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急性应激期间的脂质过氧化作用。

Lipid peroxidation during acute stress.

作者信息

Kovács P, Juránek I, Stankovicová T, Svec P

机构信息

Department of Pharmacology, Comenius University, Bratislava, Slovak Republic.

出版信息

Pharmazie. 1996 Jan;51(1):51-3.

PMID:8999436
Abstract

Lipid peroxidation (LPO) is one of the main events induced by oxidative stress. The aim of our study was to investigate the influence of 30 min cold-immobilization (model of acute stress used in this experiment) on LPO in the brain, heart, liver and stomach homogenates of the rats. LPO was determined by measuring of the contents of thiobarbituric acid reactive substances (TBARS), conjugated dienes (CD) and sulfhydryl groups (SH). Experimental stress induced enhancement of TBARS formation in the liver and increased level of the CD in the heart, stomach and liver, while in the brain both parameters were found to be decreased. The levels of TBARS were not changed in the heart and in the stomach, too. The concentrations of SH-groups were decreased in the heart, brain and stomach, while in the liver the parameter was found to be not changed. The results of this study showed the increase of LPO in the heart, stomach and liver under stress conditions. It could be supposed that LPO may be involved in mechanisms of stress injury in different tissues.

摘要

脂质过氧化(LPO)是氧化应激诱导的主要事件之一。我们研究的目的是调查30分钟冷束缚(本实验中使用的急性应激模型)对大鼠脑、心脏、肝脏和胃匀浆中LPO的影响。通过测量硫代巴比妥酸反应性物质(TBARS)、共轭二烯(CD)和巯基(SH)的含量来测定LPO。实验性应激导致肝脏中TBARS形成增加,心脏、胃和肝脏中CD水平升高,而在脑中这两个参数均降低。心脏和胃中TBARS水平也未改变。心脏、脑和胃中SH基团的浓度降低,而肝脏中的该参数未改变。本研究结果表明,应激条件下心脏、胃和肝脏中的LPO增加。可以推测,LPO可能参与不同组织的应激损伤机制。

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