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| Differential Cytotoxic Effects of Arsenic on Human and Animal Cells Environ Health Perspect Key words: arsenite, cytotoxicity, arsenic resistance, glutathione S-transferase, heme oxygenase, oxidative damage
This paper was presented at the Second International Meeting on Molecular Mechanisms of Metal Toxicity and Carcinogenicity held 10-17 January 1993 in Madonna di Campiglio, Italy, Abstract
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  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. -- Environ Health Perspect 102(Suppl 3) :101-105 (1994) . Key words: arsenite, cytotoxicity, arsenic resistance, glutathione S-transferase, heme oxygenase, oxidative damage
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