Weitberg A B
Division of Hematology/Oncology, Roger Williams Cancer Center, Providence, RI 02908.
Carcinogenesis. 1987 Nov;8(11):1619-20. doi: 10.1093/carcin/8.11.1619.
Oxidative damage to membranes initiates lipid peroxidation chain reactions and stimulation of the arachidonic acid cascade. The products of these reactions may mediate the genetic toxicity of oxygen radicals. Arachidonic acid alone induced sister chromatid exchange (SCE) formation and significantly augmented the genetic damage observed with an oxygen radical-generating system. The number of SCEs was reduced significantly in oxygen radical-treated Chinese hamster ovary cells incubated with inhibitors of the cyclo-oxygenase and lipoxygenase pathways. Vitamin E, when combined with inhibitors of arachidonic acid metabolism, protected target cells completely from oxygen radical-induced genotoxicity. These data support the hypothesis that lipid peroxidation intermediates may be involved in the genesis of radical-generated genetic lesions.
膜的氧化损伤引发脂质过氧化链式反应并刺激花生四烯酸级联反应。这些反应的产物可能介导氧自由基的遗传毒性。单独的花生四烯酸可诱导姐妹染色单体交换（SCE）形成，并显著增强用氧自由基生成系统观察到的遗传损伤。在用环氧化酶和脂氧化酶途径抑制剂孵育的经氧自由基处理的中国仓鼠卵巢细胞中，SCE的数量显著减少。维生素E与花生四烯酸代谢抑制剂联合使用时，可使靶细胞完全免受氧自由基诱导的遗传毒性。这些数据支持脂质过氧化中间体可能参与自由基产生的遗传损伤发生的假说。
