过氧化物肿瘤启动子在肝脏线粒体中产生自由基。

Radical production in liver mitochondria by peroxidic tumor promoters.

作者信息

Kennedy C H, Dyer J M, Church D F, Winston G W, Pryor W A

机构信息

Biodynamics Institute, Louisiana State University, Baton Rouge 70803.

出版信息

Biochem Biophys Res Commun. 1989 May 15;160(3):1067-72. doi: 10.1016/s0006-291x(89)80111-1.

DOI:10.1016/s0006-291x(89)80111-1

PMID:2543385

Abstract

Eleven peroxides have been tested to determine if there is a correlation between tumor-promoting activity and the ability to stimulate radical production in mitochondria. When non-respiring rat liver mitochondria are treated with these peroxidic compounds in the presence of DMPO, ESR signals are observed from the spin trapping of carbon- and oxygen-centered radicals in the case of 4 of the 7 peroxides that are known to be tumor promoters. Enhancement of carbon-centered radical production is observed in the presence of respiratory substrate. Thus there does not appear to be a correlation between tumor-promoting activity of peroxidic compounds and radical production in mitochondria. Oxidants can act as promoters either by 1- or 2-electron oxidation pathways; both types of mechanisms may be inhibited by antioxidants, which can scavenge either radicals or electrophiles.

摘要

已对11种过氧化物进行了测试，以确定肿瘤促进活性与刺激线粒体自由基产生能力之间是否存在相关性。当在DMPO存在的情况下用这些过氧化物化合物处理不呼吸的大鼠肝线粒体时，在已知为肿瘤促进剂的7种过氧化物中的4种情况下，观察到了碳中心和氧中心自由基自旋捕获产生的ESR信号。在有呼吸底物存在的情况下，观察到碳中心自由基产生增强。因此，过氧化物化合物的肿瘤促进活性与线粒体中的自由基产生之间似乎不存在相关性。氧化剂可通过单电子或双电子氧化途径充当促进剂；这两种机制都可能被抗氧化剂抑制，抗氧化剂可以清除自由基或亲电试剂。