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巯基化合物在大鼠胃上皮细胞抵御氧反应性代谢产物诱导损伤中的作用。

Role of sulphydryl compounds in the defense of rat gastric epithelial cells against oxygen reactive metabolite-induced damage.

作者信息

Romano M, Razandi M, Ivey K J

机构信息

Istituto di Medicina Generale e Metodologia Clinica, I Facoltà di Medicina, Napoli, Italy.

出版信息

Ital J Gastroenterol. 1991 Feb;23(2):55-9.

PMID:1747503
Abstract

This study evaluated the role of endogenous and exogenous sulphydryl compounds in the defense of rat gastric epithelial cells against damage brought about by oxygen reactive metabolites in vitro. Toxic oxygen species were generated by xanthine oxidase in the presence of xanthine. Cell damage was assessed by 51 chromium release assay. Our data confirm that xanthine oxidase, in the presence of xanthine damages cultured rat gastric cells in a dose dependent manner (r = 0.0885, p less than 0.05). Depletion of endogenous thiols by N-ethylmaleimide significantly increases the amount of damage induced by oxygen radicals causing, at the concentration of 0.005 mM, a 60% increase in 51 chromium release (p less than 0.001). The sulphydryl agent cysteamine did not prevent cell damage induced by oxygen reactive metabolites. In conclusion, 1) depletion of endogenous thiols significantly increases the susceptibility of rat gastric epithelial cells to oxygen radical-induced damage; 2) this damage is not prevented by an exogenous agent containing a SH group.

摘要

本研究评估了内源性和外源性巯基化合物在体外保护大鼠胃上皮细胞免受氧反应性代谢产物所致损伤中的作用。在黄嘌呤存在的情况下,通过黄嘌呤氧化酶产生有毒氧物种。通过51铬释放试验评估细胞损伤。我们的数据证实,在黄嘌呤存在的情况下,黄嘌呤氧化酶以剂量依赖性方式损伤培养的大鼠胃细胞(r = 0.0885,p小于0.05)。N - 乙基马来酰亚胺消耗内源性硫醇会显著增加氧自由基诱导的损伤量,在0.005 mM浓度下,51铬释放增加60%(p小于0.001)。巯基试剂半胱胺不能预防氧反应性代谢产物诱导的细胞损伤。总之,1)内源性硫醇的消耗显著增加大鼠胃上皮细胞对氧自由基诱导损伤的易感性;2)含有SH基团的外源性试剂不能预防这种损伤。

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