Zasukhina G D, Vasil'eva I M, Alekhina N I, Semiachkina A N
Vavilov Institute of General Genetics, Russian Academy of Sciences, Moscow, 119991 Russia.
Genetika. 2003 Dec;39(12):1630-3.
The superoxide dismutase (SOD) inhibitor, TRIEN, which enhanced the formation of gamma-induced DNA breaks in cells of healthy donors and patients with Marfan syndrome and Bloom syndrome (repair-defective hereditary diseases), had virtually no effect on the formation of radioadaptive response (RAR) in these systems. Similar results were obtained in studies on cell survival: TRIEN facilitated mortality in cells irradiated with gamma-rays but did not affect RAR formation. TRIEN also increased the deleterious effect of CdCl2, which indicates that SOD apparently plays a certain role in cell defence against this mutagen.
超氧化物歧化酶（SOD）抑制剂TRIEN可增强健康供体以及患有马凡氏综合征和布卢姆综合征（遗传性修复缺陷疾病）患者细胞中γ射线诱导的DNA断裂形成，但在这些系统中对辐射适应性反应（RAR）的形成几乎没有影响。在细胞存活研究中也得到了类似结果：TRIEN促进了γ射线照射细胞的死亡率，但不影响RAR的形成。TRIEN还增强了CdCl2的有害作用，这表明SOD显然在细胞抵御这种诱变剂中发挥了一定作用。
