Implication of Pyrethroid Neurotoxicity for Human Health: A Lesson from Animal Models

Pyrethroids, synthetic insecticides used in pest management, pose health risks, particularly neurotoxic effects, with studies linking exposure to a neurodegenerative disorder. This review examines the neurotoxic mechanisms of pyrethroids analyzing literature from animal model studies. It identifies critical targets for neurotoxicity, including ion channels, oxidative stress, inflammation, neuronal cell loss, and mitochondrial dysfunction. The review also discusses key therapeutic targets and signaling pathways relevant to Pyrethroids neurotoxicity management, including calcium, Wnt/β-catenin, mTOR, MAPK/Erk, PI3K/Akt, Nrf2, Nurr1, and PPARγ. Our findings demonstrate that pyrethroid exposure triggers multiple neurotoxic pathways that bear resemblance to the mechanisms underlying neurotoxicity. Oxidative stress and inflammation emerge as prominent factors that contribute to neuronal degeneration, alongside disrupted mitochondrial function. The investigation highlights the significance of ion channels as primary neurodegeneration targets while acknowledging the potential involvement of various other receptors and enzymes that may exacerbate neurological damage. Additionally, we elucidate how pyrethroids may interfere with therapeutic targets associated with neuronal dysfunction, potentially impairing treatment efficacy.Also, exposure to these chemicals can alter DNA methylation patterns and histone modifications, ultimately leading to changes in gene expression that may enhance susceptibility to neurological disorders. Pyrethroid neurotoxicity poses a significant public health risk, necessitating future research for protective strategies against pesticide-induced neurological disorders and understanding the interplay between neurodegenerative diseases, potentially leading to innovative therapeutic interventions.