in the livers of CCl4-treated rats while subsequent treatment with cysteine alone or together with tryptophan elevated both levels of glutathione. Using isolated hepatocytes, CCl4 caused decreases in cell viability, in release of LDH, and in [14C]leucine incorporation into protein. Treatment with CCl4 and tryptophan and/or cysteine revealed that cysteine alone or with tryptophan improved cell viability and decreased LDH release of the cells, while tryptophan alone or with cysteine improved protein synthesis. Upon cytologic evaluation, the isolated hepatocytes revealed membrane distortions after CCl4 alone but these were less marked after CCl4 plus tryptophan, cysteine, or both (most improvement). Thus, tryptophan and cysteine act in a beneficial manner against CCl4-induced hepatic injury in the rat.
研究了色氨酸和/或半胱氨酸给药对四氯化碳（CCl4）诱导的肝损伤的影响。大鼠腹腔注射CCl4（1 ml/kg），6小时后经胃管给予色氨酸（300 mg/kg）和/或半胱氨酸（950 mg/kg），24小时后处死大鼠。色氨酸、半胱氨酸或两者联合治疗均可减轻组织学观察到的肝坏死程度。虽然CCl4在体内外均可导致多核糖体解聚，并降低[14C]亮氨酸掺入肝脏蛋白质的量，但色氨酸、半胱氨酸或两者联合治疗可使多核糖体向更重的聚集方向转变，蛋白质合成增加。单独给予CCl4后，血清乳酸脱氢酶（LDH）、谷草转氨酶、谷丙转氨酶和γ-谷氨酰转肽酶活性显著升高，但随后给予半胱氨酸或色氨酸与半胱氨酸联合治疗后，这些酶活性明显降低。CCl4处理的大鼠肝脏中谷胱甘肽浓度降低，但总量保持不变，而随后单独给予半胱氨酸或与色氨酸联合治疗可提高谷胱甘肽水平。使用分离的肝细胞，CCl4可导致细胞活力降低、LDH释放减少以及[14C]亮氨酸掺入蛋白质减少。CCl4与色氨酸和/或半胱氨酸联合处理显示，单独使用半胱氨酸或与色氨酸联合使用可提高细胞活力并减少细胞LDH释放，而单独使用色氨酸或与半胱氨酸联合使用可改善蛋白质合成。在细胞学评估中，单独使用CCl4后分离的肝细胞显示细胞膜变形，但在CCl4加色氨酸、半胱氨酸或两者联合处理后（改善最明显），这种变形不那么明显。因此，色氨酸和半胱氨酸对大鼠CCl4诱导的肝损伤具有有益作用。
