Bioaccumulation and related effects of PCBs and organochlorinated pesticides in freshwater fish Hypostomus commersoni.

Few studies have investigated the bioaccumulation of persistent organic pollutants (POPs) in Brazilian native freshwater fish. In order to evaluate the bioavailability, potential risk to human exposure and the effects of POPs in the fish Hypostomus commersoni, muscle and liver samples of thirteen specimens were collected in a lake located in the city of Ponta Grossa (Parana State, Southern Brazil). Also, the liver and gills were considered for histopathological studies, and oxidative stress was investigated in the liver. Expressive concentrations of POPs were observed in the liver and muscle, with a total of 427 ± 78.7 and 69.2 ± 18.1 ng g(-1) dry weights of polychlorinated biphenyls (PCBs), respectively. Negative correlations between the concentration of several POPs and glutathione S-transferase and glucose-6-phosphate dehydrogenase were found. Otherwise, the cholinesterase activity in the muscle and brain presented positive correlations with the concentration of POPs. The hepatic bioaccumulation of some banned pesticides like aldrin, dieldrin and DDT was associated with various histopathological findings in the liver and gills. Necrotic areas, fibrosis, leukocyte infiltration, and the absence of macrophage centers were observed in the liver, indicating both chronic exposure and immunological suppression. Neoplasic changes were observed in the gills, confirming the carcinogenic potential reported for some of the investigated pollutants. The current work was the first to study the bioaccumulation of POPs in H. commersoni, an important species in ecological aspects and as a vehicle to human exposure to PCBs and organochlorine pesticides (OCPs).

Responses of hepatocytes to DDT and methyl mercury exposure.

The aim of the current work was to investigate the effects of dichlorodiphenyltrichloroethane (DDT) and monomethyl mercury (MeHg) on hepatocytes from tropical fish Hypostomus commersoni (cascudo). In order to verify DDT and MeHg impacts on the redox milieu, cells were exposed for 4 days to 50 nM of DDT, 0.25 and 2.5 microM of MeHg and to a combination of 50 nM of DDT and 0.25 microM of MeHg. These concentrations were compared with those previously published (Filipak Neto et al., 2008) for the predator fish Hoplias malabaricus (traíra). The effects were mostly noticeable on reduced glutathione concentration and delta-aminolevulinic acid dehydratase and glutathione S-transferase activity. Catalase activity increased in the group exposed to 2.5 microM of MeHg and hydrogen peroxide levels decreased in all exposed groups. Also, superoxide anion levels decreased in the groups exposed to 2.5 microM of MeHg and DDT *MeHg group. Cell viability decreased only in the DDT exposed group, demonstrating that the antioxidant defense mechanism of H. commersoni hepatocytes is more efficient than H. malabaricus. These results corroborate the resistance of H. commersoni to polluted areas and support the hypothesis that this species is more resistant to DDT and MeHg than H. malabaricus species.

The immune response of peritoneal macrophages due to exposure to inorganic lead in the house mouse Mus musculus.

Peritoneal macrophages from the house mouse (Mus musculus) were exposed to variable lead (Pb) concentrations (0.2, 2, 20 and 40 microM) to better understand lead cytotoxicity and its damage to the immune response. Phagocytes were exposed to 20 and 40 microM Pb for 72 h, and macrophages were exposed at lower concentrations (0.2, 2 and 20 microM Pb) for 24h and 72 h. Dysfunctions in macrophage immune activity were examined by measuring phagocytic activity, nitric oxide production, endosomal/lysosomal stability and cell adhesion. Lead affected all macrophage functions, even at low concentrations, by reducing the phagocytic index, nitric oxide production, endosomal/lysosomal system stability and cell adhesion, and upregulating the antioxidant enzymatic activity of catalase. We demonstrate that lead affects the redox status of the cells and suggest that the immunomodulatory effects at low dosages on mouse macrophages reduces their ability to protect the host against infectious agents.

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.