Chelating efficacy of CaNa(2) EDTA on nickel-induced toxicity in Cirrhinus mrigala (Ham.) through its effects on glutathione peroxidase, reduced glutathione and lipid peroxidation.
In this age of modern biology, aquatic toxicological research has provided potential tools for ecotoxicologic investigations. Heavy metals primarily affect protein structures and induce a stress in the organisms. The present investigation was carried out to assess the effect of nickel chloride on the selected organs of the freshwater fish Cirrhinus mrigala and how CaNa(2) EDTA counters its effects as an antidote. Toxicity experiments were conducted for different exposure periods and also in certain tissues namely gill, liver, kidney and muscle. The total protein content, reduced glutathione, glutathione peroxidase and lipid peroxidation were found to be decreased in the nickel chloride treated tissues and the treatment with CaNa(2) EDTA+nickel chloride returned to near normal levels. Histopathological observations also revealed that after the administration of nickel chloride+CaNa(2) EDTA the chelator induced reduction in nickel toxicity. It has also contributed towards reduction in the pathological damage, thus enabling the organs to attain their near normal histological appearance. The present study shown that CaNa(2) EDTA is an effective chelating agent for the removal of nickel and it has proved efficient in restoring both the biochemical variables and pathological features immediately after a sub lethal exposure of nickel chloride in fish.
Gopal
Rengaswamy
R
Department of Zoology, Annamalai University, Tamilnadu, India. rvijay1985@rediffmail.com
Narmada
S
S
Vijayakumar
Remya
R
Jaleel
Cheruth Abdul
CA
D000818:Animals; D002614:Chelating Agents / Q000494:pharmacology* / Q000627:therapeutic use; D015913:Chelation Therapy; D003530:Cyprinidae / Q000033:anatomy & histology / Q000378:metabolism*; D004353:Drug Evaluation, Preclinical / Q000662:veterinary; D004492:Edetic Acid / Q000494:pharmacology* / Q000627:therapeutic use; D005393:Fish Diseases / Q000139:chemically induced / Q000378:metabolism / Q000473:pathology; D005880:Gills / Q000737:chemistry / Q000473:pathology; D005978:Glutathione / Q000378:metabolism*; D005979:Glutathione Peroxidase / Q000378:metabolism*; D007668:Kidney / Q000737:chemistry / Q000473:pathology; D015227:Lipid Peroxidation / Q000187:drug effects*; D008099:Liver / Q000737:chemistry / Q000473:pathology; D018482:Muscle, Skeletal / Q000737:chemistry / Q000473:pathology; D009532:Nickel / Q000008:administration & dosage / Q000633:toxicity*; D010084:Oxidation-Reduction; D011506:Proteins / Q000032:analysis; D014874:Water Pollutants, Chemical / Q000008:administration & dosage / Q000633:toxicity*
D002614:Chelating Agents; D011506:Proteins; D014874:Water Pollutants, Chemical; C022838:nickel chloride; D009532:Nickel; D004492:Edetic Acid; D005979:Glutathione Peroxidase; D005978:Glutathione