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Genotoxicity studies on toxic metals and their organic compounds are very important, especially so in the investigation of the effects of these compounds on the aquatic environments where they tend to accumulate. The use of endemic aquatic organisms as biological sentinels has proved useful to environmental monitoring. We assessed the mutagenic potential of tributyltin (TBT) and inorganic lead (PbII) using samples of the fish Hoplias malabaricus (commonly called traíra) using the comet assay and the piscine micronucleus and chromosome aberration tests. Eighteen H. malabaricus were acclimatized in three individual aquariums, each containing six fish, six fish being exposed to 0.3 µg/g of body weight (bw) of TBT, six to 21 µg/g bw of PbII and six being used as controls. Exposure to TBT and PbII was achieved by feeding the fish every five days with Astyanax (a small fish that is part of the normal diet of H. malabaricus) which had been injected with solutions of TBT, PbII or with water (the control group). After two months the H. malabaricus were sacrificed and their peripheral blood collected and subjected to the comet and micronucleus assays, the chromosome aberration assay being conducted using kidney-tissue. Although the comet assay showed now mutagenic effects at the lead concentrations used but encountered results with TBT, the micronucleus and chromosome aberrations assays both indicated that TBT and PbII are potentially mutagenic (p < 0.01), the micronucleus assay showing morphological alterations of the nucleus.

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We fed immature 1+ arctic charr with a single dose of methyl[203Hg]mercury (MeHg) and quantified distribution kinetics with a new and simple three-compartment caternary model having well-perfused viscera and blood as the central compartment (VB), whereas gut (G) and the rest of body (R) constituted the peripheral compartments. The model accurately described distribution kinetics of MeHg in the fish, using either data of MeHg content in compartments or blood concentration data. Despite the known fast translocation of MeHg between binding sites at the molecular level, its translocation rate between compartments was surprisingly slow, 27 days being needed to complete 95% of the transfer from gut to blood and 48 days for the subsequent transfer to compartment R. This probably results from a limitation of the stepwise transfer rate of MeHg from red blood cells, which contain most of blood MeHg, to plasma and then to tissues due to low plasmatic concentration of small mobile sulfhydryl ligands. The model presented is a convenient tool that could be used to compare the fate of MeHg and other organometals, such as butyltins and alkylleads, in various aquatic and terrestrial animal species.

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