Abstract
Parkinson's disease (PD) is a neurodegenerative condition that typically develops as people age and is characterized by the progressive death of dopaminergic neurons in the substantia nigra area of the midbrain. The etiology of PD includes both genetic and environmental components. Epidemiological studies have shown that pesticide exposure is an important contributory risk factor for PD. Fenpropathrin has been shown to have neurotoxic effects on rodents, but the exact mechanism and its ability to replicate the pathological features associated with PD remain unclear. Therefore, the present study investigated the neurotoxic effects of Fenpropathrin in D. melanogaster. Fenpropathrin was added to the food at various concentrations, and adult male flies were allowed to consume it for 96 h, after which the LC50 value was determined. The administration of Fenpropathrin resulted in notable impairments in the climbing, jumping, and crawling abilities of adult male flies and larvae, along with a significant dose-dependent reduction in their lifespan. Moreover, it significantly extended the developmental life cycle of D. melanogaster. In addition, Fenpropathrin exposure altered oxidative stress responses through a dose-dependent biphasic modulation of Nrf2 expression and suppressed the expression of B-cell lymphoma 2 (Bcl-2) and tyrosine hydroxylase (TH) expression in the brain tissue of male flies. This resulted in the impairment of dopaminergic neurons and subsequent neuronal death through apoptosis. The results of this study suggest that Fenpropathrin exhibits potent neurotoxicity toward dopaminergic (DA) neurons, implicating it as a notable environmental factor contributing to the risk of PD.
