St Clair D K, Wan X S, Oberley T D, Muse K E, St Clair W H
Graduate Center for Toxicology, University of Kentucky, Lexington 40506-0054.
Mol Carcinog. 1992;6(4):238-42. doi: 10.1002/mc.2940060404.
Manganese superoxide dismutase (MnSOD) scavenges toxic superoxide radicals produced in the mitochondria. Transfection of the human MnSOD gene into mouse C3H 10T1/2 cells resulted in production of active MnSOD, which was properly transported into mitochondria. Overexpression of MnSOD protected cells from radiation-, but not chemically-induced neoplastic transformation. This finding demonstrates that oxidative stress that occurs in the mitochondria plays an important role in the development of neoplastic transformation.
锰超氧化物歧化酶(MnSOD)可清除线粒体中产生的有毒超氧自由基。将人类MnSOD基因转染到小鼠C3H 10T1/2细胞中可产生活性MnSOD,其能被正确转运到线粒体中。MnSOD的过表达可保护细胞免受辐射诱导的肿瘤转化,但不能保护细胞免受化学诱导的肿瘤转化。这一发现表明,线粒体中发生的氧化应激在肿瘤转化的发生中起重要作用。