The heart as a target for deltamethrin toxicity: Inhibition of Nrf2/HO-1 pathway induces oxidative stress and results in inflammation and apoptosis.

As a synthetic pyrethroid pesticide, deltamethrin (DLM) is widely employed in veterinary medicine and farming, and DLM-triggered oxidative stress largely causes serious harm to the organism. It is well-known that nuclear factor erythroid-2-related factor 2/heme oxygenase-1 (Nrf2/HO-1), a pivotal endogenous anti-oxidative pathway, acts on inhibiting oxidative stress-induced cell injury under the activated state. The purpose of this research was to observe the impact and molecular mechanism of DLM on inflammation and apoptosis in quail cardiomyocytes based on the Nrf2/HO-1 signaling route. In this research, quails were established as a cardiac injury model through gastric infusion of various doses of DLM (0, 15, 30, and 45 mg/kg b. w.) for 12 weeks. Our results showed that DLM could induced cardiomyocyte injury in a dose-dependent manner though weakening antioxidant defense via down-regulating Nrf2 and its downstream protein HO-1. Furthermore, DLM stimulation induced apoptosis in quail heart by decreasing the protein expressions of B-cell lymphoma-extra large and B-cell lymphoma gene 2 (Bcl-2), as well as increasing P53, caspase 3, and Bcl-2-associated X protein levels. Meanwhile, relative levels of nuclear factor-kappa B and interleukin-1β in quail hearts were up-regulated under DLM intervention progressively. Collectively, our study demonstrates that chronic exposure to DLM can induce quail cardiomyocyte inflammation and apoptosis by mediating Nrf2/HO-1 signaling pathway-related oxidative stress.