Abstract: BACKGROUND AND AIM: Inorganic arsenic is a ubiquitous carcinogen, teratogen and mutagen, where it occurs mainly in the pentavalent form in the aquatic environment. The genotoxic effects of arsenate to intact animals are still unclear. In order to understand the potential genotoxic effects of arsenate and the underlying mechanisms, the nematode Caenorhabditis elegans were employed in this study. The studies presented here investigated the effects and the underlying mechanisms of arsenate on the brood size, germ cell cycle arrest and apoptosis of C. elegans. MATERIALS AND METHODS: The C. elegans adult hermaphrodites were exposed to 0.0, 2.5, 5.0, 10.0 or 20.0 mmol/L of arsenate, the brood size, germ cell cycle arrest and apoptosis were assayed after exposure. RESULTS: From arsenate exposure of 5.0 to 20.0 mmol/L, the brood size was significantly smaller(P<0.05). From the concentrations of 2.5 to 20.0 mmol/L,arsenate exposure caused germ cell cycle arrest and apoptosis in a dose-dependent manner(P<0.05). Germ cell apoptosis could be detected as early as 6 h after arsenate exposure. The addition of dimethyl sulphoxide (DMSO) could significantly rescue arsenate-induced germ cell cycle arrest and partially reduced apoptosis. CONCLUSION: Arsenate exhibited genotoxic effects, causing germ cell cycle arrest and apoptosis in C. elegans.

Key words: Caenorhabditis elegans, arsenate, cell cycle, apoptosis