Abstract
XRS-5, 是輻射線敏感的細胞株, 但同樣對許多自由基氧產生之藥物例如 過氧化氫、硫化亞鐵、亞砷酸鈉等亦較敏感. 本研究發現, XRS-5 細胞內 麩胱甘胜過氧化酵素(glutathione peroxidase)、過氧化氫酵素( catalase)的活性比其母細胞株 CHO-K1 分別低了7及6倍之多. 但麩胱甘 胜(glutathione)的含量, 麩胱甘胜轉移酵素 (glutathione S- transferase),麩胱甘胜還原酵素(glutathione reductase)的活性皆無差 別. 為了說明在 XRS-5 細胞中, 較低的麩胱甘胜過氧化酵素活性與 X射 線, 過氧化氫, 亞砷酸鈉較敏感的關聯, 首先將麩胱甘胜過氧化酵素加入 培養液內以微小核球的形成來研究遺傳毒性. 實驗結果發現麩胱甘胜過氧 化酵素可以保護 XRS-5細胞免於過氧化氫及亞砷酸鈉的微小核球產生, 但 無法保護由 X射線引起的微小核球產生. 硒可以提高 CHO-K1 細胞內的 麩胱甘胜過氧化酵素活性, 也可以降低由亞砷酸鈉、過氧化氫引起的微小 核球的產生, 但是無法降低由 X射線引起的微小核球的產生. 這些結果顯 示麩胱甘胜過氧化酵素參與亞砷酸鈉及過氧化氫的解毒, 但是在 X射線引 起的基因毒性上則無重要的角色。 本研究的結果顯示,在 XRS-5 細胞 中, 抗氧化酵素的缺失雖然與其它產生自由基之藥物的高敏感性有關, 但 其對 X射線的高敏感度則並無直接關係。 XRS-5 cell, an X-ray-sensitive cell line, was cross-sensitive to other oxygen-radical-generating agents, such as hydrogen peroxide, ferrous sulfate, and sodium arsenite. The activities of glutathione peroxidase and catalase in XRS-5 cells were 7- and 6-fold lower than those in CHO-K1 cells, respectively. However, there was no difference in the levels of glutathione and the activities of glutathione S-transferase and glutathione reductase. To elucidate the relationship among the lower glutathione peroxidase activity, hyper-sensitivity of XRS-5 cells to X-ray, sodium arsenite and hydrogen peroxide, glutathione peroxidase was added to the culture medium before micronucleus assay. Addition of glutathione peroxidase to the culture medium protected XRS-5 cells against the genotoxicity effect of hydrogen peroxide and sodium arsenite but not that of X-ray. Selenite increased the intracellular glutathione peroxidase activity and decreased the micronuclei induction frequency of sodium arsenite and hydrogen peroxide, but not that of X-ray in CHO-K1 cells. These results suggest that glutathione peroxidase plays a role in the detoxification of sodium arsenite and hydrogen peroxide but not in protecting against the X-ray-induced genotoxicity. It follows that the deficiency of antioxidant enzymes such as catalase and glutathione peroxidase, seems not to be responsible for the hyperadiosensitivity of XRS-5 cells.