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大鼠心脏中的氧化应激:低水平化学发光研究

Oxidative stress in the rat heart, studies on low-level chemiluminescence.

作者信息

Ursini F, Barsacchi R, Pelosi G, Benassi A

机构信息

Department of Biological Chemistry, University of Padova, Italy.

出版信息

J Biolumin Chemilumin. 1989 Jul;4(1):241-4. doi: 10.1002/bio.1170040134.

DOI:10.1002/bio.1170040134
PMID:2801215
Abstract

Detection of ultraweak chemiluminescence (CL) emission from the surface of the organ is a sensitive and non-disruptive tool to evaluate the oxidative stress in rat heart. Indeed, an increased photon emission rate can be observed when cellular antioxidants such as glutathione or vitamin E are depleted, or when organic hydroperoxides are infused. We used CL recording to demonstrate in rat heart that: (i) different diets may lead to different heart sensitivity to an oxidative stress; and (ii) post-ischaemic reoxygenation induces an oxidative stress. CL emission induced by an oxidative stress is accompanied by an increased release of eicosanoids. However, while non-steroid anti-inflammatory drugs (aspirin, indomethacin and ibuprofen) prevented eicosanoid release, these compounds dramatically enhanced hydroperoxide-dependent CL. The nature of this phenomenon is still obscure, but the increase of steady-state concentration of excited species caused by anti-inflammatory drugs seems to be pathophysiologically relevant, since in all our experimental conditions tissue damage was proportional to CL emission rate.

摘要

检测器官表面的超微弱化学发光(CL)发射是评估大鼠心脏氧化应激的一种敏感且非侵入性的工具。事实上,当细胞抗氧化剂如谷胱甘肽或维生素E耗尽时,或者当注入有机氢过氧化物时,可以观察到光子发射率增加。我们使用CL记录来证明在大鼠心脏中:(i)不同的饮食可能导致心脏对氧化应激的敏感性不同;(ii)缺血后复氧会诱导氧化应激。氧化应激诱导的CL发射伴随着类花生酸释放的增加。然而,虽然非甾体抗炎药(阿司匹林、吲哚美辛和布洛芬)可阻止类花生酸的释放,但这些化合物却显著增强了氢过氧化物依赖性CL。这种现象的本质仍然不清楚,但抗炎药引起的激发态物种稳态浓度的增加似乎在病理生理学上具有相关性,因为在我们所有的实验条件下,组织损伤与CL发射率成正比。

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