ArticleAntioxidants (Basel, Switzerland)2020
Oral Bisphenol A Worsens Liver Immune-Metabolic and Mitochondrial Dysfunction Induced by High-Fat Diet in Adult Mice: Cross-Talk between Oxidative Stress and Inflammasome Pathway.
Article in Antioxidants (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 48 citations in OpenAlex.
- Endoplasmic reticulum stress is associated with cardiac effects of bisphenol S independently of a high-fat diet.Histochemistry and cell biology · 2026Article
- L. carnitine modulates oxidative stress, steroidogenic gene disturbance, and testicular histopathology induced by Bisphenol A in male rats.Veterinary research communications · 2026Article
- Carnosic Acid Protects against Bisphenol A-Induced NLRP3 Inflammasome Activation by Attenuating Oxidative Stress in Human Microglial Cells.Inflammation · 2026Article
- Astaxanthin attenuates bisphenol A-induced testicular toxicity in Wistar rats by reducing apoptosis and fibrosis via Bax/Bcl-2 balance and collagen gene expression.Biomolecules & biomedicine · 2026Article
- Bisphenol A exacerbates dry eye disease via the CASP1/GSDMD-mediated pyroptotic axis: network toxicology, mendelian randomization, and experimental validation.Frontiers in pharmacology · 2026Article
- Liver disorders and phytotherapy.Toxicology reports · 2025Review
- Anti-Inflammatory Effect ofAntioxidants (Basel, Switzerland) · 2025Article
- Early-life bisphenol A exposure causes neuronal pyroptosis in juvenile and adult male rats through the NF-κB/IL-1β/NLRP3/caspase-1 signaling pathway: exploration of age and dose as effective covariates using an in vivo and in silico modeling approach.Molecular and cellular biochemistry · 2025Article
- Endocrine Disrupting Toxicity of Bisphenol A and Its Analogs: Implications in the Neuro-Immune Milieu.Journal of xenobiotics · 2025Review
- Bisphenols exposure and non-alcoholic fatty liver disease: from environmental trigger to molecular pathogenesis.Frontiers in endocrinology · 2025Review
- Endocrine disruptors, obesity, and metabolic syndrome.Turkish journal of medical sciences · 2025Review
- Medaka liver developed Human NAFLD-NASH transcriptional signatures in response to ancestral bisphenol A exposure.Research square · 2024Article
- Liver and Pancreatic Toxicity of Endocrine-Disruptive Chemicals: Focus on Mitochondrial Dysfunction and Oxidative Stress.International journal of molecular sciences · 2024Review
- Sex-specific expression of the human NAFLD-NASH transcriptional signatures in the liver of medaka with a history of ancestral bisphenol A exposure.bioRxiv : the preprint server for biology · 2024Article
- Deciphering the molecular mechanism of NLRP3 in BPA-mediated toxicity: Implications for targeted therapies.Heliyon · 2024Review
- Bisphenol A (BPA) and Cardiovascular or Cardiometabolic Diseases.Journal of xenobiotics · 2023Review
- Effects ofFoods (Basel, Switzerland) · 2023Article
- Activation of NLRP3 Inflammasome in Liver of Long Evans Lactating Rats and Its Perinatal Effects in the Offspring after Bisphenol F Exposure.International journal of molecular sciences · 2023Article
- Zinc Deficiency Exacerbates Bisphenol A-Induced Hepatic and Renal Damage: Delineation of Molecular Mechanisms.Biological trace element research · 2023Article
- Sulforaphane ameliorates bisphenol A-induced hepatic lipid accumulation by inhibiting endoplasmic reticulum stress.Scientific reports · 2023Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lines of evidence have shown the embryogenic and transgenerational impact of bisphenol A (BPA), an endocrine-disrupting chemical, on immune-metabolic alterations, inflammation, and oxidative stress, while BPA toxic effects in adult obese mice are still overlooked. Here, we evaluate BPA's worsening effect on several hepatic maladaptive processes associated to high-fat diet (HFD)-induced obesity in mice. After 12 weeks HFD feeding, C57Bl/6J male mice were exposed daily to BPA (50 μg/kg per os) along with HFD for 3 weeks. Glucose tolerance and lipid metabolism were examined in serum and/or liver. Hepatic oxidative damage (reactive oxygen species, malondialdehyde, antioxidant enzymes), and mitochondrial respiratory capacity were evaluated. Moreover, liver damage progression and inflammatory/immune response were determined by histological and molecular analysis. BPA amplified HFD-induced alteration of key factors involved in glucose and lipid metabolism, liver triglycerides accumulation, and worsened mitochondrial dysfunction by increasing oxidative stress and reducing antioxidant defense. The exacerbation by BPA of hepatic immune-metabolic dysfunction induced by HFD was shown by increased toll-like receptor-4 and its downstream pathways (i.e., NF-kB and NLRP3 inflammasome) amplifying inflammatory cytokine transcription and promoting fibrosis progression. This study evidences that BPA exposure represents an additional risk factor for the progression of fatty liver diseases strictly related to the cross-talk between oxidative stress and immune-metabolic impairment due to obesity.
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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.