Untitled

Abstract

Bisphenol-A (BPA), 2,2-bis(4-hydroxyphenyl) propane is an emerging environmental toxicant with endocrine disrupting properties and toxic effects on living organisms. BPA is ubiquitously present in consumer products current in our daily lives. As it is released from consumer products and deposited in the environment, thus creating the potential for human exposure through oral, inhaled, and dermal routes. BPA exposure might be able to cause oxidative damage by disturbing the balance between reactive oxygen species (ROS) and the antioxidant defense system of eukaryotic cells, resulting in the development of oxidative stress-related diseases. From the available information, it can be inferred that a wide variety of BPA intake through any mode results into a generation of reactive oxygen species (ROS), altering the antioxidant balance of eukaryotic cells, induces mitochondrial dysfunction, and affects cell signaling pathways related to oxidative stress. BPA induced oxidative stress might be able to cause sperm damage, mitochondrial dysfunction, and impairment of the structure and function of spermatozoa resulting in male infertility. Here, a review of the current literature examining literature related to BPA exposure, induction of ROS or oxidative stress and concludes that it alters reproductive system functions through induced oxidative stress pathways and negatively affects the fertility of male and females.

Exposure to environmental pollutant bisphenol A causes oxidative damage and lipid accumulation in Zebrafish larvae: Protective role of WL15 peptide derived from cysteine and glycine‐rich protein 2

“…The enzymatic and nonenzymatic production of radicals by BPA can result in the generation of ROS. [5] Also, exposure to high doses of BPA causes impaired glucose metabolism and insulin resistance.…”