ArticleScientific reports2016
Effects of Bisphenol A Metabolite 4-Methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene on Lung Function and Type 2 Pulmonary Alveolar Epithelial Cell Growth.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 26 citations in OpenAlex.
- 4-Methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene (MBP) exposure induces hepatotoxicity and nephrotoxicity - role of oxidative stress, mitochondrial dysfunction and pathways of cytotoxicity.Toxicology research · 2024Article
- YTHDC1 delays cellular senescence and pulmonary fibrosis by activating ATR in an m6A-independent manner.The EMBO journal · 2024Article
- Transfer of Bisphenol A and Trace Metals from Plastic Packaging to Mineral Water in Ouagadougou, Burkina Faso.International journal of environmental research and public health · 2023Article
- Protective Effects of Selenium Nanoparticles against Bisphenol A-Induced Toxicity in Porcine Intestinal Epithelial Cells.International journal of molecular sciences · 2023Article
- Volatilomics as an Emerging Strategy to Determine Potential Biomarkers of Female Infertility: A Pilot Study.Biomedicines · 2022Article
- Endocrine-Disrupting Chemicals and Their Adverse Effects on the Endoplasmic Reticulum.International journal of molecular sciences · 2022Review
- Lycopene attenuates bisphenol A-induced lung injury in adult albino rats: a histological and biochemical study.Environmental science and pollution research international · 2021Article
- Exploratory Study Using Urinary Volatile Organic Compounds for the Detection of Hepatocellular Carcinoma.Molecules (Basel, Switzerland) · 2021Article
- 4-Methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene, a Major Active Metabolite of Bisphenol A, Triggers Pancreatic β-Cell Death via a JNK/AMPKα Activation-Regulated Endoplasmic Reticulum Stress-Mediated Apoptotic Pathway.International journal of molecular sciences · 2021Article
- Ultrafine silicon dioxide nanoparticles cause lung epithelial cells apoptosis via oxidative stress-activated PI3K/Akt-mediated mitochondria- and endoplasmic reticulum stress-dependent signaling pathways.Scientific reports · 2020Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bisphenol A (BPA) is recognized as a major pollutant worldwide. 4-Methyl-2,4-bis(4-hydroxyphenyl)pent-1-ene (MBP) is a major active metabolite of BPA. The epidemiological and animal studies have reported that BPA is harmful to lung function. The role of MBP in lung dysfunction after BPA exposure still remains unclear. This study investigated whether MBP would induce lung alveolar cell damage and evaluated the role of MBP in the BPA exposure-induced lung dysfunction. An in vitro type 2 alveolar epithelial cell (L2) model and an ex vivo isolated reperfused rat lung model were used to determine the effects of BPA or MBP on cell growth and lung function. MBP, but not BPA, dose-dependently increased the mean artery pressure (Pa), pulmonary capillary pressure (Pc), pulmonary capillary filtration coefficient (K
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Registered trials
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