Parshad R, Sanford K K, Tarone R E, Jones G M, Baeck A E
Cancer Res. 1979 Mar;39(3):929-33.
Exposure of mouse cells in culture to fluorescent light has been shown to produce chromatid breaks and exchanges. Hydrogen peroxide formed in the cell during illumination has been implicated as the causative agent. The present results indicate that susceptibility to light-induced chromosome damage increases with time in culture and seems to be associated with or requisite for the spontaneous malignant transformation of mouse cells. All three cell lines followed during long-term culture that either became tumorigenic or showed cytological evidence of neoplastic transformation developed a concomitant increase in susceptibility. In three additional cell lines, susceptibility to light-induced chromatid damage was significantly increased in the spontaneously transformed malignant cells as compared with their nonneoplastic precursors. The increased susceptibility is not simply the result of long-term culture, since three other nonneoplastic cell lines after prolonged culture were significantly less susceptible than their malignant counterparts. Increased susceptibility to light-induced chromatid damage could result from impaired DNA repair or from the loss of defense mechanisms for destroying H2O2 or scavenging free radicals.
已证明,培养中的小鼠细胞暴露于荧光下会产生染色单体断裂和交换。光照期间细胞中形成的过氧化氢被认为是致病因素。目前的结果表明,对光诱导的染色体损伤的易感性会随着培养时间的增加而增加,并且似乎与小鼠细胞的自发恶性转化相关或为其必要条件。在长期培养过程中追踪的所有三个细胞系,无论是变成致瘤性的还是显示出肿瘤转化的细胞学证据,其对光的易感性都随之增加。在另外三个细胞系中,与它们的非肿瘤前体细胞相比,自发转化的恶性细胞对光诱导的染色单体损伤的易感性显著增加。易感性增加并非仅仅是长期培养的结果,因为另外三个非肿瘤细胞系在长时间培养后比它们的恶性对应物的易感性显著降低。对光诱导的染色单体损伤易感性增加可能是由于DNA修复受损,或者是由于破坏过氧化氢或清除自由基的防御机制丧失所致。