EVIDENCE FOR CHLORDECONE-STIMULATED OXIDATIVE STRESS IN DIFFERENT TISSUES OF THE CICHLID FISH, Pseudetroplus maculatus (Bloch, 1795)

EVIDENCE FOR CHLORDECONE-STIMULATED OXIDATIVE STRESS IN DIFFERENT TISSUES OF THE CICHLID FISH, Pseudetroplus maculatus (Bloch, 1795)Download fileoriginal scientific paper
EVIDENCE FOR CHLORDECONE-STIMULATED OXIDATIVE STRESS IN DIFFERENT TISSUES OF THE CICHLID FISH, Pseudetroplus maculatus (Bloch, 1795)Asifa, K. P., Chitra, K. C.Keywords:
oxidative stressbrainlivergillchlordecone

DOI number: http://dx.doi.org/10.1515/cjf-2017-0010

Volume: 75
Issue: 2
Pages: 67 - 75

Summary

The present study was designed to assess the effect of chlordecone on the stimulation of oxidative stress in gill, liver and brain tissues of the cichlid fish, Pseudetroplus maculatus. Fishes were exposed to chlordecone at two sublethal concentrations - 3.5 and 7 µg/L - for 24, 72 and 96 h, maintaining ten animals in each group. Chlordecone treatment did not alter the body weight of the animal. However, significant increase in the secretion of mucous and decrease in the weights of gill, brain and hepatosomatic index were observed at 7 µg/L of chlordecone treatment only after 96 h. Gill tissue showed significant increase in the activities of superoxide dismutase, catalase and glutathione reductase along with elevated levels of hydrogen peroxide and lipid peroxidation in concentration and time-dependent manner. This could be the defensive mechanism of gill tissue to escape the toxic effects of chlordecone. In the liver tissue, superoxide dismutase activity was increased by 39% at 3.5 µg/L and by 73% at 7 µg/L of chlordecone treatment. Activities of catalase and glutathione reductase were decreased 3 to 9 times at 3.5 and 7 µg/L concentrations, respectively, with concomitant increase in hydrogen peroxide generation (17 to 28 times) and lipid peroxidation (3 to 7 times) at the end of 96 h, which reveals the failure of hepatic antioxidant system to prevent free radical generation owing to chlordecone exposure. Activities of all antioxidant enzymes in the brain were inhibited by 29 to 80% along with the induction of hydrogen peroxide (13 to 20 times) and lipid peroxidation (6 to 11 times), thereby indicating imbalance in the antioxidant status. Activities of gill and liver marker enzyme - alkaline phosphatase - and acetylcholinesterase in brain were decreased. Therefore, imbalance in the antioxidant defence system as a result of chlordecone toxicity could lead to susceptible oxidative stress in various tissues of the fish.