Induction of oxidative stress by bisphenol A and its pleiotropic effects

Abstract

Bisphenol A (BPA) has become a target of intense public scrutiny since concerns about its association with human diseases such as obesity, diabetes, reproductive disorders, and cancer have emerged. BPA is a highly prevalent chemical in consumer products, and human exposure is thought to be ubiquitous. Numerous studies have demonstrated its endocrine disrupting properties and attributed exposure with cytotoxic, genotoxic, and carcinogenic effects; however, the results of these studies are still highly debated and a consensus about BPA's safety and its role in human disease has not been reached. One of the contributing factors is a lack of molecular mechanisms or modes of action that explain the diverse and pleiotropic effects observed after BPA exposure. The increase in BPA research seen over the last ten years has resulted in more studies that examine molecular mechanisms and revealed links between BPA-induced oxidative stress and human disease. Here, a review of the current literature examining BPA exposure and the induction of reactive oxygen species (ROS) or oxidative stress will be provided to examine the landscape of the current BPA literature and provide a framework for understanding how induction of oxidative stress by BPA may contribute to the pleiotropic effects observed after exposure.

Bisphenol A aggravates renal ischemia–reperfusion injury by disrupting mitochondrial homeostasis and N‐acetylcysteine mitigates the injurious outcomes

“…It should be mentioned here that our study focuses on the aggravated effect of BPA on AKI and the protection by NAC under a concentration of BPA at 50 mg/kg. Publications regarding BPA did not show a unity on the appropriate BPA concentration that should be used to investigate its detrimental health effects . However, BPA at the dose of 50 mg/kg given orally for 4–8 weeks is one of the regimens repeatedly reported in a rat model to study the BPA outcomes in several organ systems for example, liver, heart, and testis .…”

“…Publications regarding BPA did not show a unity on the appropriate BPA concentration that should be used to investigate its detrimental health effects. 1 However, BPA at the dose of 50 mg/kg given orally for 4-8 weeks is one of the regimens repeatedly reported in a rat model to study the BPA outcomes in several organ systems for example, liver, 44 heart, 45 and testis. 46 Importantly, BPA 50 mg/kg administered via intraperitoneal injection for 5 weeks has been reported in one study on the kidney.…”

“…Bisphenol A (BPA) is one of the high‐volume chemicals used worldwide as a precursor in the production of polycarbonate plastics and epoxy resins. BPA contamination is common in everyday life due to the increase in BPA‐based products, especially food and beverage packaging as well as various plastic products . Epidemiological data reveal that over 90% of population have BPA detected in the urine, implying that human exposure to BPA is almost unavoidable.…”

“…BPA contamination is common in everyday life due to the increase in BPA-based products, especially food and beverage packaging as well as various plastic products. 1 Epidemiological data reveal that over 90% of population have BPA detected in the urine, 2 implying that human exposure to BPA is almost unavoidable. Experimental evidence in the past few years have also shown the associations between BPA exposure and adverse health outcomes.…”

Oxidant-Antioxidant Status and c-myc Expression in BPAand DEHP-Exposed Zebrafish Embryos

“…ROS are generated during normal cellular metabolism, such as superoxide anions, peroxides, and hydroxyl radicals, and cells have developed antioxidant mechanisms to regulate and scavenge excess ROS to prevent deleterious effects. If this balance is disrupted by environmental toxicants or EDCs, the same ROS that were beneficial to the cell can cause mutations, unchecked cell growth, and impair cellular signals (21,22). Moreover, increased oxidative stress is related to aging, cardiovascular disease, neuronal degeneration, and the development and progression of cancers (22).…”