In vitro studies
No data are available on point mutations in bacteria after
exposure to inorganic mercury compounds.
Information on other genotoxicity is available mostly on mercuric
chloride. Mercuric chloride binds to the chromatin of rat fibroblasts (Rozalski
& Wierzbicki 1983) and Chinese hamster ovary cells (Cantoni et al.,
1984a,b). Mercuric chloride can damage DNA in rat and mouse embryo fibroblasts
(Zasukhina et al., 1983), and several studies using Chinese hamster ovary
cells have demonstrated that mercuric chloride induces single-strand breaks
in DNA (Cantoni et al., 1982, 1984a,b; Cantoni & Costa, 1983; Christie
et al., 1984, 1986). Strand breaks have also been observed in rat and mouse
embryo fibroblasts (Zasukhina et al., 1983). Howard et al. (1991) observed
an increase in chromosomal aberrations and sister chromatid exchange in
Chinese hamster ovary cells treated with mercuric chloride. Oberly et al.
(1982) reported that doses of mercuric chloride (4.4 and 5.9 Κg mercury/ml)
approaching severely cytotoxic levels induced a weak mutagenic response
in mouse lymphoma L5178Y cells in the presence of auxiliary metabolic activation.
Mercuric chloride also induced spindle disturbances in Indian muntjak fibroblasts
and human lymphocytes in vitro, cell transformation in Syrian hamster cells
in vitro (Casto et al., 1979; Verschaeve et al., 1984), and sister chromatid
exchanges and chromosomal aberrations in human lymphocytes in vitro (Morimoto
et al., 1982; Verschaeve et al., 1985). Mercuric chloride was positive
in the Bacillus subtilis rec-assay (Kanematsu et al. 1980), but failed
to enhance lethality in a DNA repair-deficient strain of Escherichia coli
(Brandi et al., 1990).
Mercurous chloride was also positive in the Bacillus subtilis
rec-assay (Kanematsu et al., 1980).
Mercuric acetate induced chromosomal aberrations in mouse oocytes
in vitro at a concentration of 35 mg/litre (Jagiello & Lin, 1973),
but failed to induce anchorage-independent growth in human foreskin fibroblasts
in vitro (Biedermann & Landolph, 1987).
In vivo studies
A dose-related increase in chromosomal aberrations was observed in
the bone marrow of mice administered a single oral dose of mercuric chloride
at levels of at least 4.4 mg mercury/kg body weight (Ghosh et al., 1991).
Chromatid breaks were the most common aberration. In contrast, no increase
in chromosomal aberrations was observed in spermatogonia of mice or oocytes
of Syrian hamsters after an equally large or larger parenteral dose (Poma
et al., 1981; Watanabe et al., 1982).
Mercuric chloride administered orally for 12 months (0.18-1.8 mg
mercury/kg body weight per day) induced a weak but dose-related increase
in dominant lethal mutations (Zasukhina et al., 1983). A weakly positive
result in a dominant lethal assay was also reported in an early study in
mice after a single intraperitoneal dose (Suter, 1975).
Mercuric acetate failed to induce chromosomal aberrations in mouse
oocytes in vivo after subcutaneous or intravenous administration (Jagiello
& Lin, 1973)