Abstract
The effects of cysteine on dimethylarsinic acid (DMA)‐induced cytotoxicity and chromosomal aberration were studied using Chinese hamster V79 cells. The IC 50 of DMA, i.e. the concentration resulting in a 50% decrease in cell population of viable cells, was 130 µg ml^−1^ (0.94 mM), whereas that in the presence of 50 µg ml^−1^ (0.28 mM) cysteine was 20 µg ml^−1^ (0.14 mM). The mitotic index with co‐administration of 50 µg ml^−1^ (0.36 mM) DMA and 50 µg ml^−1^ cysteine was 1.4 times that with 50 µg ml^−1^ DMA alone. Whereas 82% of cells divided twice with 25 µg ml^−1^ (0.18 mM) DMA alone, most cells divided only once with co‐administration of 25 µg ml^−1^ DMA and 50 µg ml^−1^ cysteine. These results indicated that the increase in mitotic index by cysteine was due to enhancement of mitotic arrest by DMA. With co‐administration of 25 µg ml^−1^ DMA and 50 µg ml^−1^ cysteine, tetraploidy was 14.3% higher and fivefold by that with 25 µg ml^−1^ DMA only. Cysteine at 50 µg ml^−1^ enhanced induction of chromosomal aberrant cells by DMA. 100 µg ml^−1^ (0.72 mM) DMA induced 91% chromosomal aberrant cells in the presence of cysteine, and 12% in the absence of cysteine. Chromatid breaks and chromatid gaps were the most frequent types of aberration induced by co‐administration of DMA and cysteine or DMA alone. Co‐administration of DMA and cysteine produced many attenuated chromosomal figures. The attenuated chromosomal figures always had several chromatid gaps and chromatid breaks. Our findings may provide clues to arsenic carcinogenesis in humans. Copyright © 2002 John Wiley & Sons, Ltd.