Bisphenol-A acts as a potent estrogen via non-classical estrogen triggered pathways

@article{AlonsoMagdalena2012BisphenolAAA,
  title={Bisphenol-A acts as a potent estrogen via non-classical estrogen triggered pathways},
  author={Paloma Alonso-Magdalena and Ana Bel{\'e}n Ropero and Sergi Soriano and Marta Garc{\'i}a-Ar{\'e}valo and Cristina Ripoll and Esther Fuentes and Iv{\'a}n Quesada and Angel Nadal},
  journal={Molecular and Cellular Endocrinology},
  year={2012},
  volume={355},
  pages={201-207}
}
Bisphenol-A: Epigenetic Reprogramming and Effects on Reproduction and Behavior
TLDR
This review will draw on both human and animal studies in an attempt to synthesize the literature and examine the effects of BPA exposure on reproduction, behavior, and carcinogenesis with a focus on the potential epigenetic mechanisms by which it acts.
Bisphenol A, an endocrine-disruptor compund, that modulates the immune response to infections.
TLDR
It appears that BPA, while by such an impact might be useful in the control of certain disease states that are helped by an inflmmatory response, it can worsen the prognosis of diseases that are adversely affected by inflammation.
Bisphenols as a Legacy Pollutant, and Their Effects on Organ Vulnerability
TLDR
Bisphenols are widely used in the synthesis of polycarbonate plastics, epoxy resins, and thermal paper, which are used in manufacturing items of daily use and deserve a critical assessment of their uses.
Bisphenol A stimulates steroidogenic acute regulatory protein expression via an unknown mechanism in adrenal cortical cells
TLDR
It is demonstrated that BPA increases StAR protein levels through an unknown mechanism independent of StAR gene transcription, translation, and protein half‐life, which is likely mediated by ERα and/or ERβ.
Low-dose exposure to bisphenols A, F and S of human primary adipocyte impacts coding and non-coding RNA profiles
TLDR
The analysis of upstream regulators of deregulated genes highlighted hormones or hormone-like chemicals suggesting that BPS and BPF can be suspected to interfere, just like BPA, with hormonal regulation and have to be considered as endocrine disruptors.
Bisphenol a exposure promotes the migration of NCM460 cells via estrogen receptor‐mediated integrin β1/MMP‐9 pathway
TLDR
Results indicate that environmental concentration of BPA exposure promotes cell migration through activating ERβ‐mediated integrin β1/MMP‐9 pathway, suggesting exposure to BPA in the colon may present a potential cancer risk.
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References

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Bisphenol A interacts with the estrogen receptor α in a distinct manner from estradiol
The activity of bisphenol A depends on both the estrogen receptor subtype and the cell type.
TLDR
The results indicate that BPA only acts as an agonist of estrogen via ERbeta whereas it has dual actions asan agonist and antagonist in some types of cells via ERalpha.
Problems for risk assessment of endocrine-active estrogenic compounds.
TLDR
The results show that synthetic and phytoestrogens are weakly estrogenic but induce distinct patterns of ER agonist/antagonist activities that are cell context- and promoter-dependent, suggesting that these compounds will induce tissue-specific (in vivo)ER agonist or antagonist activities.
In vitro and in vivo interactions of bisphenol A and its metabolite, bisphenol A glucuronide, with estrogen receptors alpha and beta.
TLDR
Results demonstrate that BPA competes more effectively for binding to ERbeta, but induces ERalpha- and ERbeta-mediated gene expression with comparable efficacy, while BPA-G did not exhibit any in vitro estrogenic activity.
Bisphenol-A, an environmental contaminant that acts as a thyroid hormone receptor antagonist in vitro, increases serum thyroxine, and alters RC3/neurogranin expression in the developing rat brain.
TLDR
It is reported that dietary exposure to BPA of Sprague Dawley rats during pregnancy and lactation causes an increase in serum total T4 in pups on postnatal d 15, but serum TSH was not different from controls, suggesting that BPA acts as a TH antagonist on the beta-TR, which mediates the negative feedback effect of TH on the pituitary gland.
In Vitro and in Vivo Interactions of Bisphenol A and Its Metabolite, Bisphenol A Glucuronide, with Estrogen Receptors α and β
TLDR
Results demonstrate that BPA competes more effectively for binding to ERbeta, but induces ERalpha- and ERbeta-mediated gene expression with comparable efficacy, while BPA-G did not exhibit any in vitro estrogenic activity.
In vivo effects of bisphenol A in laboratory rodent studies.
In vitro molecular mechanisms of bisphenol A action.
Low doses of the endocrine disruptor Bisphenol‐A and the native hormone 17β‐estradiol rapidly activate the transcription factor CREB
TLDR
It is shown that the environmental estrogen Bisphenol‐A and the native hormone 17β‐E2 activate the transcription factor, cAMP‐responsive element binding protein (CREB) with the same potency, involving a non‐classical membrane estrogen receptor.
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