Bisphenol a promotes cell survival following oxidative DNA damage in mouse fibroblasts
Bisphenol A (BPA) is a biologically active industrial chemical used in production of consumer products. BPA has become a target of intense public scrutiny following concerns about its association with human diseases such as obesity, diabetes, reproductive disorders, and cancer. Recent studies link B...
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Published in | PloS one Vol. 10; no. 2; p. e0118819 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
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Public Library of Science
18.02.2015
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Abstract | Bisphenol A (BPA) is a biologically active industrial chemical used in production of consumer products. BPA has become a target of intense public scrutiny following concerns about its association with human diseases such as obesity, diabetes, reproductive disorders, and cancer. Recent studies link BPA with the generation of reactive oxygen species, and base excision repair (BER) is responsible for removing oxidatively induced DNA lesions. Yet, the relationship between BPA and BER has yet to be examined. Further, the ubiquitous nature of BPA allows continuous exposure of the human genome concurrent with the normal endogenous and exogenous insults to the genome, and this co-exposure may impact the DNA damage response and repair. To determine the effect of BPA exposure on base excision repair of oxidatively induced DNA damage, cells compromised in double-strand break repair were treated with BPA alone or co-exposed with either potassium bromate (KBrO3) or laser irradiation as oxidative damaging agents. In experiments with KBrO3, co-treatment with BPA partially reversed the KBrO3-induced cytotoxicity observed in these cells, and this was coincident with an increase in guanine base lesions in genomic DNA. The improvement in cell survival and the increase in oxidatively induced DNA base lesions were reminiscent of previous results with alkyl adenine DNA glycosylase-deficient cells, suggesting that BPA may prevent initiation of repair of oxidized base lesions. With laser irradiation-induced DNA damage, treatment with BPA suppressed DNA repair as revealed by several indicators. These results are consistent with the hypothesis that BPA can induce a suppression of oxidized base lesion DNA repair by the base excision repair pathway. |
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AbstractList | Bisphenol A (BPA) is a biologically active industrial chemical used in production of consumer products. BPA has become a target of intense public scrutiny following concerns about its association with human diseases such as obesity, diabetes, reproductive disorders, and cancer. Recent studies link BPA with the generation of reactive oxygen species, and base excision repair (BER) is responsible for removing oxidatively induced DNA lesions. Yet, the relationship between BPA and BER has yet to be examined. Further, the ubiquitous nature of BPA allows continuous exposure of the human genome concurrent with the normal endogenous and exogenous insults to the genome, and this co-exposure may impact the DNA damage response and repair. To determine the effect of BPA exposure on base excision repair of oxidatively induced DNA damage, cells compromised in double-strand break repair were treated with BPA alone or co-exposed with either potassium bromate (KBrO3) or laser irradiation as oxidative damaging agents. In experiments with KBrO3, co-treatment with BPA partially reversed the KBrO3-induced cytotoxicity observed in these cells, and this was coincident with an increase in guanine base lesions in genomic DNA. The improvement in cell survival and the increase in oxidatively induced DNA base lesions were reminiscent of previous results with alkyl adenine DNA glycosylase-deficient cells, suggesting that BPA may prevent initiation of repair of oxidized base lesions. With laser irradiation-induced DNA damage, treatment with BPA suppressed DNA repair as revealed by several indicators. These results are consistent with the hypothesis that BPA can induce a suppression of oxidized base lesion DNA repair by the base excision repair pathway. Bisphenol A (BPA) is a biologically active industrial chemical used in production of consumer products. BPA has become a target of intense public scrutiny following concerns about its association with human diseases such as obesity, diabetes, reproductive disorders, and cancer. Recent studies link BPA with the generation of reactive oxygen species, and base excision repair (BER) is responsible for removing oxidatively induced DNA lesions. Yet, the relationship between BPA and BER has yet to be examined. Further, the ubiquitous nature of BPA allows continuous exposure of the human genome concurrent with the normal endogenous and exogenous insults to the genome, and this co-exposure may impact the DNA damage response and repair. To determine the effect of BPA exposure on base excision repair of oxidatively induced DNA damage, cells compromised in double-strand break repair were treated with BPA alone or co-exposed with either potassium bromate (KBrO 3 ) or laser irradiation as oxidative damaging agents. In experiments with KBrO 3 , co-treatment with BPA partially reversed the KBrO 3 -induced cytotoxicity observed in these cells, and this was coincident with an increase in guanine base lesions in genomic DNA. The improvement in cell survival and the increase in oxidatively induced DNA base lesions were reminiscent of previous results with alkyl adenine DNA glycosylase-deficient cells, suggesting that BPA may prevent initiation of repair of oxidized base lesions. With laser irradiation-induced DNA damage, treatment with BPA suppressed DNA repair as revealed by several indicators. These results are consistent with the hypothesis that BPA can induce a suppression of oxidized base lesion DNA repair by the base excision repair pathway. Bisphenol A (BPA) is a biologically active industrial chemical used in production of consumer products. BPA has become a target of intense public scrutiny following concerns about its association with human diseases such as obesity, diabetes, reproductive disorders, and cancer. Recent studies link BPA with the generation of reactive oxygen species, and base excision repair (BER) is responsible for removing oxidatively induced DNA lesions. Yet, the relationship between BPA and BER has yet to be examined. Further, the ubiquitous nature of BPA allows continuous exposure of the human genome concurrent with the normal endogenous and exogenous insults to the genome, and this co-exposure may impact the DNA damage response and repair. To determine the effect of BPA exposure on base excision repair of oxidatively induced DNA damage, cells compromised in double-strand break repair were treated with BPA alone or co-exposed with either potassium bromate (KBrO.sub.3) or laser irradiation as oxidative damaging agents. In experiments with KBrO.sub.3, co-treatment with BPA partially reversed the KBrO.sub.3 -induced cytotoxicity observed in these cells, and this was coincident with an increase in guanine base lesions in genomic DNA. The improvement in cell survival and the increase in oxidatively induced DNA base lesions were reminiscent of previous results with alkyl adenine DNA glycosylase-deficient cells, suggesting that BPA may prevent initiation of repair of oxidized base lesions. With laser irradiation-induced DNA damage, treatment with BPA suppressed DNA repair as revealed by several indicators. These results are consistent with the hypothesis that BPA can induce a suppression of oxidized base lesion DNA repair by the base excision repair pathway. Bisphenol A (BPA) is a biologically active industrial chemical used in production of consumer products. BPA has become a target of intense public scrutiny following concerns about its association with human diseases such as obesity, diabetes, reproductive disorders, and cancer. Recent studies link BPA with the generation of reactive oxygen species, and base excision repair (BER) is responsible for removing oxidatively induced DNA lesions. Yet, the relationship between BPA and BER has yet to be examined. Further, the ubiquitous nature of BPA allows continuous exposure of the human genome concurrent with the normal endogenous and exogenous insults to the genome, and this co-exposure may impact the DNA damage response and repair. To determine the effect of BPA exposure on base excision repair of oxidatively induced DNA damage, cells compromised in double-strand break repair were treated with BPA alone or co-exposed with either potassium bromate (KBrO 3 ) or laser irradiation as oxidative damaging agents. In experiments with KBrO 3 , co-treatment with BPA partially reversed the KBrO 3 -induced cytotoxicity observed in these cells, and this was coincident with an increase in guanine base lesions in genomic DNA. The improvement in cell survival and the increase in oxidatively induced DNA base lesions were reminiscent of previous results with alkyl adenine DNA glycosylase-deficient cells, suggesting that BPA may prevent initiation of repair of oxidized base lesions. With laser irradiation-induced DNA damage, treatment with BPA suppressed DNA repair as revealed by several indicators. These results are consistent with the hypothesis that BPA can induce a suppression of oxidized base lesion DNA repair by the base excision repair pathway. |
Audience | Academic |
Author | Jaruga, Pawel Wilson, Samuel H Stefanick, Donna F Coskun, Erdem Horton, Julie K Dizdaroglu, Miral Gassman, Natalie R |
AuthorAffiliation | University of South Alabama Mitchell Cancer Institute, UNITED STATES 3 Faculty of Pharmacy, Gazi University, Ankara, Turkey 2 Biomolecular Measurement Division, National Institute of Standards and Technology, Gaithersburg, MD 20899, United States of America 1 Genomic Integrity and Structural Biology Laboratory, NIEHS, National Institutes of Health, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709, United States of America |
AuthorAffiliation_xml | – name: 2 Biomolecular Measurement Division, National Institute of Standards and Technology, Gaithersburg, MD 20899, United States of America – name: 1 Genomic Integrity and Structural Biology Laboratory, NIEHS, National Institutes of Health, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709, United States of America – name: University of South Alabama Mitchell Cancer Institute, UNITED STATES – name: 3 Faculty of Pharmacy, Gazi University, Ankara, Turkey |
Author_xml | – sequence: 1 givenname: Natalie R surname: Gassman fullname: Gassman, Natalie R organization: Genomic Integrity and Structural Biology Laboratory, NIEHS, National Institutes of Health, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709, United States of America – sequence: 2 givenname: Erdem surname: Coskun fullname: Coskun, Erdem organization: Biomolecular Measurement Division, National Institute of Standards and Technology, Gaithersburg, MD 20899, United States of America; Faculty of Pharmacy, Gazi University, Ankara, Turkey – sequence: 3 givenname: Donna F surname: Stefanick fullname: Stefanick, Donna F organization: Genomic Integrity and Structural Biology Laboratory, NIEHS, National Institutes of Health, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709, United States of America – sequence: 4 givenname: Julie K surname: Horton fullname: Horton, Julie K organization: Genomic Integrity and Structural Biology Laboratory, NIEHS, National Institutes of Health, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709, United States of America – sequence: 5 givenname: Pawel surname: Jaruga fullname: Jaruga, Pawel organization: Biomolecular Measurement Division, National Institute of Standards and Technology, Gaithersburg, MD 20899, United States of America – sequence: 6 givenname: Miral surname: Dizdaroglu fullname: Dizdaroglu, Miral organization: Biomolecular Measurement Division, National Institute of Standards and Technology, Gaithersburg, MD 20899, United States of America – sequence: 7 givenname: Samuel H surname: Wilson fullname: Wilson, Samuel H organization: Genomic Integrity and Structural Biology Laboratory, NIEHS, National Institutes of Health, 111 T.W. Alexander Drive, Research Triangle Park, NC 27709, United States of America |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/25693136$$D View this record in MEDLINE/PubMed |
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Notes | Competing Interests: The authors have declared that no competing interests exist. Conceived and designed the experiments: NRG DFS JKH SHW. Performed the experiments: NRG EC. Analyzed the data: NRG EC PJ MD SHW. Contributed reagents/materials/analysis tools: NRG EC PJ MD SHW. Wrote the paper: NRG MD SHW. |
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Snippet | Bisphenol A (BPA) is a biologically active industrial chemical used in production of consumer products. BPA has become a target of intense public scrutiny... |
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SubjectTerms | Adenine Animals Base excision repair Benzhydryl Compounds - adverse effects Biological activity Biology Bisphenol A Bromates - pharmacology Cancer Cell cycle Cell Line Cell survival Cell Survival - drug effects Consumer products Cytotoxicity Deoxyribonucleic acid Diabetes mellitus DNA DNA - drug effects DNA - radiation effects DNA damage DNA Damage - drug effects DNA glycosylase DNA methylation DNA polymerase DNA repair DNA Repair - drug effects DNA Repair - radiation effects Double-strand break repair Enzymes Exposure Fibroblasts Fibroblasts - cytology Fibroblasts - drug effects Fibroblasts - radiation effects Gene expression Genomes Genomics Guanine Guanine - metabolism Impact damage Irradiation Laboratories Laser damage Lasers Lesions Low-Level Light Therapy - adverse effects Mice Obesity Oxidative stress Oxidative Stress - drug effects Oxygen Phenols Phenols (Class of compounds) Phenols - adverse effects Potassium Potassium bromate Purines Radiation damage Reactive oxygen species Repair Reproductive disorders Survival Toxicity |
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Title | Bisphenol a promotes cell survival following oxidative DNA damage in mouse fibroblasts |
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