Resveratrol mitigates diazinon-induced neurotoxicity during fetal brain development.

OBJECTIVES

Disruption of transcriptional programs governing fetal neurogenesis represents a critical but underexplored mechanism of diazinon (DZN)-induced developmental neurotoxicity. This research examines whether resveratrol (RV) influences the expression of genes associated with neurogenesis and survival after prenatal exposure to DZN.

MATERIALS AND

METHODS

Twenty-four pregnant Wistar rats were divided into DZN (40 mg/kg) group, RV (10 mg/kg), DZN+RV (40 mg/kg + 10 mg/kg), and Control. On day 21 of pregnancy, rats were cesarean sectioned, and the neonatal brains were examined using HPLC, GC-MS, real-time PCR, and histology techniques to assess RV's neuroprotective effects against DZN-induced toxicity. Data were statistically analyzed using SPSS and GraphPad Prism.

RESULTS

DZN significantly reduced neuronal survival and altered gene expression in fetal brains, with lower Ptf1α, SOX2, BDNF, and BCL2 levels and higher BAX levels compared to controls. The simultaneous administration of RV partially restored these molecular changes. Histological findings indicated that RV mitigated neuronal damage associated with DZN, resulting in decreased dark neuron formation and preserved myelin integrity in the hippocampus and thalamus.

CONCLUSION

Collectively, these findings suggest that DZN exposure correlates with changes in the molecular and structural composition of the fetal brain, and that RV may help regulate these effects.