尾孢菌素诱导的脂质过氧化可能是其毒性的一个决定因素。

Lipid peroxidation induced by cercosporin as a possible determinant of its toxicity.

作者信息

Cavallini L, Bindoli A, Macrì F, Vianello A

出版信息

Chem Biol Interact. 1979 Dec;28(2-3):139-46. doi: 10.1016/0009-2797(79)90156-x.

Abstract

The photodynamic action of cercosporin was assayed in various kinds of natural and artificial membranes. Cerosporin induces lipoperoxidation of liposomes, rat liver and pea internode mitochondria and microsomes, estimated both as malondialdehyde (MDA) formation and O2 consumption. Cercosporin-induced lipoperoxidation is inhibited by either singlet oxygen quenchers, free radical trapping agents or EDTA. Superoxide anion (O2-), hydrogen peroxide and hydroxyl radicals (.OH) are not involved in the activity of cercosporin. In addition cercosporin, by chelating iron, lowers the lipoperoxidation induced by such a metal. Therefore cercosporin stimulates, through singlet oxygen production, the hydroperoxide formation but, at the same time, it inhibits the continuation of the iron-mediated free radical chain. The present results suggest that cellular lipid peroxidation has a certain relevance to toxic activity of cercosporin.

摘要

在各种天然和人工膜中检测了尾孢菌素的光动力作用。尾孢菌素可诱导脂质体、大鼠肝脏、豌豆节间线粒体和微粒体发生脂质过氧化，这可通过丙二醛（MDA）的形成和氧气消耗来估算。尾孢菌素诱导的脂质过氧化可被单线态氧猝灭剂、自由基捕获剂或乙二胺四乙酸（EDTA）抑制。超氧阴离子（O2-）、过氧化氢和羟基自由基（·OH）不参与尾孢菌素的活性。此外，尾孢菌素通过螯合铁，降低了这种金属诱导的脂质过氧化。因此，尾孢菌素通过产生单线态氧刺激氢过氧化物的形成，但同时，它抑制了铁介导的自由基链的延续。目前的结果表明，细胞脂质过氧化与尾孢菌素的毒性活性有一定关联。