Lee T C, Ho I C
Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan, Republic of China.
Environ Health Perspect. 1994 Sep;102 Suppl 3(Suppl 3):101-5. doi: 10.1289/ehp.94102s3101.
Human fibroblasts (HFW) were 10-fold more susceptible than Chinese hamster ovary (CHO-K1) cells to sodium arsenite. Comparison of cellular antioxidant enzyme activities showed that CHO-K1 cells contained 3- and 8-fold more glutathione-peroxidase and catalase activities, respectively, than HFW cells. Since vitamin E, methylamine, and benzyl alcohol could prevent, in part, the arsenite-induced killing of HFW cells, we suggest that arsenite can induce oxidative damage in HFW cells. We have also established arsenic-resistant cells, SA7 and CL3R, from CHO cells and from a human lung adenocarcinoma cell line (CL3), respectively. The arsenic resistance of SA7 cells was attributed mainly to elevation of glutathione S-transferase pi levels, and that of CL3R cells was possibly due to an increase in heme oxygenase activity. Since induction of heme oxygenase is a general response to oxidative stress, we suspect that the differential toxicity of arsenic to human and animal cells could be due to arsenic's more efficient induction of oxidative damage in human cells.
人成纤维细胞（HFW）对亚砷酸钠的敏感性比中国仓鼠卵巢（CHO-K1）细胞高10倍。细胞抗氧化酶活性的比较表明，CHO-K1细胞中的谷胱甘肽过氧化物酶和过氧化氢酶活性分别比HFW细胞高3倍和8倍。由于维生素E、甲胺和苯甲醇可以部分预防亚砷酸盐诱导的HFW细胞死亡，我们认为亚砷酸盐可在HFW细胞中诱导氧化损伤。我们还分别从CHO细胞和人肺腺癌细胞系（CL3）建立了抗砷细胞SA7和CL3R。SA7细胞的抗砷性主要归因于谷胱甘肽S-转移酶pi水平的升高，而CL3R细胞的抗砷性可能是由于血红素加氧酶活性的增加。由于血红素加氧酶的诱导是对氧化应激的普遍反应，我们怀疑砷对人和动物细胞的不同毒性可能是由于砷在人细胞中更有效地诱导氧化损伤。
