ArticlePloS one2015
Bisphenol a promotes cell survival following oxidative DNA damage in mouse fibroblasts.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 58 citations in OpenAlex.
- Bombesin-like receptor 3 expression induced by bisphenol A is likely associated with reduced cell proliferation by inhibiting DNA synthesis and inducing inflammation in liver cells.Molecular biology reports · 2024Article
- Evaluating the Toxicity Induced by Bisphenol F inScientifica · 2024Article
- Transcriptome-Wide Analysis of Low-Concentration Exposure to Bisphenol A, S, and F in Prostate Cancer Cells.International journal of molecular sciences · 2023Article
- Re-evaluation of the risks to public health related to the presence of bisphenol A (BPA) in foodstuffs.EFSA journal. European Food Safety Authority · 2023Article
- Combined Toxic Effects of BPA and Its Two Analogues BPAP and BPC in a 3D HepG2 Cell Model.Molecules (Basel, Switzerland) · 2023Article
- Article
- Bisphenol A Interferes with Redox Balance and the Nrf2 Signaling Pathway inAnimals : an open access journal from MDPI · 2022Article
- Bisphenol A Promotes the Progression of Colon Cancer Through Dual-Targeting of NADPH Oxidase and Mitochondrial Electron-Transport Chain to Produce ROS and Activating HIF-1α/VEGF/PI3K/AKT Axis.Frontiers in endocrinology · 2022Article
- Dihydroxyacetone suppresses mTOR nutrient signaling and induces mitochondrial stress in liver cells.PloS one · 2022Article
- Bisphenol A Induces Histopathological, Hematobiochemical Alterations, Oxidative Stress, and Genotoxicity in Common Carp (Oxidative medicine and cellular longevity · 2022Article
- Endocrine-Disrupting Chemicals' (EDCs) Effects on Tumour Microenvironment and Cancer Progression: Emerging Contribution of RACK1.International journal of molecular sciences · 2020Review
- Oxidative Stress and BPA Toxicity: An Antioxidant Approach for Male and Female Reproductive Dysfunction.Antioxidants (Basel, Switzerland) · 2020Review
- Bisphenol A co-exposure effects: a key factor in understanding BPA's complex mechanism and health outcomes.Critical reviews in toxicology · 2019Review
- Defective base excision repair in the response to DNA damaging agents in triple negative breast cancer.PloS one · 2019Article
- Association of Bisphenol A Exposure with LINE-1 Hydroxymethylation in Human Semen.International journal of environmental research and public health · 2018Article
- Camptothecin Efficacy to Poison Top1 Is Altered by Bisphenol A in Mouse Embryonic Fibroblasts.Chemical research in toxicology · 2018Article
- DNA polymerase β: A missing link of the base excision repair machinery in mammalian mitochondria.DNA repair · 2017Article
- Review
- Formation and repair of oxidatively generated damage in cellular DNA.Free radical biology & medicine · 2017Review
- Induction of oxidative stress by bisphenol A and its pleiotropic effects.Environmental and molecular mutagenesis · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.