Phillips B J, James T E, Anderson D
Mutat Res. 1984 May;126(3):265-71. doi: 10.1016/0027-5107(84)90006-x.
The genetic toxicity of active oxygen species produced during the enzymic oxidation of xanthine has been investigated using Chinese hamster ovary (CHO) cells. Incubation of cells with xanthine plus xanthine oxidase resulted in extensive chromosome breakage and sister-chromatid exchange and gave a small increase in frequency of thioguanine-resistant cells (HGPRT test). Inclusion of superoxide dismutase or catalase in the xanthine/xanthine oxidase system inhibited chromosome breakage, whereas only catalase prevented SCE and mutant induction. It is concluded that hydrogen peroxide is responsible for most of the genetic effects observed in CHO cells exposed to xanthine/xanthine oxidase but that superoxide plays a key role in chromosome breakage.
利用中国仓鼠卵巢(CHO)细胞研究了黄嘌呤酶促氧化过程中产生的活性氧的遗传毒性。将细胞与黄嘌呤加黄嘌呤氧化酶一起孵育,导致广泛的染色体断裂和姐妹染色单体交换,并使硫代鸟嘌呤抗性细胞的频率略有增加(次黄嘌呤 - 鸟嘌呤磷酸核糖转移酶试验)。在黄嘌呤/黄嘌呤氧化酶系统中加入超氧化物歧化酶或过氧化氢酶可抑制染色体断裂,而只有过氧化氢酶可防止姐妹染色单体交换和突变诱导。得出的结论是,过氧化氢是暴露于黄嘌呤/黄嘌呤氧化酶的CHO细胞中观察到的大多数遗传效应的原因,但超氧化物在染色体断裂中起关键作用。