GENOTOXICITY OF MERCURY-COMPOUNDS - A REVIEW

This article reviews literature data concerning the genotoxicity of 29 mercury-containing agents, including laboratory compounds as well as ingredients of preparations used as fungicides, dyes, disinfectants an d drugs. A variety of genetic end-points were investigated in bacteria , yeasts, moulds, plants, insects, cultured cells from fishes, rodents or humans, aquatic organisms, amphibians, mammalia and exposed humans . The overall evaluation is quite complex. Mercury compounds failed to induce point mutations in bacteria but often exerted clastogenic effe cts in eukaryotes, especially by binding SII groups and acting as spin dle inhibitors, thereby causing c-mitosis and consequently aneuploidy and/or polyploidy. Inorganic mercury compounds were also found to indu ce the generation of reactive oxygen species and glutathione depletion in cultured mammalian cells. Although different mercury compounds ten ded to produce qualitatively comparable genetic effects, which suggest s the involvement of a common toxic entity, methylmercury derivatives and other ionizable organomercury compounds were more active in short- term tests than either non-ionizable mercury compounds (e.g., dimethyl mercury) or inorganic mercury salts (e.g., mercuric chloride). The res ults of cytogenetic monitoring in peripheral blood lymphocytes of indi viduals exposed to elemental mercury or mercury compounds from acciden tal, occupational or alimentary sources were either negative or border line or uncertain as to the actual role played by mercury in some posi tive findings. Both genotoxic and non-genotoxic mechanisms may contrib ute to the renal carcinogenicity of mercury, which so far has been con vincingly demonstrated only in male rodents treated with methylmercury chloride.