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[禁食期间谷胱甘肽的施用及脂质过氧化作用]

[Administration of glutathione and lipid peroxidation induced during fasting].

作者信息

Angelini P, Cirelli F, Quarticelli A, Chicco D, Vendemiale G, Altomare E

机构信息

Istituto di Clinica Medica 1, Università di Bari.

出版信息

Boll Soc Ital Biol Sper. 1990 Nov;66(11):1097-104.

PMID:2095820
Abstract

It is well known that lipid peroxidation may be initiated or exaggerated by conditions leading to hepatic GSH depletion or altered GSH/GSSG ratio. In our study we evaluated the effects of GSH administration on hepatic, bile and plasma GSH, GSSG and MDA in rats depleted of the tripeptide by a prolonged. fasting. An exteriorized biliary-duodenal fistula was established and GSH or saline solution was administered i.p. for a period of 6h. Rats treated with GSH exhibited an increased GSH and decreased GSSG biliary excretion. Whereas in control rats an opposite pattern was observed, namely enhanced GSSG and decreased GSH biliary excretion. While hepatic GSH and GSSG concentrations were comparable in the two groups, a significant increase in liver and plasma MDA production was found in controls compared to GSH treated rats. Our data suggest a protective role of GSH against the production of lipoperoxidation as evidenced by the decrease of hepatic, biliary and plasma MDA levels and by a decreased percentage of biliary GSSG. In addition, the significant increase of biliary GSH excretion, observed in rats treated with GSH compared to controls, may be due to an increased supply of the tripeptide which is known to be preferentially excreted into bile in the reduced form.

摘要

众所周知,导致肝脏谷胱甘肽(GSH)耗竭或GSH/氧化型谷胱甘肽(GSSG)比值改变的情况可能引发或加剧脂质过氧化。在我们的研究中,我们评估了给通过长期禁食使三肽耗竭的大鼠腹腔注射GSH后,其肝脏、胆汁和血浆中GSH、GSSG和丙二醛(MDA)的变化。建立了体外胆管十二指肠瘘,腹腔注射GSH或生理盐水,持续6小时。用GSH治疗的大鼠胆汁中GSH排泄增加,GSSG排泄减少。而在对照大鼠中观察到相反的模式,即胆汁中GSSG排泄增加,GSH排泄减少。虽然两组大鼠肝脏中GSH和GSSG的浓度相当,但与GSH治疗的大鼠相比,对照组肝脏和血浆中MDA的生成显著增加。我们的数据表明,GSH对脂质过氧化的产生具有保护作用,这一点通过肝脏、胆汁和血浆中MDA水平的降低以及胆汁中GSSG百分比的降低得到证明。此外,与对照组相比,用GSH治疗的大鼠胆汁中GSH排泄显著增加,可能是由于三肽供应增加,已知三肽优先以还原形式排泄到胆汁中。

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