Bisphenol A stimulates NO synthesis through a non-genomic estrogen receptor-mediated mechanism in mouse endothelial cells

Noguchi, Soichi; Nakatsuka, Mikiya; Asagiri, Kazuo; Habara, Toshihiro; Takata, Masashi; Konishi, Hideyuki; Kudo, Takafumi

doi:10.1016/s0378-4274(02)00252-7

Cited by 44 publications

(28 citation statements)

References 28 publications

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“…Further, ERa triggers mitogenactivated protein (MAP) kinases to enhance eNOS expression (Chen et al, 1999;Noguchi et al, 2002). Nitrite (NO 2 À ) levels of the tissue indicate NO action and in the present study, BPA increased the NO 2 À level by three times indicating a greater increase in NO activity (Fig.…”

Section: Discussionsupporting

confidence: 54%

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Bisphenol A depresses monosynaptic and polysynaptic reflexes in neonatal rat spinal cord in vitro involving estrogen receptor-dependent NO-mediated mechanisms

Pandey

Deshpande

2015

Neuroscience

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Section: Discussionsupporting

confidence: 54%

“…Using endothelial cells, it is shown that ERa activation by estrogen/BPA increased endothelial nitric oxide synthase (eNOS) expression (Chen et al, 1999;Noguchi et al, 2002). Further, ERa triggers mitogenactivated protein (MAP) kinases to enhance eNOS expression (Chen et al, 1999;Noguchi et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

Bisphenol A depresses monosynaptic and polysynaptic reflexes in neonatal rat spinal cord in vitro involving estrogen receptor-dependent NO-mediated mechanisms

Pandey

Deshpande

2015

Neuroscience

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“…In the endothelial cell line MSS31, BPA enhances NO synthesis independently of protein synthesis at concentrations 100-to 1,000-fold than 17b-estradiol. This effect is likely to take place via ERa, since ERb has not been detected by immunoblotting and the effect is completely blocked by ICI182,780 [62]. Evidence for a non-genomic effect of BPA has also been found in neurones of the chick ciliary ganglion.…”

Section: Actions Through Alternative Pathways Involving Classic Ersmentioning

confidence: 99%

“…Evidence indicate that ERs are involved in the effect of bisphenol-A [BPA, 2,2-bis(4-hydroxyphenyl)-propane] on NO synthesis in endothelial cells [62]. BPA is a polycarbonate plastic monomer to which humans are exposed widely.…”

Section: Actions Through Alternative Pathways Involving Classic Ersmentioning

confidence: 99%

Disentangling the molecular mechanisms of action of endogenous and environmental estrogens

Nadal

Alonso-Magdalena

Ripoll

et al. 2004

Pflugers Arch - Eur J Physiol

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The gonadal hormone 17beta-estradiol is involved in numerous cellular processes. In many cases, 17beta-estradiol actions are imitated by synthetic and natural chemicals in the environment. Their actions differ depending on the target tissue, the receptors involved and the molecular pathways activated. The plethora of estrogenic actions is triggered by different receptors and other specific structures that activate different signalling pathways. This amount of information may lead to a maze of effects triggered by endogenous and environmental estrogens that we intend to clarify in this review. Understanding the variety of estrogen receptors, their different locations and the signalling pathways activated by estrogenic ligands is fundamental for understanding the diversity of actions that estrogens have in different tissues and cells.

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“…31) Immunohistochemistry showed BPAtreated embryos and BPA-treated VYSs express abnormal iNOS compared to controls, which might be another mechanism of BPA action.…”

Section: Discussionmentioning

confidence: 95%

Developmental Toxicity of Bisphenol-A on Post-Implantation Rat Embryos Cultured in Vitro

Liu

Fan

et al. 2010

JOURNAL OF HEALTH SCIENCE

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We studied the developmental toxicity and possible mechanisms of bisphenol A (BPA) damage of rat embryos in vitro. Whole-embryo culture was used to study the damage of BPA on visceral yolk sacs (VYSs) and embryos. Micromass culture was used to investigate the effects of BPA on differentiation and proliferation of embryonic midbrain cells. Neutral red staining was used to detect cell death. Immunohistochemistry was used to evaluate the expression of inducible nitric oxide synthase (iNOS) in VYSs and embryos. Our results as following, BPA could cause damage to embryonic development and morphological differentiation in a dose-dependent manner. At the highest dose, 80 and 100 mg/l BPA delayed cardiac tube growth and differentiation of VYSs, and induced various embryonic defects. BPA also induced excessive cell death and inhibited both proliferation and differentiation of rat midbrain cells. Immunohistochemical staining showed that BPA induces abnormal expression of iNOS protein in treated VYSs and embryos. Our results indicated that BPA is a potential teratogen and has toxicity on cultured rat embryo development. BPA-related developmental toxicity is caused by damage to the VYS, excessive cell death, inhibition of cell proliferation and differentiation, and abnormal expression of iNOS.

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Bisphenol A stimulates NO synthesis through a non-genomic estrogen receptor-mediated mechanism in mouse endothelial cells

Cited by 44 publications

References 28 publications

Bisphenol A depresses monosynaptic and polysynaptic reflexes in neonatal rat spinal cord in vitro involving estrogen receptor-dependent NO-mediated mechanisms

Bisphenol A depresses monosynaptic and polysynaptic reflexes in neonatal rat spinal cord in vitro involving estrogen receptor-dependent NO-mediated mechanisms

Disentangling the molecular mechanisms of action of endogenous and environmental estrogens

Developmental Toxicity of Bisphenol-A on Post-Implantation Rat Embryos Cultured in Vitro

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