Carvacrol Prevents Bisphenol A-Induced Behavioral Changes And Oxidative Stress in Zebrafish Through Modulating Brain Antioxidant Defense Mechanism

Abstract

It has been discovered that bisphenol A (BPA), an established anthropogenic xenoestrogen, is a causal factor in developing cancer, cognitive impairment, neurotoxicity, oxidative stress, and other harmful effects in humans and other species. Although there is some research into the mechanisms of BPA-induced toxicity, it is unclear whether there is a chance of amelioration through natural intervention. Zebrafish (Danio rerio) were used in this study after waterborne exposure to BPA, to assess whether carvacrol co-supplementation could reduce the destructive potential of the compound. All the chemicals and reagents utilized in the current investigations were purchased from Sigma-Aldrich, Ottochem, India. 5-7month-old zebrafish were acquired from a local fish store in Kolathur, Chennai and kept in a 50-L tank at a constant temperature of 25±2ºC. There were no animal ethical issues involved to carry out this research. Laboratory studies were conducted to determine whether the antioxidant nature of carvacrol might protect the zebrafish brain from BPA-induced altered behavioural responses and oxidative stress. The current data demonstrates that carvacrol is effective in alleviating the altered behavioural response caused by BPA. Biochemical investigations in the zebrafish brain suggest that carvacrol may have therapeutic potential in treating oxidative stress induced by BPA. In addition, the zebrafish brain is protected by carvacrol against BPA-induced toxicity. These preliminary data suggest that carvacrol may be a helpful intervention in treating BPA-induced toxicity in zebrafish by inhibiting the reactive oxygen species production. Novel therapeutic approaches for treating BPA-induced predisposition to severe illnesses could emerge from future research on signaling cascades.