Yamanaka K, Hasegawa A, Sawamura R, Okada S
Department of Pharmacy, Nihon University College of Science and Technology, Tokyo, Japan.
Biochem Biophys Res Commun. 1989 Nov 30;165(1):43-50. doi: 10.1016/0006-291x(89)91031-0.
In order to study the genotoxicity of arsenics, we focused our attention on dimethylarsinic acid (DMAA) which was a main metabolite of inorganic arsenics in mammals. ICR mice were orally administered DMAA-Na (1500mg/kg). DNA single-strand breaks occurred specifically in lung at 12h after administration. An in vitro experiment indicated that the breaks were not caused directly by DMAA but by dimethylarsine, a further metabolite of DMAA. Furthermore, the dimethylarsine-induced breaks were diminished by the addition of SOD and catalase, suggesting that active oxygen produced by dimethylarsine was involved in the induction of DNA damage.
为了研究砷的遗传毒性，我们将注意力集中在二甲基次砷酸（DMAA）上，它是无机砷在哺乳动物体内的主要代谢产物。给ICR小鼠口服DMAA-Na（1500mg/kg）。给药后12小时，DNA单链断裂特异性地出现在肺部。体外实验表明，这些断裂不是由DMAA直接引起的，而是由DMAA的进一步代谢产物二甲基胂引起的。此外，添加超氧化物歧化酶（SOD）和过氧化氢酶可减少二甲基胂诱导的断裂，这表明二甲基胂产生的活性氧参与了DNA损伤的诱导。
