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体内暴露于低氧环境的大鼠小肠中的谷胱甘肽转运及谷胱甘肽依赖性解毒作用

GSH transport and GSH-dependent detoxication in small intestine of rats exposed in vivo to hypoxia.

作者信息

Bai C, Jones D P

机构信息

Department of Biochemistry, Emory University School of Medicine, Atlanta, Georgia 30322, USA.

出版信息

Am J Physiol. 1996 Oct;271(4 Pt 1):G701-6. doi: 10.1152/ajpgi.1996.271.4.G701.

DOI:10.1152/ajpgi.1996.271.4.G701
PMID:8897891
Abstract

The effects of hypoxia on glutathione (GSH) concentration and GSH-related enzyme and transport systems were studied in the small intestine of rats exposed to 8-10 days of 10.5% O2. Exposure to hypoxia resulted in a 40% lower GSH concentration in enterocytes and a 50% lower concentration in blood plasma. Activities of GSH-related detoxication enzymes in the intestinal epithelium were largely unaffected by hypoxic exposure. GSH degradation and synthesis rates in enterocytes isolated from hypoxic rats were comparable with rates in normoxic controls, but GSH uptake rate was decreased by 30%. Stimulation of absorption of GSH by phenylephrine, such as occurs in control rats, was not detectable in isolated, vascularly perfused intestines of hypoxic rats. Decreased GSH uptake was associated with enhanced transepithelial appearance of thiobarbituric acid-reactive substances in everted intestinal sacs incubated with peroxidized methyl linoleate. These results suggest that chronic hypoxia results in impaired uptake of GSH in the small intestine, and this may result in impaired GSH-related defense mechanisms in the small intestine.

摘要

研究了低氧对暴露于10.5%氧气环境8 - 10天的大鼠小肠中谷胱甘肽(GSH)浓度以及与GSH相关的酶和转运系统的影响。暴露于低氧环境导致肠细胞中GSH浓度降低40%,血浆中浓度降低50%。肠上皮中与GSH相关的解毒酶活性在很大程度上不受低氧暴露的影响。从低氧大鼠分离出的肠细胞中GSH降解和合成速率与常氧对照组相当,但GSH摄取率降低了30%。在低氧大鼠分离的、经血管灌注的小肠中,未检测到如在对照大鼠中发生的去氧肾上腺素对GSH吸收的刺激作用。GSH摄取减少与在过氧化亚油酸甲酯孵育的外翻肠囊中硫代巴比妥酸反应性物质的跨上皮出现增加有关。这些结果表明,慢性低氧导致小肠中GSH摄取受损,这可能导致小肠中与GSH相关的防御机制受损。

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