Chapter 3: Bisphenol A Associated Signaling Pathways in Human Diseases

Divya Adiga, G. Nadeem Khan, Sangavi Eswaran, S. Sriharikrishnaa, Sanjiban Chakrabarty, Padmalatha S. Rai, Shama Prasada Kabekkodu

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Citations (Scopus)


Bisphenol A (BPA) is a ubiquitous chemical contaminant found in the environment due to anthropogenic activities. BPA is still being used worldwide despite the longstanding concern over safety, as it has been challenging to develop safe and economical replacements. BPA has been reported to induce disease in various lifeforms, including humans. BPA can exert its toxic effects by inducing genetic and epigenetic alterations, oxidative stress, mitochondrial dysfunction, and endocrine disruption, and by modulating cell signaling pathways. Many experimental and epidemiological studies have described the association between high levels of free BPA in body fluids with different chronic health complications such as obesity, cancer, cardiovascular disorders, hepatotoxicity, diabetes, and neurological, reproductive, and developmental disorders. BPA can modulate key oncogenic signaling pathways, including epithelial-mesenchymal transition, Wnt, MAPK, PI3K/AKT, NF-κB, cytokine signaling, senescence, apoptosis, calcium homeostasis, and receptor-driven signaling cascades. This chapter describes the molecular alterations associated with BPA exposure and different human ailments, with a detailed note on the intricate signaling cascades involved in BPA-mediated carcinogenesis.

Original languageEnglish
Title of host publicationBisphenol A
Subtitle of host publicationA Multi-modal Endocrine Disruptor
EditorsNatalie R. Gassman
PublisherRoyal Society of Chemistry
Number of pages45
ISBN (Electronic)9781839162060
Publication statusPublished - 2022

Publication series

NameIssues in Toxicology
ISSN (Print)1757-7179
ISSN (Electronic)1757-7187

All Science Journal Classification (ASJC) codes

  • Toxicology
  • Pharmacology
  • Health, Toxicology and Mutagenesis


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