白三烯B4、C4、D4和E4被羟基自由基灭活。

Leukotriene B4, C4, D4 and E4 inactivation by hydroxyl radicals.

作者信息

Henderson W R, Klebanoff S J

出版信息

Biochem Biophys Res Commun. 1983 Jan 14;110(1):266-72. doi: 10.1016/0006-291x(83)91290-1.

Abstract

Leukotriene B4 chemotactic activity and leukotriene C4, D4 and E4 slow reacting substance activity were rapidly decreased by hydroxyl radicals generated by two different iron-supplemented acetaldehyde-xanthine oxidase systems. At low Fe2+, leukotriene inactivation was inhibited by catalase, superoxide dismutase, mannitol and ethanol, suggesting involvement of hydroxyl radicals generated by the iron-catalyzed interaction of superoxide and H2O2 (Haber-Weiss reaction). Leukotriene inactivation increased at high Fe2+ concentrations, but was no longer inhibitable by superoxide dismutase, suggesting that inactivation resulted from a direct interaction between H2O2 and Fe2+ to form hydroxyl radicals (Fenton reaction). The inactivation of leukotrienes by hydroxyl radicals suggests that oxygen metabolites generated by phagocytes may play a role in modulating leukotriene activity.

摘要

两种不同的铁强化乙醛 - 黄嘌呤氧化酶系统产生的羟基自由基可迅速降低白三烯B4趋化活性以及白三烯C4、D4和E4慢反应物质活性。在低铁离子浓度下，过氧化氢酶、超氧化物歧化酶、甘露醇和乙醇可抑制白三烯的失活，这表明超氧化物与过氧化氢通过铁催化相互作用产生的羟基自由基参与其中（哈伯 - 韦斯反应）。在高铁离子浓度下，白三烯失活增加，但不再受超氧化物歧化酶抑制，这表明失活是由过氧化氢与铁离子直接相互作用形成羟基自由基所致（芬顿反应）。羟基自由基对白三烯的失活作用表明，吞噬细胞产生的氧代谢产物可能在调节白三烯活性中发挥作用。