Parshad R, Taylor W G, Sanford K K, Camalier R F, Gantt R, Tarone R E
Mutat Res. 1980 Nov;73(1):115-24. doi: 10.1016/0027-5107(80)90140-2.
Exposure of human fibroblasts (IMR-90) to cool-white fluorescent light causes chromatid breaks and exchanges. This chromatid damage is caused largely by the production of hydrogen peroxide (H2O2) since it can be prevented almost completely by the addition of catalase. In support of this conclusion, exogenous H2O2 is shown to induce chromatid breaks. The clastogenic amounts of H2O2 generated during light exposure are formed within the cell since cells illuminated in saline showed the same extent of damage as cells in culture medium. Addition of selenite to the cultures during light exposure significantly decreases the chromatid damage in a dose-related manner and may be necessary to maintain sufficient activity of glutathione peroxidase. The free hydroxyl radical, . OH, appears to be partially responsible for the light-induced chromatid damage. Of the free-radical scavengers tested, i.e., mannitol, vitamin E, and dimethyl sulfoxide, only mannitol, which scavenges . OH, significantly decreases the light-induced chromatid damage. Thus, both . OH and H2O2 formed within the cell during light exposure are agents that directly or indirectly cause chromatid damage.
将人成纤维细胞（IMR - 90）暴露于冷白色荧光灯下会导致染色单体断裂和交换。这种染色单体损伤主要是由过氧化氢（H₂O₂）的产生引起的，因为添加过氧化氢酶几乎可以完全防止这种损伤。为支持这一结论，外源性H₂O₂被证明可诱导染色单体断裂。光照期间产生的具有致断裂作用的H₂O₂量是在细胞内形成的，因为在盐溶液中光照的细胞与在培养基中的细胞显示出相同程度的损伤。在光照期间向培养物中添加亚硒酸盐以剂量相关的方式显著降低染色单体损伤，并且可能是维持谷胱甘肽过氧化物酶足够活性所必需的。游离羟基自由基·OH似乎部分导致了光照诱导的染色单体损伤。在所测试的自由基清除剂中，即甘露醇、维生素E和二甲基亚砜，只有能够清除·OH的甘露醇显著降低了光照诱导的染色单体损伤。因此，光照期间在细胞内形成的·OH和H₂O₂都是直接或间接导致染色单体损伤的因素。
