Abstract
ABSTRACTThe nickel impacts on antioxidant enzymes’ activities such as superoxide dismutase (SOD), glutathione peroxidase (GPx), catalase (CAT) and hepatic enzymes’ activity were studied in freshwater carassius auratus. Probite analysis was used to determine acute toxicity of nickel to the goldfish. Fish were subjected to selected concentrations of nickel (control 0, 10, 20, 50, 100, 150, 200, 250 and 300 ppm) and the mortality data were determined after 24, 48, 72 and 96 h. The 96 h LC50 value of nickel to the fish was found to be 95.39 ± 0.73 ppm. SOD, GPx and CAT activities were monitored in the liver. These were determined in goldfish exposed to sub-lethal concentrations (40% and 80% LC50 at 7 days of exposure). There was a marked increase in SOD within both exposure groups and GPx was observed in this tissue having exposure to nickel (P < .05) but CAT was decreased in both the groups (P < .05). AST, ALP, ALT enzymes’ activity in both groups (40% and 80% LC50) was increased significantly when compared to that of the control group (P < .05). This result implied that increasing the dosage of nickel exposure induced antioxidant and hepatic enzymes’ activity in the goldfish.
Highlights
Heavy metals’ chronic contamination in the marine environment is found to be an adverse issue, especially in water bodies
Fish inhabiting polluted areas are frequently exposed to toxic compounds, many of them occurring due to cytotoxic impacts by the production of reactive oxygen species (ROS; Di Giulio et al 1989)
The superoxidase that appeared in the xanthine/xanthine-oxidase superoxide generation system inhibited the formation of nitrite from hydroxylammoniumchloride (Ji et al 1991)
Summary
Heavy metals’ chronic contamination in the marine environment is found to be an adverse issue, especially in water bodies. Nickel is an important chemical species in natural waters In aquatic ecosystems, it interacts with many mineral and organic compounds and occurs as soluble salts adsorbed onto materials belonging to various chemical origins (Us epa 1980). It interacts with many mineral and organic compounds and occurs as soluble salts adsorbed onto materials belonging to various chemical origins (Us epa 1980) Many of such pathways are additive or synergistic in causing adverse effects, and some are antagonistic as well. Once ROS generation caused by xenobiotics exceeds the thresholds, impairments to cellular components occur. This process is called oxidative stress (Oakes & Van der Kraak 2003). Oxidative activities were measured in carassius auratusas as biomarkers of environmental contamination (Van der Oost et al 2003)
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