BPA-toxicity via superoxide anion overload and a deficit in β-catenin signaling in human bone mesenchymal stem cells

Yea Hyun Leem, Seikwan Oh, Hong Je Kang, Jung Hwa Kim, Juno Yoon, Jae Suk Chang

Research output: Contribution to journalArticlepeer-review

28 Scopus citations

Abstract

Bisphenol A (BPA), used in the manufacture of products based on polycarbonate plastics and epoxy resins, is well known as an endocrine-disrupting monomer. In the current study, BPA increased cytotoxicity in hBMSCs in a dose- and time-dependent manner, concomitantly with increased lipid peroxidation. Increased cell death in BPA-treated cells was markedly blocked by pretreatment with the superoxide dismutase mimetic MnTBAP and MnTMPyP, but not by catalase, glutathione, the glutathione peroxidase mimetic ebselen, the NOS inhibitor NAME, or the xanthine oxidase inhibitor allopurinol. Furthermore, the decline in nuclear β-catenin and cyclin D1 levels in hBMSCs exposed to BPA was reversed by MnTBAP treatment. Finally, treatment of hBMSCs with the GSK3β inhibitor LiCl2 increased nuclear β-catenin levels and significantly attenuated cytotoxicity compared with BPA treatment. Our current results in hBMSCs exposed to BPA suggest that BPA causes a disturbance in β-catenin signaling via a superoxide anion overload.

Original languageEnglish
Pages (from-to)344-352
Number of pages9
JournalEnvironmental Toxicology
Volume32
Issue number1
DOIs
StatePublished - 1 Jan 2017

Keywords

  • GSK3β
  • MnTBAP
  • bisphenol A
  • human bone mesenchymal stem cells
  • superoxide dismutase
  • β-catenin

Fingerprint

Dive into the research topics of 'BPA-toxicity via superoxide anion overload and a deficit in β-catenin signaling in human bone mesenchymal stem cells'. Together they form a unique fingerprint.

Cite this