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Exploring novel insights into the molecular mechanisms underlying Bisphenol A-induced toxicity: A persistent threat to human health.

Authors :
Ahmad I
Kaur M
Tyagi D
Singh TB
Kaur G
Afzal SM
Jauhar M
Source :
Environmental toxicology and pharmacology [Environ Toxicol Pharmacol] 2024 Jun; Vol. 108, pp. 104467. Date of Electronic Publication: 2024 May 17.
Publication Year :
2024

Abstract

Bisphenol A (BPA) is a ubiquitous industrial chemical used in the production of polycarbonate plastics and epoxy resins, found in numerous consumer products. Despite its widespread use, its potential adverse health effects have raised significant concerns. This review explores the molecular mechanisms and evidence-based literature underlying BPA-induced toxicities and its implications for human health. BPA is an endocrine-disrupting chemical (EDC) which exhibits carcinogenic properties by influencing various receptors, such as ER, AhR, PPARs, LXRs, and RARs. It induces oxidative stress and contributes to cellular dysfunction, inflammation, and DNA damage, ultimately leading to various toxicities including but not limited to reproductive, cardiotoxicity, neurotoxicity, and endocrine toxicity. Moreover, BPA can modify DNA methylation patterns, histone modifications, and non-coding RNA expression, leading to epigenetic changes and contribute to carcinogenesis. Overall, understanding molecular mechanisms of BPA-induced toxicity is crucial for developing effective strategies and policies to mitigate its adverse effects on human health.<br />Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.<br /> (Copyright © 2024 Elsevier B.V. All rights reserved.)

Details

Language :
English
ISSN :
1872-7077
Volume :
108
Database :
MEDLINE
Journal :
Environmental toxicology and pharmacology
Publication Type :
Academic Journal
Accession number :
38763439
Full Text :
https://doi.org/10.1016/j.etap.2024.104467