ArticleCell death & disease2015
Evaluation of low doses BPA-induced perturbation of glycemia by toxicogenomics points to a primary role of pancreatic islets and to the mechanism of toxicity.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 62 citations in OpenAlex.
- Individual and combined antagonism of aryl hydrocarbon receptor (AhR) and estrogen receptors (ERs) offers distinct level of protection against Bisphenol A (BPA)-induced pancreatic islet cell toxicity in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- BPA and low-Se exacerbate apoptosis and mitophagy in chicken pancreatic cells by regulating the PTEN/PI3K/AKT/mTOR pathway.Journal of advanced research · 2025Article
- Analysis of bisphenol A-modulated expression of hypothalamic thyroid, estrogen, and peroxisome proliferator-activated receptors and concurrent mitochondrial dynamics following short-term exposure in mice.Current research in toxicology · 2025Article
- Liver and Pancreatic Toxicity of Endocrine-Disruptive Chemicals: Focus on Mitochondrial Dysfunction and Oxidative Stress.International journal of molecular sciences · 2024Review
- Endocrine disruptors in plastics alter β-cell physiology and increase the risk of diabetes mellitus.American journal of physiology. Endocrinology and metabolism · 2023Review
- Chronic Exposure to Chlorpyrifos Damages Thyroid Activity and Imbalances Hepatic Thyroid Hormones Signaling and Glucose Metabolism: Dependency of T3-FOXO1 Axis by Hyperglycemia.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
- Application of In Vitro Models for Studying the Mechanisms Underlying the Obesogenic Action of Endocrine-Disrupting Chemicals (EDCs) as Food Contaminants-A Review.International journal of molecular sciences · 2023Review
- Screening of Metabolism-Disrupting Chemicals on Pancreatic α-Cells Using In Vitro Methods.International journal of molecular sciences · 2022Article
- Bisphenol A is a carcinogen that induces lipid accumulation, peroxisome proliferator‑activated receptor‑γ expression and liver disease.Experimental and therapeutic medicine · 2022Article
- In Vitro Assays to Identify Metabolism-Disrupting Chemicals with Diabetogenic Activity in a Human Pancreatic β-Cell Model.International journal of molecular sciences · 2022Article
- Article
- Reconceptualization of Hormetic Responses in the Frame of Redox Toxicology.International journal of molecular sciences · 2021Review
- Effectiveness of N-Acetylcysteine in the Treatment of Renal Deterioration Caused by Long-Term Exposure to Bisphenol A.Biomolecules · 2021Article
- Microplastics in the environment: Occurrence, perils, and eradication.Chemical engineering journal (Lausanne, Switzerland : 1996) · 2021Article
- Characterization of Estrogenic Activity and Site-Specific Accumulation of Bisphenol-A in Epididymal Fat Pad: Interfering Effects on the Endocannabinoid System and Temporal Progression of Germ Cells.International journal of molecular sciences · 2021Article
- The phenotypic and transcriptomic effects of developmental exposure to nanomolar levels of estrone and bisphenol A in zebrafish.The Science of the total environment · 2021Article
- Role of TET Dioxygenases and DNA Hydroxymethylation in Bisphenols-Stimulated Proliferation of Breast Cancer Cells.Environmental health perspectives · 2020Article
- A mini review of bisphenol A (BPA) effects on cancer-related cellular signaling pathways.Environmental science and pollution research international · 2019Article
- Redox stress and signaling during vertebrate embryonic development: Regulation and responses.Seminars in cell & developmental biology · 2018Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epidemiologic and experimental studies have associated changes of blood glucose homeostasis to Bisphenol A (BPA) exposure. We took a toxicogenomic approach to investigate the mechanisms of low-dose (1 × 10(-9 )M) BPA toxicity in ex vivo cultures of primary murine pancreatic islets and hepatocytes. Twenty-nine inhibited genes were identified in islets and none in exposed hepatocytes. Although their expression was slightly altered, their impaired cellular level, as a whole, resulted in specific phenotypic changes. Damage of mitochondrial function and metabolism, as predicted by bioinformatics analyses, was observed: BPA exposure led to a time-dependent decrease in mitochondrial membrane potential, to an increase of ROS cellular levels and, finally, to an induction of apoptosis, attributable to the bigger Bax/Bcl-2 ratio owing to activation of NF-κB pathway. Our data suggest a multifactorial mechanism for BPA toxicity in pancreatic islets with emphasis to mitochondria dysfunction and NF-κB activation. Finally, we assessed in vitro the viability of BPA-treated islets in stressing condition, as exposure to high glucose, evidencing a reduced ability of the exposed islets to respond to further damages. The result was confirmed in vivo evaluating the reduction of glycemia in hyperglycemic mice transplanted with control and BPA-treated pancreatic islets. The reported findings identify the pancreatic islet as the main target of BPA toxicity in impairing the glycemia. They suggest that the BPA exposure can weaken the response of the pancreatic islets to damages. The last observation could represent a broader concept whose consideration should lead to the development of experimental plans better reproducing the multiple exposure conditions.
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