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邻菲罗啉对哺乳动物细胞的保护作用:免受活性氧产生的致死和DNA损伤效应影响

Protection of mammalian cells by o-phenanthroline from lethal and DNA-damaging effects produced by active oxygen species.

作者信息

de Mello Filho A C, Meneghini R

出版信息

Biochim Biophys Acta. 1985 Oct 30;847(1):82-9. doi: 10.1016/0167-4889(85)90156-9.

Abstract

Active oxygen species are suspected as being a cause of the cellular damage that occurs at the site of inflammation. Phagocytic cells accumulate at these sites and produce superoxide ion, hydrogen peroxide and hydroxyl radical. The ultimate killing species, the cellular target and the mechanism whereby the lethal injury is produced are unknown. We exposed mouse fibroblasts to xanthine oxidase and acetaldehyde, a system which mimics the membrane of phagocytic cells in terms of production of oxygen species. We observed that the generation of these species produced DNA strand breaks and cellular death. The metal chelator o-phenanthroline completely abolished the former effect, and at the same time it effectively protected the cells from lethal injuries. Because complexing iron o-phenanthroline prevents the formation of hydroxyl radical by the Fendon reaction (Fe(II) + H2O2----Fe(III) + OH- + OH.), it is proposed that most of the cell death and DNA damage are brought about by OH radical, produced from other species by iron-mediated reactions.

摘要

活性氧被怀疑是炎症部位发生细胞损伤的一个原因。吞噬细胞聚集在这些部位并产生超氧离子、过氧化氢和羟基自由基。最终的杀伤物质、细胞靶点以及产生致命损伤的机制尚不清楚。我们将小鼠成纤维细胞暴露于黄嘌呤氧化酶和乙醛中,该体系在产生活性氧方面模拟吞噬细胞膜。我们观察到这些物质的产生导致了DNA链断裂和细胞死亡。金属螯合剂邻菲罗啉完全消除了前者的效应,同时有效地保护细胞免受致命损伤。由于邻菲罗啉与铁络合可通过芬顿反应(Fe(II) + H2O2→Fe(III) + OH- + OH.)阻止羟基自由基的形成,因此有人提出,大多数细胞死亡和DNA损伤是由铁介导反应从其他物质产生的羟基自由基所致。

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