Sublethal toxicity of carbofuran on the African catfish Clarias gariepinus: Hormonal, enzymatic and antioxidant responses

The present study examined the impacts of carbofuran on endocrinology of the catfish, Clarias gariepinus, for the first time and evaluated cortisol (CRT), triiodothyronine (T3), thyroxin (T4), 17 beta-estradiol (E2) and testosterone (TST) and the oxidative stress markers including SOD, CAT, GSTs, GSH. The toxic effects on the metabolic enzymes, G6PDH and LDH, in addition to lipid peroxidation (LPO) and DNA damage as biomarkers in Nile catfish, to sublethal exposures of carbofuran (0.16 and 0.49 mg/L, for 35 days) were studied. Statistically significant differences between selected parameters between control and carbofuran-treated fish were recorded. Carbofuran caused a significant (p < 0.05) increase in CRT and T3 levels; the mean levels of T4, TST, E2 exhibited significant decreases (p < 0.05) in carbofuran-treated fish. Toxicity of carbofuran on liver, kidney, gills, gonads and muscles after 35 days of exposure was found. Glycogen levels showed a highly significant decrease in liver and gills (p < 0.001), a significant decrease (p < 0.05) in kidney and muscles, and insignificant changes (p > 0.05) in gonads of treated fish. The two metabolic enzymes G6PDH and LDH in all tissues exhibited significant decreases (p < 0.05) in treated fish. SOD, CAT, GSH and GST levels showed significant decreases (p < 0.05) in all tissues of fish after exposure to carbofuran. LPO levels increased significantly (p < 0.05) in all tissues except gonads after 5 weeks of exposure to carbofuran. There was a significant (p < 0.05) increase in DNA fragmentation percentage in treated fish. Our results provide a clear evidence on the response of C gariepinus to sublethal doses of carbofuran and allow us to consider catfish as a good bioindicator to reflect the endocrine disrupting impacts of carbofuran, and reflect the potential of this pesticide to cause disturbance in antioxidant defense system as well as metabolism and induction of lipid peroxidation (LPO) and DNA damage in contaminated ecosystems. (C) 2014 Elsevier Inc. All rights reserved.