Genotoxic evaluation of different doses of inorganic lead (PbII) in Hoplias malabaricus.

Different genetic biomarkers have been used to evaluate the pollution effects of mutagenic agents such as metals and also a great variety of chemicals delivered on the environment by human activities. This way, the aim of the present report was to evaluate the effects of inorganic lead in fishes through the frequency of piscine micronuclei and nuclear morphological alterations in peripheral cells, chromosomal aberration frequency and comet assays in blood and kidney cells. Specimens of Hoplias malabaricus received different doses of lead by intra-peritoneal injections at time of 96 h. There was not a significant difference between control and treated groups for the piscine micronucleus and chromosomal aberration assays. In the comet assays there was a significant difference between control and contaminated groups. However, a significant difference between the applied doses was not observed. The results obtained with the comet assays also show that blood presented a higher sensibility than the kidney tissue, possibly due to the acute contamination. Although the results showed the genotoxic potential of lead at the 21 and 63 microg Pb(2 + )/g doses for both tissues, the lowest dose is considered more appropriate for future bioassays.

Use of hepatocytes from Hoplias malabaricus to characterize the toxicity of a complex mixture of lipophilic halogenated compounds.

Organisms are continuously exposed to a plethora of anthropogenic toxicants daily released to the environment. In the present study, the effects of a mixture of halogenated organic compounds (HOCs) extracted from hepatic lipids were evaluated on the primary hepatocyte culture from fish Hoplias malabaricus. Cells were isolated through non-enzymatic perfusion protocol and cultured during 3 days to allow attachment. Two concentrations of the mixture of HOCs (10 ng ml(-1) [Mix10] and 50 ng ml(-1) [Mix50]) were tested in cells for 2 days by medium replacement. The control groups, with and without solvent (DMSO) were run in the same conditions. Both tested concentrations of HOCs increased the catalase and GST activities, but only the Mix50 increase the DNA damage and decreased the GSH concentration and cell viability. Lipid peroxidation increased in the Mix10 group, but it seems to be more a consequence of DMSO presence than the HOCs themselves. The DMSO at 0.1% increased the lipid peroxidation, GSH concentration, apoptosis and DNA damage. The present data suggest that DMSO interferes with the hepatocytes of H. malabaricus in culture and that the mixture of HOCs tested alters the redox state of the hepatocytes.

Cell death and DNA damage in peritoneal macrophages of mice (Mus musculus) exposed to inorganic lead.

Lead is a heavy metal of considerable environmental and occupational concern and there is growing evidence that it is toxic to the human immune system. In this regard, this study examined the effect of lead (Pb) exposure to peritoneal macrophages (Mvarphis) of mice (Mus musculus) cultivated in DMEM medium supplemented with fetal bovine serum, in order to investigate cell damage related to cell death. Cells were exposed to two concentrations of inorganic lead [Pb(II)] for 4, 24 and 72h. Cell viability declined during the treatment, with responses including cell death, cellular damage and DNA damage. Cell death images were found in treated cells with an increase in Bax expression, but the inorganic lead failed to induce the loss of membrane asymmetry (Annexin V conjugates), suggesting that cell death was mainly due to necrosis induction. The effects of Pb(II) on the mechanisms of cell death is not completely understood, but the immunosuppression due to DNA damage and Mvarphis death is discussed here. We have previously shown the effect of inorganic lead in mitochondria and phagocytosis in Mvarphis, suggesting here a pathway for the effect of the metal on mechanisms of cell death, also discussing its effects on the immune system.