Weitberg A B
Division of Hematology/Oncology, Roger Williams Cancer Center, Providence, Rhode Island.
Am J Med Sci. 1990 Jan;299(1):50-3. doi: 10.1097/00000441-199001000-00011.
Oxygen radical-induced genetic damage may be mediated by products of lipid peroxidation, in particular, arachidonic acid. Several isomeric hydroxy- and hydroperoxy-6,8,11,14-eicosatetraenoic acids (HETEs and HPETEs), intermediates of arachidonic acid metabolism, were evaluated for their ability to cause sister chromatid exchanges (SCEs) in Chinese hamster ovary (CHO) cells. Both HETEs and HPETEs induced SCEs in a dose-dependent fashion at concentrations of 5, 10, and 20 microM. At each concentration, HETEs were more effective in producing SCEs than the corresponding HPETEs. Each of the isomeric forms used were equally effective in producing genetic damage. Antioxidants (superoxide dismutase, catalase and mannitol) were protective suggesting an intermediate role for the hydroxyl radical. Iron chelation by desferrioxamine suppressed SCE induction by 45% and an additional 33% inhibition was observed upon the addition of the calcium chelator EGTA.
氧自由基诱导的遗传损伤可能由脂质过氧化产物介导，尤其是花生四烯酸。对花生四烯酸代谢的几种异构体羟基和氢过氧基-6,8,11,14-二十碳四烯酸（HETEs和HPETEs）在中国仓鼠卵巢（CHO）细胞中引起姐妹染色单体交换（SCEs）的能力进行了评估。HETEs和HPETEs在5、10和20微摩尔浓度下均以剂量依赖方式诱导SCEs。在每个浓度下，HETEs在产生SCEs方面比相应的HPETEs更有效。所使用的每种异构体形式在产生遗传损伤方面同样有效。抗氧化剂（超氧化物歧化酶、过氧化氢酶和甘露醇）具有保护作用，表明羟基自由基起中间作用。去铁胺的铁螯合作用使SCE诱导减少45%，加入钙螯合剂EGTA后又观察到33%的抑制作用。
