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MERCURY 285
2. HEALTH EFFECTS
sensitivity preclude an extrapolation of the relevance of these findings to humans. Refer to Table 2-11 for a
further summary of these results.
Several in vitro assays employing human cells were located. Both structural and numerical chromosomal
aberrations were observed following the exposure of human lymphocytes to methylmercury chloride or
dimethylmercury in vitro (Betti et al. 1992). Although the smoking status of the donor was not reported, all
of the cells came from the same donor, and no aberrations were observed in the control cultures. Mercuric
acetate caused single-strand breaks in DNA from human KB-cells (Williams et al. 1987). Methylmercuric
chloride treatment of human lymphocytes resulted in the formation of chromosome and chromatid
aberrations (Betti et al. 1993b). Further, it was found to be a weak inducer of sister chromatid exchange, but
that effect did not increase with an increasing dosage. Methylmercuric chloride was also found to be capable
of producing aneuploidy (particularly hyperdiploidy). At low doses, more chromosomal aberrations were
observed in the second metaphases than in the first, suggesting that several premutational lesions induced by
that organomercurial survived through one cell cycle. Thus, the damage produced by methylmercuric
chloride appeared to be stable and could lead to chromosome segregation errors. Betti et al. (1993b)
concluded that methylmercuric chloride was capable of producing long-lasting damage, which in turn gives
rise to both structural and numerical chromosome abnormalities. Bala et al. (1993) reported that methylmercuric
chloride in concentrations of 10 -5 , 10-6 , and 10-7 M induced aberrant metaphases (including gaps) in
cultured human peripheral lymphocytes in a dose-dependent manner (p