Behavioural, neurochemical, and neurohistological effects of bisphenol A and vanadium following chronic co-administration in mice

Abstract

Bisphenol A (BPA) and vanadium are industrial chemicals known to disrupt hormones and cause neurotoxicity. BPA is commonly found in food packaging and poses risks to human health through various exposure routes, while vanadium exposure can occur near power plants. Both chemicals induce oxidative stress, disrupt neurotransmission, and cause neuronal damage, yet research on their combined effects is limited. To examine the behavioral, neurochemical, and neurohistological changes associated with co-exposure to BPA and vanadium, we utilized 40 male BALB/c mice, divided into four groups: the control group, the BPA-exposed group, the vanadium-exposed group, and the BPA +vanadium co-exposed group. Mice in the control group received dimethyl sulfoxide (DMSO) only. The BPA-exposed group was administered 10 µg/kg bw/day of BPA, while the vanadium-exposed group received 1.2 mg/kg bw/day of vanadyl sulphate. Mice in the BPA +vanadium co- exposed group received both 10 µg/kg bw/day of BPA and 1.2 mg/kg bw/day of vanadyl sulphate. Each group underwent this oral administration daily for 56 consecutive days. Moreover, we conducted behavioral, histological and neurochemical analyses on the prefrontal cortex of the mice. Our findings revealed that co- exposure to BPA and vanadium significantly exacerbated impairments in behavioral and neurochemical indicators. Notably, the histoarchitectural profile of the prefrontal cortex indicated evidence of neuronal cell death. In conclusion, our study suggests that co-exposure to BPA and vanadium correlates with detrimental effects on behaviors associated with the prefrontal cortex, alongside substantial neurochemical disruptions and compromised structural integrity.