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丙烯醛诱导的氧自由基形成。

Acrolein-induced oxygen radical formation.

作者信息

Adams J D, Klaidman L K

机构信息

Department of Molecular Pharmacology and Toxicology, School of Pharmacy, University of Southern California, Los Angeles 90033.

出版信息

Free Radic Biol Med. 1993 Aug;15(2):187-93. doi: 10.1016/0891-5849(93)90058-3.

Abstract

The mechanism of acrolein-induced lipid peroxidation is unknown. This study found that acrolein and its glutathione adduct, glutathionylpropionaldehyde, induce oxygen radical formation. These oxygen radicals may be responsible for the induction of lipid peroxidation by acrolein. The enzymes xanthine oxidase and aldehyde dehydrogenase were found to interact with glutathionylpropionaldehyde to produce O2.- and HO(.). Acrolein was oxidized by xanthine oxidase to produce acroleinyl radical and O2(.-). Aldehyde dehydrogenase metabolized acrolein to form O2.- but not acroleinyl radical. The fact that glutathionylpropionaldehyde is a more potent stimulator of oxygen radical formation than acrolein indicates that glutathionylpropionaldehyde is a toxic metabolite of acrolein and may be responsible for some of the in vivo toxicity of acrolein.

摘要

丙烯醛诱导脂质过氧化的机制尚不清楚。本研究发现,丙烯醛及其谷胱甘肽加合物谷胱甘肽丙醛可诱导氧自由基形成。这些氧自由基可能是丙烯醛诱导脂质过氧化的原因。研究发现,黄嘌呤氧化酶和醛脱氢酶与谷胱甘肽丙醛相互作用产生超氧阴离子(O2.-)和羟基自由基(HO(.))。黄嘌呤氧化酶将丙烯醛氧化生成丙烯醛自由基和超氧阴离子(O2(.-))。醛脱氢酶将丙烯醛代谢生成超氧阴离子(O2.-),但不生成丙烯醛自由基。谷胱甘肽丙醛比丙烯醛更能有效地刺激氧自由基形成,这一事实表明谷胱甘肽丙醛是丙烯醛的一种毒性代谢产物,可能是丙烯醛体内部分毒性的原因。

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