Bisphenol A leads to oxidative DNA damage and alters the damage response in mouse fibroblasts

Published

February 18, 2015

Author(s)

Pawel Jaruga, Natalie R. Gassman, Erdem Coskun, Donna F. Stefanick, Julie K. Horton, M Miral Dizdar, Samuel H. Wilson

Abstract

Metabolism of bisphenol A (BPA) generates reactive oxygen species causing DNA strand breaks and damaged DNA bases. Base excision repair (BER) is responsible for removing oxidatively induced DNA base lesions and for repairing single strand breaks (SSBs), yet the relationship between BPA and BER has yet to be examined. To determine the effect of BPA exposure on repair of oxidatively induced DNA damage, Ku70-proficient and Ku70-deficient cells lines were co-exposed to BPA and the oxidizing agent, potassium bromate (KBrO3), or to laser delivered irradiation. Ku70-deficient cells were more sensitive to KBrO3-generated DNA damage than isogenic wild-type cells. However, in the presence of BPA, an enhanced cell survival was observed that was coupled with increased oxidized guanine content in genomic DNA. This cellular protective effect, and the increased DNA lesion load, resembles the DNA glycosylase-deficient cell phenotype, suggesting that BPA suppresses repair of guanine lesions during the first 4 h after exposure to KBrO3

Citation

PLoS One

Volume

10

Issue

2

Pub Type

Journals

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Citation

Jaruga, P. , Gassman, N. , Coskun, E. , Stefanick, D. , Horton, J. , , M. and Wilson, S. (2015), Bisphenol A leads to oxidative DNA damage and alters the damage response in mouse fibroblasts, PLoS One, [online], https://tsapps.nist.gov/publication/get_pdf.cfm?pub_id=916441 (Accessed October 16, 2025)