Delineating involvement of MAPK/NF-κB pathway during mitigation of permethrin-induced oxidative damage in fish gills by melatonin

Present study evaluated involvement of transcription factors during permethrin-induced gill toxicity and its amelioration by melatonin. First, adult Notoptertus notopterus females were exposed to permethrin at nominal concentrations [C: 0.0, P1: 0.34, P2: 0.68 mu g/L] for 15 days followed by intramuscular melatonin administration (100 mu g/kg body weight) for 7 days. Gill MDA, XO, LDH levels increased, while Na+-K+-ATPase, SDH, cytochrome C oxidase levels decreased with increasing permethrin concentrations. Glutathione, SOD, CAT, GST, GRd levels increased in P1 than C, but decreased in P2 than P1, C. Melatonin administration restored gill enzyme and antioxidant levels in P1, P2. Next, isolated gill tissues were exposed to permethrin at 25, 50 mu M doses along with melatonin administration (100 mu g/mL). NF-kappa B, NRF2, Keap1, ERK, Akt, caspases protein expression changed significantly during permethrin-induced gill damage. Melatonin administration amended permethrin-induced molecular imbalance through modulation of caspase proteins and MAPK/NF-kappa B signal transduction pathway via melatonin receptor 1.

Automated summary

This study evaluated the involvement of transcription factors in permethrin-induced gill toxicity and its amelioration by melatonin. The results showed that permethrin exposure led to oxidative stress and inflammation in gill tissues, while melatonin administration restored the enzyme activity and antioxidant levels in the gills. Furthermore, melatonin was found to modulate caspase proteins and the MAPK/NF-kappa B signaling pathway to ameliorate the molecular imbalance caused by permethrin.