Bisphenol A (BPA) shown to interfere with the T3 and thyroid hormone receptor interaction. This study even showed that BPA inhibited thyroid receptor transcription.
Animal study finds that Bisphenol A exposure in utero has profound different effects in male offspring versus female offspring. In the male offspring there appears to be an up regulation of the HPA axis. The opposite appears true in the female off spring. Additionally, the receptors are effected differently as well.
really interesting abstract. Bisphenol A (BPA) is a xenoestrogen. This animal study finds that BPA down regulated ER-beta in the brains of male rats. It also blocked the production of GABA(A)alpha 2 receptor. These long term effects were evident in anxiety and depression in adult mice.
Pregnancy exposure would set up an ER-alpha dominance in the male brain increasing risk of continuous ER alpha stim.
Another strike against BPA. This time, BPA exposure during development increased hormone-dependent cancer risk in the prostate through its interaction with prostate stem-progenitor cells. Again, we are being altered prior to birth.
Prenatal exposure to BPA has been shown to alter a variety of reproductive endocrine parameters, such as testosterone and luteinizing hormone levels
arly onset of sexual maturation of female mice
imbalanced T-helper (TH)1/TH2 immune responses have been demonstrated on exposure to BPA
indicating that BPA exerted its effects by reducing the number of Treg cells.
Exposure to BPA by subcutaneous injection in adulthood significantly promoted antigen-stimulated production of IL-4, IL-10, and IL-13 in TH2-skewed
BPA can leak from the placenta and accumulate in the fetus
We showed that prenatal exposure to BPA increased the production of a TH1 cytokine, IFN-γ, and a TH2 cytokine, IL-4, after the offspring developed, suggesting that prenatal exposure to BPA can induce persistent immunologic effects lasting into adulthood.
These results are consistent with a previous report that fetal exposure to BPA augmented TH1 and TH2 immune responses
our results clearly demonstrate that the production of TH2 cytokines is promoted by BPA in adult mice and in offspring during developmental exposure.
The decrease of Treg cells would predispose to immune dysfunction in aged individuals, explaining their higher risk of immune-mediated diseases, cancer, and infections.
BPA might cause these diseases. Thus, avoiding exposure to or promoting the excretion of BPA and other EDCs would help in preventing diseases and adverse health effects.
Very low levels of BPA shown to be present in pregnant and unborn children. These levels exceed the levels at which documented receptor change occurs as the result of BPA.
Study finds that men exposed to BPA have lower androstenedione and free testosterone compared to those not exposed. Also of note, SHBG is increased, which is what one would expect with xenoestrogen exposure.