Selenite prevents the induction of sister-chromatid exchanges by methyl mercury and mercuric chloride in human whole-blood cultures.

The protective effect of sodium selenite (Na2SeO3) against the cytogenetic toxicity of methyl mercury (CH3HgCl) and mercuric chloride (HgCl2) were investigated on human whole-blood cultures in relation to induction of sister-chromatid exchange (SCE). Both mercurials caused a dose-dependent increase in SCEs, methyl mercury being about 5 times more potent than mercuric chloride. Sodium selenite also induced SCEs. However, the simultaneous addition of selenite (1 x 10(-7) -3 x 10(-5) M) to cell cultures containing either methyl mercury (3 x 10(-6) M) or mercuric chloride (1 x 10(-5) M) prevented the induction of SCEs by the mercurial in a clear dose-related manner. When selenite and mercurial were simultaneously added at a molar ratio of 1:2 Na2SeO3:CH3HgCl, or 1:1 Na2SeO3:HgCl2, cells from treated cultures showed no increase in the SCE frequency. These results indicate that selenite and mercury mutually antagonize their ability to cause DNA damage leading to the formation of SCEs. The formation of bis(methylmercuric)selenide, (CH3Hg)2Se, from Na2SeO3 and CH3HgCl, or a high molecular complex consisting of glutathione-Se-Hg from Na2SeO3 and HgCl2 involving the participation of glutathione in RBCs might play a key role in this antagonism between mercury and selenium.