Deltamethrin is the most common type II synthetic pyrethroid insecticide, and has posed widespread residues to environment. However, whether deltamethrin has potential toxic effects on quail cerebrum remains greatly obscure. Accordingly, we investigated the impact of chronic exposure to deltamethrin on oxidative stress and apoptosis in quail cerebrum. Quails upon 12-week exposure of deltamethrin (0, 15, 30, or 45 mg/kg body weight intragastric administration) were used as a cerebrum injury model. The results showed that deltamethrin treatment led to cerebral injury dose-dependently through the weakened antioxidant defense by downregulating nuclear factor erythroid-2-related factor 2 (Nrf2) and its downstream proteins levels and mRNA expression. Furthermore, deltamethrin treatment induced apoptosis in cerebrum by decreasing B-cell lymphoma gene 2 (Bcl-2) level, as well as increasing Jun N-terminal kinase3, caspase-3, and Bcl-2-associated X protein levels. Simultaneously, toll-like receptor 4 (TLR4) downstream inflammation-related genes or proteins were significantly up-regulated by deltamethrin dose-dependently. Altogether, our study demonstrated that chronic exposure to deltamethrin induces inflammation and apoptosis in quail cerebrums by promoting oxidative stress linked to inhibition of the Nrf2/TLR4 signaling pathway. These results provide a novel knowledge on the chronic toxic effect of deltamethrin, and establish a theoretical foundation for the evaluation of pesticide-induced health risk.
Keywords: Apoptosis; Cerebral toxicity; Deltamethrin; Nrf2/TLR4; Oxidative stress; Pyrethroid insecticide.
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