巯基物质在氧自由基损伤离体胃粘膜细胞中的作用  

ROLE OF SULFHYDRYL COMPOUNDS IN THE OXYGEN RADICAL INDUCED INJURY OF ISOLATED GASTRIC MUCOSAL CELLS

作　　者：李铁[1] 张席锦[1] 

机构地区：[1]北京医科大学生理学教研室,北京100083

出　　处：《生理学报》1992年第4期386-393,共8页Acta Physiologica Sinica

摘　　要：本文用离体胃粘膜细胞研究了细胞内流基物质在活性氧诱发细胞损伤中的作用。实验采用pronase-EDTA法分离大鼠胃粘膜细胞并进行短期孵育,以黄嘌呤氧化酶(XO)-黄嘌呤(X)系统产生氧自由基损伤细胞。实验结果表明,用XO-X损伤胃粘膜细胞时,细胞存活率显著降低,乳酸脱氨酶(LDH)漏出量增多,同时细胞内非蛋白质巯基(NPSH)和蛋白质巯基(PSH)含量均不同程度地下降;N-乙基顺丁烯二酰亚胺(NEM)在耗竭细胞内NPSH和PSH的同时,引起细胞死亡和LDH漏出增加,这一作用与NEM的作用时间和浓度是显著依从关系;在细胞孵育液中预先加入含-SH的化合物还原型谷胱甘肽(GSH)或半胱胺,可剂量依赖性地减轻XO-X引起的细胞损伤。上述结果提示,胃粘膜细胞内的巯基物质在自身防御机制中具有重要作用,氧自由基损伤胃粘膜细胞的机制之一可能与破坏细胞内巯基的稳态有夫。Gastric mucosal cells were separated by pronase-EDTA method and cultur-ed. The cellular injury was produced by oxygen radicals provided by xanthineoxidase(XO)-xanthine(X) system. When the cells were subjected to the actionof XO-X system, the cellular viability was decreased and leakage of lactate dehy-drogenase (LDH) from the cells was significantly increased. In addition, the cel-lular contents of nonprotein sulfhydryls (NPSH) and protein sulfhydryls (PSH)were decreased. When the intracellular sulfhydryl content was decreased by N-ethylmaleimide (NEM, a depletor of endogenous sulfhydryls), the cell mortality andLDH leakage were increased in a time-dependent and dose-dependent manner. Ifglutathione or cysteamine (compounds containing-SH) was administrated intothe media, the cellular injury induced by XO-X system was notably inhibited, alsoin a dose-dependent manner. The above results suggest that sulfhydryls may playan important role in the cell defending mechanism against injury of gastric mu-cosal cells by oxygen radicals.

关 键 词：胃粘膜细胞 氧自由基 巯基 

分 类 号：R363[医药卫生—病理学]