scholarly journals Understanding the molecular mechanisms of bisphenol A action in spermatozoa

2019 ◽  
Vol 46 (3) ◽  
pp. 99-106 ◽  
Author(s):  
Md Saidur Rahman ◽  
Myung-Geol Pang
Keyword(s):  
Bisphenol A ◽  
Molecular Mechanisms

scholarly journals Author Correction: Molecular mechanisms involved in the non-monotonic effect of bisphenol-a on Ca2+ entry in mouse pancreatic β-cells

2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Sabrina Villar-Pazos ◽  
Juan Martinez-Pinna ◽  
Manuel Castellano-Muñoz ◽  
Paloma Alonso-Magdalena ◽  
Laura Marroqui ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Molecular Mechanisms ◽  
Β Cells ◽  
Pancreatic Β Cells

scholarly journals In utero Bisphenol A Exposure Is Linked with Sex Specific Changes in the Transcriptome and Methylome of Human Amniocytes

2019 ◽  
Vol 105 (2) ◽  
pp. 453-467
Author(s):  
Amita Bansal ◽  
Nicole Robles-Matos ◽  
Paul Zhiping Wang ◽  
David E Condon ◽  
Apoorva Joshi ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Bisphenol A ◽  
Gestational Age ◽  
Molecular Mechanisms ◽  
In Utero ◽  
Metabolic Dysfunction ◽  
Altered Expression ◽  
Obesity And Diabetes ◽  
Genome Wide

Abstract Context Prenatal exposure to bisphenol A (BPA) is linked to obesity and diabetes but the molecular mechanisms driving these phenomena are not known. Alterations in deoxyribonucleic acid (DNA) methylation in amniocytes exposed to BPA in utero represent a potential mechanism leading to metabolic dysfunction later in life. Objective To profile changes in genome-wide DNA methylation and expression in second trimester human amniocytes exposed to BPA in utero. Design A nested case-control study was performed in amniocytes matched for offspring sex, maternal race/ethnicity, maternal age, gestational age at amniocentesis, and gestational age at birth. Cases had amniotic fluid BPA measuring 0.251 to 23.74 ng/mL. Sex-specific genome-wide DNA methylation analysis and RNA-sequencing (RNA-seq) were performed to determine differentially methylated regions (DMRs) and gene expression changes associated with BPA exposure. Ingenuity pathway analysis was performed to identify biologically relevant pathways enriched after BPA exposure. In silico Hi-C analysis identified potential chromatin interactions with DMRs. Results There were 101 genes with altered expression in male amniocytes exposed to BPA (q < 0.05) in utero, with enrichment of pathways critical to hepatic dysfunction, collagen signaling and adipogenesis. Thirty-six DMRs were identified in male BPA-exposed amniocytes and 14 in female amniocyte analysis (q < 0.05). Hi-C analysis identified interactions between DMRs and 24 genes with expression changes in male amniocytes and 12 in female amniocytes (P < 0.05). Conclusion In a unique repository of human amniocytes exposed to BPA in utero, sex-specific analyses identified gene expression changes in pathways associated with metabolic disease and novel DMRs with potential distal regulatory functions.

scholarly journals Potential Mechanisms of Bisphenol A (BPA) Contributing to Human Disease

2020 ◽  
Vol 21 (16) ◽  
pp. 5761 ◽  
Author(s):  
Ilaria Cimmino ◽  
Francesca Fiory ◽  
Giuseppe Perruolo ◽  
Claudia Miele ◽  
Francesco Beguinot ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Human Health ◽  
Cancer Progression ◽  
Molecular Mechanisms ◽  
Dental Materials ◽  
Reproductive Function ◽  
Epigenetic Changes ◽  
Synthetic Compound ◽  
Male Reproductive Function ◽  
Thermal Paper

Bisphenol A (BPA) is an organic synthetic compound serving as a monomer to produce polycarbonate plastic, widely used in the packaging for food and drinks, medical devices, thermal paper, and dental materials. BPA can contaminate food, beverage, air, and soil. It accumulates in several human tissues and organs and is potentially harmful to human health through different molecular mechanisms. Due to its hormone-like properties, BPA may bind to estrogen receptors, thereby affecting both body weight and tumorigenesis. BPA may also affect metabolism and cancer progression, by interacting with GPR30, and may impair male reproductive function, by binding to androgen receptors. Several transcription factors, including PPARγ, C/EBP, Nrf2, HOX, and HAND2, are involved in BPA action on fat and liver homeostasis, the cardiovascular system, and cancer. Finally, epigenetic changes, such as DNA methylation, histones modification, and changes in microRNAs expression contribute to BPA pathological effects. This review aims to provide an extensive and comprehensive analysis of the most recent evidence about the potential mechanisms by which BPA affects human health.

scholarly journals Molecular Mechanisms Underlying the Rapid Arrhythmogenic Action of Bisphenol A in Female Rat Hearts

Endocrinology ◽  
2013 ◽  
Vol 154 (12) ◽  
pp. 4607-4617 ◽  
Author(s):  
Xiaoqian Gao ◽  
Qian Liang ◽  
Yamei Chen ◽  
Hong-Sheng Wang
Keyword(s):  
Bisphenol A ◽  
Molecular Mechanisms ◽  
Female Rat ◽  
Rat Hearts

scholarly journals Cardiovascular Effects and Molecular Mechanisms of Bisphenol A and Its Metabolite MBP in Zebrafish

2018 ◽  
Vol 53 (1) ◽  
pp. 463-474 ◽  
Author(s):  
A. Ross Brown ◽  
Jon M. Green ◽  
John Moreman ◽  
Lina M. Gunnarsson ◽  
Sulayman Mourabit ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Molecular Mechanisms ◽  
Cardiovascular Effects

1884 THE MOLECULAR MECHANISMS IN RAT SERTOLI CELL INDUCED BY BISPHENOL A

2010 ◽  
Vol 183 (4S) ◽  
Author(s):  
Koji Chiba ◽  
Kohei Yamaguchi ◽  
Makoto Ando ◽  
Masato Fujisawa
Keyword(s):  
Bisphenol A ◽  
Sertoli Cell ◽  
Molecular Mechanisms

scholarly journals Bisphenol A and Phthalates in Diet: An Emerging Link with Pregnancy Complications

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 525 ◽  
Author(s):  
Tiziana Filardi ◽  
Francesca Panimolle ◽  
Andrea Lenzi ◽  
Susanna Morano
Keyword(s):  
Bisphenol A ◽  
Pregnancy Complications ◽  
Molecular Mechanisms ◽  
Metabolic Diseases ◽  
Endocrine Disrupting Chemicals ◽  
Preventive Measure ◽  
Adverse Outcomes ◽  
Pancreatic Β Cell ◽  
Β Cell ◽  
Cell Dysfunction

Endocrine-disrupting chemicals (EDCs) are exogenous substances that are able to interfere with hormone action, likely contributing to the development of several endocrine and metabolic diseases. Among them, Bisphenol A (BPA) and phthalates contaminate food and water and have been largely studied as obesogenic agents. They might contribute to weight gain, insulin resistance and pancreatic β-cell dysfunction in pregnancy, potentially playing a role in the development of pregnancy complications, such as gestational diabetes mellitus (GDM), and adverse outcomes. Pregnancy and childhood are sensitive windows of susceptibility, and, although with not univocal results, preclinical and clinical studies have suggested that exposure to BPA and phthalates at these stages of life might have an impact on the development of metabolic diseases even many years later. The molecular mechanisms underlying this association are largely unknown, but adipocyte and pancreatic β-cell dysfunction are suspected to be involved. Remarkably, transgenerational damage has been observed, which might be explained by epigenetic changes. Further research is needed to address knowledge gaps and to provide preventive measure to limit health risks connected with exposure to EDCs.

scholarly journals Counteracting Environmental Chemicals with Coenzyme Q10: An Educational Primer for Use with “Antioxidant CoQ10 Restores Fertility by Rescuing Bisphenol A-Induced Oxidative DNA Damage in the Caenorhabditis elegans Germline”

Genetics ◽  
2020 ◽  
Vol 216 (4) ◽  
pp. 879-890
Author(s):  
Beatrix R. Bradford ◽  
Nicole E. Briand ◽  
Nina Fassnacht ◽  
Esabelle D. Gervasio ◽  
Aidan M. Nowakowski ◽  
...  
Keyword(s):  
Dna Damage ◽  
Caenorhabditis Elegans ◽  
Bisphenol A ◽  
Coenzyme Q10 ◽  
Oxidative Dna Damage ◽  
Molecular Mechanisms ◽  
Fluorescent Microscopy ◽  
Environmental Chemicals ◽  
Background Information ◽  
Environmental Toxicants

Environmental toxicants are chemicals that negatively affect human health. Although there are numerous ways to limit exposure, the ubiquitous nature of certain environmental toxicants makes it impossible to avoid them entirely. Consequently, scientists are continuously working toward developing strategies for combating their harmful effects. Using the nematode Caenorhabditis elegans, a model with many genetic and physiological similarities to humans, researchers in the Colaiácovo laboratory have identified several molecular mechanisms by which the toxic agent bisphenol A (BPA) interferes with reproduction. Here, we address their recent discovery that a widely available compound, Coenzyme Q10 (CoQ10), can rescue BPA-induced damage. This work is significant in that it poses a low-cost method for improving reproductive success in humans. The goal of this primer is to assist educators and students with navigating the paper entitled “Antioxidant CoQ10 Restores Fertility by Rescuing Bisphenol A-Induced Oxidative DNA Damage in the Caenorhabditis elegans Germline.” It is ideally suited for integration into an upper-level undergraduate course such as Genetics, Cell and Molecular Biology, Developmental Biology, or Toxicology. The primer provides background information on the history of BPA, the utility of the C. elegans germ line as a model for studying reproductive toxicity, and research methods including assessment of programmed cell death, fluorescent microscopy applications, and assays to quantify gene expression. Questions for deeper exploration in-class or online are provided.Related article in GENETICS: Hornos Carneiro MF, Shin N, Karthikraj R, Barbosa F Jr, Kannan K, Colaiácovo MP. Antioxidant CoQ10 restores fertility by rescuing bisphenol A-induced oxidative DNA damage in the Caenorhabditis elegans Germline. Genetics 214:381–395.

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