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Induction of mitotic arrest and aneuploidy by organic arsenic compounds in human lymphocytes

✍ Scribed by K. Iwami; K. Kuroda; G. Endo

Publisher: John Wiley and Sons
Year: 1997
Tongue: English
Weight: 261 KB
Volume: 11
Category: Article
ISSN: 0268-2605
DOI: 10.1002/(sici)1099-0739(199709)11:9<743::aid-aoc642>3.0.co;2-q

No coin nor oath required. For personal study only.

✦ Synopsis

Inorganic arsenic is methylated in the mammalian body to methylarsonic acid (MMA), dimethylarsinic acid (DMA) and trimethylarsine oxide (TMA). To achieve a more precise understanding of arsenic carcinogenicity, we examined the genotoxic effects of organic arsenic compounds on human lymphocytes by assessing induction of mitotic arrest, sister chromatid exchange (SCE) and aneuploidy. MMA, DMA and TMA arrested mitosis, DMA induced hyperdiploid cells, and DMA and TMA induced tetraploid cells. Of the three arsenic metabolites tested, DMA had the strongest effects on cell mitosis and aneuploidy induction. DMA arrested mitosis and induced c-mitosis significantly. These results suggest that DMA arrests mitosis and induces aneuploidy through spindle disruptions similar to those observed with known spindle poisons, such as colchicine or vinblastine. Since aneuploidy has been thought to be associated with tumor induction or neoplastic transformation, induction of aneuploidy by organic metabolites of arsenic may play a major role in arsenic carcinogenesis in humans.

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