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大鼠小肠中硒酸盐的吸收:与谷胱甘肽的相互作用。

Absorption of selenite in the rat small intestine: interactions with glutathione.

作者信息

Anundi I, Högberg J, Ståhl A

出版信息

Acta Pharmacol Toxicol (Copenh). 1984 Apr;54(4):273-7. doi: 10.1111/j.1600-0773.1984.tb01930.x.

Abstract

Incubation of isolated rat intestinal epithelial cells with selenite resulted in a rapid decrease of intracellular glutathione (GSH) and about 5 nmol of Se (added as 75Se labelled selenite, 50 microM) was accumulated per 10(6) cells during 20 min. Addition of exogenous GSH enhanced cellular accumulation of Se, while the gamma-glutamyl transferase inhibitor, serine-borate, decreased uptake. The added exogenous GSH was rapidly consumed (oxidized) by selenite. Depletion of GSH by diethylmaleate (DEM) inhibited selenite uptake both in in situ isolated intestinal loop, everted gut sacs and in isolated intestinal cells. The findings indicate that both intracellular and extracellular GSH, and gamma-glutamyltransferase, play a role in the absorption of selenite in the intestine.

摘要

用亚硒酸盐孵育分离的大鼠肠上皮细胞,导致细胞内谷胱甘肽(GSH)迅速减少,在20分钟内每10⁶个细胞积累约5 nmol的硒(以75Se标记的亚硒酸盐形式添加,50 μM)。添加外源性GSH可增强细胞对硒的积累,而γ-谷氨酰转移酶抑制剂丝氨酸硼酸盐则降低摄取量。添加的外源性GSH被亚硒酸盐迅速消耗(氧化)。马来酸二乙酯(DEM)消耗GSH抑制了亚硒酸盐在原位分离肠袢、外翻肠囊和分离肠细胞中的摄取。这些发现表明,细胞内和细胞外的GSH以及γ-谷氨酰转移酶在肠道中亚硒酸盐的吸收中起作用。

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