Li T, Zhang X J
Department of Physiology, Beijing Medical University.
Sheng Li Xue Bao. 1992 Aug;44(4):386-93.
Gastric mucosal cells were separated by pronase-EDTA method and cultured. The cellular injury was produced by oxygen radicals provided by xanthine oxidase(XO)-xanthine(X) system. When the cells were subjected to the action of XO-X system, the cellular viability was decreased and leakage of lactate dehydrogenase (LDH) from the cells was significantly increased. In addition, the cellular 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 and LDH leakage were increased in a time-dependent and dose-dependent manner. If glutathione or cysteamine (compounds containing-SH) was administered into the media, the cellular injury induced by XO-X system was notably inhibited, also in a dose-dependent manner. The above results suggest that sulfhydryls may play an important role in the cell defending mechanism against injury of gastric mucosal cells by oxygen radicals.
采用胰蛋白酶-乙二胺四乙酸(EDTA)法分离并培养胃黏膜细胞。通过黄嘌呤氧化酶(XO)-黄嘌呤(X)系统产生的氧自由基造成细胞损伤。当细胞受到XO-X系统作用时,细胞活力降低,细胞内乳酸脱氢酶(LDH)泄漏显著增加。此外,非蛋白巯基(NPSH)和蛋白巯基(PSH)的细胞含量降低。当用N-乙基马来酰亚胺(NEM,一种内源性巯基消耗剂)降低细胞内巯基含量时,细胞死亡率和LDH泄漏呈时间依赖性和剂量依赖性增加。如果将谷胱甘肽或半胱胺(含-SH的化合物)加入培养基中,XO-X系统诱导的细胞损伤也会受到显著抑制,且同样呈剂量依赖性。上述结果表明,巯基可能在胃黏膜细胞抵御氧自由基损伤的细胞防御机制中发挥重要作用。