Lee T C, Ho I C
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, Republic of China.
Arch Toxicol. 1995;69(7):498-504. doi: 10.1007/s002040050204.
Many studies have shown that oxygen radicals can be produced during arsenic metabolism. We report here that in human fibroblasts (HFW cells) sodium arsenite exposure caused increased formation of fluorescent dichlorofluorescein (DCF) by oxidation of the nonfluorescent form. The enhanced DCF fluorescence was inhibited by a radical scavenger, butylated hydroxytoluene. The effects of sodium arsenite treatment on cellular antioxidant activities were then examined. Treatment of HFW cells with sodium arsenite resulted in a significant increase in heme oxygenase activity and ferritin level. Sodium arsenite-enhanced heme oxygenase synthesis was inhibited by co-treatment of cells with the antioxidants sodium azide and dimethyl sulfoxide. Furthermore, sodium arsenite treatment did not apparently affect glucose-6-phosphate dehydrogenase activity, but resulted in significantly increased glutathione levels and superoxide dismutase activity, slightly decreased glutathione peroxidase activity, and significantly decreased catalase activity. Sodium arsenite toxicity was partly reduced by addition of catalase to the culture medium. These results imply that arsenite can enhance oxidative stress in HFW cells.
许多研究表明，砷代谢过程中会产生氧自由基。我们在此报告，在人成纤维细胞（HFW细胞）中，亚砷酸钠暴露会通过非荧光形式的氧化导致荧光二氯荧光素（DCF）的形成增加。自由基清除剂丁基羟基甲苯可抑制增强的DCF荧光。然后研究了亚砷酸钠处理对细胞抗氧化活性的影响。用亚砷酸钠处理HFW细胞导致血红素加氧酶活性和铁蛋白水平显著增加。细胞与抗氧化剂叠氮化钠和二甲基亚砜共同处理可抑制亚砷酸钠增强的血红素加氧酶合成。此外，亚砷酸钠处理显然不影响葡萄糖-6-磷酸脱氢酶活性，但导致谷胱甘肽水平和超氧化物歧化酶活性显著增加，谷胱甘肽过氧化物酶活性略有降低，过氧化氢酶活性显著降低。向培养基中添加过氧化氢酶可部分降低亚砷酸钠的毒性。这些结果表明，亚砷酸盐可增强HFW细胞中的氧化应激。
