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Expression of Heme Oxygenase in Arsenic-resistant Human Lung Adenocarcinoma Cells¹

Institute of Biomedical Sciences, Academia Sinica, Taipei, Taiwan 115, Republic of China

We have established arsenic-resistant cells (CL3R) and their subciones from a human lung adenocarcinoma cell line (CL3). CL3R cells and their subclones were maintained in the presence of 4 µM sodium arsenite. They were 6-fold more resistant than CL3 cells to arsenite. Heme oxygenase was expressed in CL3R cells and their subclones, as demonstrated by electrophoretic analysis, Northern blotting, and enzyme activity assay. When CL3R15 cells were grown in arsenite-free medium, their arsenite resistance declined in parallel with their decreasing heme oxygenase activity. Tin-protoporphyrin, a heme oxygenase inhibitor, was found to increase the toxicity of arsenic to CL3R cells. Expression of heme oxygenase might therefore be involved in the mechanism of arsenic resistance. CL3R cells were also shown to be cross-resistant to oxygen-radical generating agents, such as menadione and Adriamycin. Furthermore, sodium arsenite treatment dose-dependently increased the dichlorofluorescein fluorescence in CL3 cells but not in CL3R15 cells. These results suggest that heme oxygenase plays an important role in reducing cellular oxidants that are enhanced by sodium arsenite treatment.

¹ This study was supported in part by Academia Sinica and by a grant from the National Science Council, Republic of China.

² To whom requests for reprints should be addressed.

Received 10/ 7/93. Accepted 1/25/94.

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