Effectiveness of melatonin to restore fish brain activity in face of permethrin induced toxicity.
Present study demonstrates permethrin induced oxidative damage in fish brain and explores effectiveness of melatonin to ameliorate brain function. Adult female Notopterus notopterus were exposed to nominal permethrin concentrations at 1/20th (0.34 μg/l) and 1/10th (0.68 μg/l) of LC50 for 15 days. The measured permethrin concentrations using gas chromatography (GC-ECD) were 0.28 μg/l and 0.57 μg/l, respectively. Some fish were sacrificed to collect brain tissue after 15 days of exposure. Remaining fish from both groups were administered exogenous melatonin (50 μg/kg, 100 μg/kg body weight) for 7 days and brain tissues were collected. Brain enzymes, ntioxidant factors, HSP70, HSP90, nuclear factor-kappa binding (NFkB), melatonin receptor (MT1R) proteins were measured. Permethrin treatment significantly (P < 0.05) decreased the levels of glutathione and brain enzymes. Malondialdehyde (MDA), xanthine oxidase (XO), HSPs increased at each concentration of permethrin. However, superoxide dismutase, glutathione s-transferase levels increased at low permethrin concentration followed by sharp decrease at higher concentration. Expression of NFkB and MT1R increased significantly (P < 0.05). Melatonin administration reinstated activity of brain enzymes, reduced MDA, XO levels and modulated HSPs. Melatonin also increased expression of NFkB and MT1R. Exogenous melatonin improves oxidative status in permethrin stressed fish brain. Melatonin modulates expression of HSPs that enables brain to become stress tolerant and survive by initiating NFkB translocation. Melatonin could act through melatonin receptor protein to induce synthesis of antioxidant proteins. Therefore the study successfully evaluates the potential of melatonin application for better culture and management of fish against pesticide toxicity.