The Oxidant Effect of Bisphenol A (BPA) Can be Decoupled from its Endocrine Disruptor Property

Bisphenol A (BPA) is an environmental defilement released mainly from polycarbonate plastic and epoxy resins. The main toxicological impact of BPA is its endocrine disruptor activities. Its structural features confer the ability to bind to both estrogen receptor (ER) subtypes. Furthermore, we recently reported that BPA aggravates male reproductive hormones. In addition to its endocrine disruptor properties, we have also reported that BPA possesses oxidant activity which is able to trigger oxidative stress. Several types of research previously reported that oxidative stress may cause hormonal imbalance and vice versa. However, the relation of both the toxicological properties of BPA is poorly understood. In this study, we found that oral testosterone undecanoate treatment in BPA-induced rats does not prevent decreasing serum superoxide dismutase, glutathione peroxidase, and catalase, and increasing serum malondialdehyde. Oral N-acetyl cysteine (NAC) in BPA-induced rats also does not attenuate decreasing total testosterone levels. These results suggest that the oxidant effect and endocrine disruptor property of BPA can be separated and might not interfere with one another. Therefore, future treatment in any pathological condition resulting from BPA exposure has to be carried out with more comprehensive approaches rather than focusing on its endocrine disruptor activity.