A plurality of molecular targets: The receptor ecosystem for bisphenol-A (BPA)

  title={A plurality of molecular targets: The receptor ecosystem for bisphenol-A (BPA)},
  author={Harry Mackay and Alfonso Abizaid},
  journal={Hormones and Behavior},
Molecular modelling methods in food safety: Bisphenols as case study.
  • F. Cavaliere, S. Lorenzetti, P. Cozzini
  • Chemistry
    Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • 2020
Effects of endocrine disruptors on Phallusia mammillata embryonic development
This PhD project is aimed at deciphering the toxicity of BPA on embryonic development of the marine invertebrate chordate Phallusia mammillata (Tunicata), and finds that BPA is toxic in a dose-dependent manner and induces neurodevelopmental toxicity by impairing differentiation of the ascidian pigmented sensory organ (PSO).
Comparative Neurodevelopment Effects of Bisphenol A and Bisphenol F on Rat Fetal Neural Stem Cell Models
Comparing the neurodevelopmental effects of BPA and its major replacement Bisphenol F on rat fetal neural stem cells shows that fetal rNSCs exposed to either BPA or BPF lead to comparable changes in the cellular differentiation, proliferation, and arborization processes.
The effects of endocrine disruptors on the male germline: an intergenerational health risk
The different modes of action by which the spermatozoa represent a key target for endocrine-disrupting chemicals are examined, and the consequences of environmentally induced changes in sperm genetic and epigenetic information for subsequent generations are analyzed.
Prenatal Bisphenol A Exposure in Mice Induces Multitissue Multiomics Disruptions Linking to Cardiometabolic Disorders.
This multitissue, multiomics investigation provides strong evidence that BPA perturbs diverse molecular networks in central and peripheral tissues and offers insights into the molecular targets that link BPA to human cardiometabolic disorders.


Bisphenol A affects androgen receptor function via multiple mechanisms.
Structural and mechanistic insights into bisphenols action provide guidelines for risk assessment and discovery of bisphenol A substitutes
The mechanisms by which BPA and two congeners bind to and activate estrogen receptors (ER) α and β differ from that used by 17β-estradiol, providing a wealth of tools and information that could be used for the development of BPA substitutes devoid of nuclear hormone receptor-mediated activity and more generally for environmental risk assessment.
Bisphenol‐A can bind to human glucocorticoid receptor as an agonist: an in silico study
It is found that the mode of interactions and binding energy of BPA were similar to that of DEXA and cortisol, two known agonists of GR, which reveals that BPA can bind to GR as an agonist and may produce biological effectssimilar to that produced by glucocorticoids.
Effects of bisphenol A and triclocarban on brain-specific expression of aromatase in early zebrafish embryos
It is confirmed that, like estrogen, the well-studied xenoestrogen bisphenol A (BPA, a plastics monomer), induces strong brain-specific overexpression of aromatase, and that exposures to combinations of certain hormonally active pollutants can have outcomes that are not easily predicted from their individual effects.
Thyroid hormone action is disrupted by bisphenol A as an antagonist.
The results suggest that BPA could displace T(3) from the TR and recruit a transcriptional repressor, resulting in gene suppression, the first report that B PA can antagonize T( 3) action at the transcriptional level.
Bisphenol A: An endocrine disruptor with widespread exposure and multiple effects
  • B. Rubin
  • Biology
    The Journal of Steroid Biochemistry and Molecular Biology
  • 2011
Estrogen‐related receptor γ is an in vivo receptor of bisphenol A
It is concluded that ERRγ mediates the otic vesicle phenotype generated by BPA, suggesting that the range of pathways perturbed by this compound and its potential harmful effect are larger than expected.
Bisphenol A interacts with the estrogen receptor α in a distinct manner from estradiol
Laccase treatment impairs bisphenol A‐induced cancer cell proliferation affecting estrogen receptor α‐dependent rapid signals
Laccase appears to impair BPA action(s), representing an invaluable bioremediation enzyme that participates to BPA‐induced cytotoxicity.