Antioxidant responses and metal accumulation in tissues of Nile tilapia Oreochromis niloticus under Zn, Cd and Zn + Cd exposures.
ABSTRACT We investigated the effects of Zn, Cd and a Zn + Cd mixture on antioxidant parameters and metal accumulation in Oreochromis niloticus. Fish were exposed to 0.5 and 5.0 mg l(-1) Zn, 0.1 and 1.0 mg l(-1) Cd, and 0.5 mg l(-1) Zn + 0.1 mg l(-1) Cd and 5.0 mg l(-1) Zn + 1.0 mg l(-1) Cd mixtures for 7 and 28 days to determine Zn and Cd accumulation, reduced glutathione (GSH) level and glucose-6-phosphate dehydrogenase (G6PD) activity in gill and liver. There was increasing accumulation of the metals in the tissues with increasing concentrations of metals in the exposure medium and with increasing duration of exposure (except at the lower concentration of Zn). Concentration of metals in the tissues of fish exposed to the Zn + Cd combination were significantly lower than in fish exposed to the single metal. The highest metal accumulation was observed in the liver. Exposure to the heavy metals affected the antioxidant parameters in the tissues, with both GSH level and G6PD activity in the gill and liver being increased under Zn, Cd and Zn + Cd exposures, especially in their higher concentrations. These increases in the antioxidant responses were higher with the Cd alone, and in combination with Zn, than with Zn alone. Furthermore, GSH level and G6PD activity increased with increasing exposure period only for Cd alone, and in Cd combination with Zn. The results indicate that O. niloticus resisted oxidative stress induced by heavy metal exposure by antioxidant mechanisms.
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ABSTRACT: Anguilla anguilla L. were caged for 8 and 48 h in harbor water of Aveiro Lagoon, Portugal. Respiratory burst activity (RBA) of peritoneal, head kidney, and gill phagocytes was measured. Lipid peroxidation (LPO) was estimated in gill, kidney, and liver. Liver ethoxyresorufin-O-deethylase (EROD) activity, cytochrome P450 (Cyt P450) content, and bile metabolites were assayed. Various antioxidant enzymes, viz., glutathione peroxidase, catalase, and glutathione S-transferase and nonenzymatic antioxidant, viz., total reduced glutathione were also studied. Harbor water xenobiotics induced a significant RBA increase in gill after 8 h; whereas in peritoneum and head kidney it increased after 48 h exposure. These responses were adversely associated with tissue-specific peroxidative damage since significant LPO increase was observed in gill (8 and 48 h), kidney (48 h), and liver (48 h). The tissue most affected was gill. Moreover, liver EROD activity, Cyt P450 content and bile metabolites remain unaltered after 8 h; in contrast, 48 h exposure showed significant EROD activity decrease and pyrene-type bile metabolites increase. Decreased EROD activity may be associated with concomitant liver damage, as increased LPO was observed after 48 h. Furthermore, the tissue-specific damage corresponded to the differences in the antioxidant potentials of the tissues, since the initial exposure period caused a significant increase in liver antioxidant activities, whereas gill and kidney showed a significant decrease, demonstrating that liver is highly adaptive to oxidative damage. However, at 48 h exposure gill, kidney, and liver showed a suppressive antioxidant effect, probably due to PAHs, since a significant induction at PAH-type bile metabolites has been seen. Our results demonstrate that phagocyte activation and associated peroxidative damage are concomitantly corroborated with enzymatic and nonenzymatic antioxidant activity differences. In addition, hepatic antioxidant induction after short-term exposure may serve as a potent biomarker for water pollutants in fish.Ecotoxicology and Environmental Safety 04/2004; 57(3):290-302. · 2.20 Impact Factor
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ABSTRACT: Zinc is an essential trace element with many enzymatic functions that include antioxidant properties. To investigate whether an excess of Zn in the cells produces cytotoxicity or tissue damage or an imbalance in the antioxidant systems, marine clams (Ruditapes decussatus) were exposed to two sublethal Zn concentrations (100 and 1000 microg L(-1)) for 28 days. The effects of Zn on the activities of protective antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase, both total and selenium-dependent), lipid peroxidation, and metallothionein induction were followed in the gills and digestive gland of these clams. The results indicate that the effect of Zn exposure in this clam species depends not only on the tissue but also on the Zn concentration present. In the gills, catalase activity was enhanced by Zn exposure, whereas total glutathione peroxidase activity was inhibited. Lipid peroxidation occurred only in the clams exposed to the highest Zn concentration. In the digestive gland, the impact of Zn exposure on metabolic activity was less evident than in the gills. The most evident effect in both tissues was the enhancement of catalase activity by Zn exposure. Catalase and total glutathione peroxidase activities as well as lipid peroxidation are promising biomarkers to assess the effects of Zn in the gills of R. decussatus.Ecotoxicology and Environmental Safety 04/2004; 57(3):399-409. · 2.20 Impact Factor
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ABSTRACT: Sodium dichromate [Cr(VI)] and cadmium chloride [Cd(II)] are both cytotoxic and mutagenic. This study examined the toxic and apoptotic potentials of these two cations on three cell types in vitro, namely, human chronic myelogenous leukemic (CML) K562 cells, promyelocytic leukemic HL-60 cells, and normal human peripheral blood mononuclear cells. The cells were incubated with 0-100 microM concentrations of the two cations for 0, 24, or 48 hours at 37 degrees C. Both Cr(VI) and Cd(II) induced changes in intracellular oxidized states of cells, which were detected using laser scanning confocal microscopy. Cell cycle modulation and apoptosis of the K562 cells by Cr(VI) and Cd(II) were determined by flow cytometry. Significant decreases in the G2/M phase were observed in the Cr(VI) and Cd(II) treated CML cells compared with untreated cells. At 12.5 microM, Cr(VI) induced greater apoptosis in K562 cells as compared with Cd(II). In the K562 cells, 2.2- and 3.0-fold increases in DNA fragmentation were observed following incubation with 12.5 and 25 microM Cr(VI), respectively, and 1.2- and 1.7-fold increases in DNA fragmentation were observed with Cd(II). Furthermore, approximately 2.7- and 4.9-fold increases in cytochrome c reduction were observed following incubation with 12.5 and 25 microM Cr(VI), respectively, and 1.6- and 3.3-fold increases in cytochrome c reduction were observed with Cd(II), demonstrating enhanced production of superoxide anion. Approximately 3.1 to 6-fold increases in hydroxyl radical production were observed following incubation of the K562 cells with these cations at 12.5 and 25 microM concentrations. These results in K562 cells were compared with promyelocytic leukemic HL-60 cells and normal human peripheral blood mononuclear cells. More pronounced effects were observed on K562 and HL-60 cells, and much lesser effects were observed on normal human peripheral blood mononuclear cells. The results demonstrate that both cations are toxic, producing oxidative tissue damage and apoptosis. Furthermore, more drastic effects were observed on K562 and HL-60 cells as compared with normal human peripheral blood mononuclear cells.Journal of Biochemical and Molecular Toxicology 02/2000; 14(1):33-41. · 1.60 Impact Factor