@article{MTMT:3159049, title = {Bisphenol A influences oestrogen- and thyroid hormone-regulated thyroid hormone receptor expression in rat cerebellar cell culture}, url = {https://m2.mtmt.hu/api/publication/3159049}, author = {Somogyi, Virág and Horváth, Tamás and Tóth, István and Bartha, Tibor and Frenyó V., László and Kiss, Dávid Sándor and Jócsák, Gergely and Kerti, Annamária and Naftolin, Frederick and Zsarnovszky, Attila}, doi = {10.1556/004.2016.046}, journal-iso = {ACTA VET HUNG}, journal = {ACTA VETERINARIA HUNGARICA}, volume = {64}, unique-id = {3159049}, issn = {0236-6290}, abstract = {Thyroid hormones (THs) and oestrogens are crucial in the regulation of cerebellar development. TH receptors (TRs) mediate these hormone effects and are regulated by both hormone families. We reported earlier that THs and oestradiol (E2) determine TR levels in cerebellar cell culture. Here we demonstrate the effects of low concentrations (10-10 M) of the endocrine disruptor (ED) bisphenol A (BPA) on the hormonal (THs, E2) regulation of TRα,β in rat cerebellar cell culture. Primary cerebellar cell cultures, glia-containing and glia-destroyed, were treated with BPA or a combination of BPA and E2 and/or THs. Oestrogen receptor and TH receptor mRNA and protein levels were determined by real-time qPCR and Western blot techniques. The results show that BPA alone decreases, while BPA in combination with THs and/or E2 increases TR mRNA expression. In contrast, BPA alone increased receptor protein expressions, but did not further increase them in combination with THs and/or E2. The modulatory effects of BPA were mediated by the glia; however, the degree of changes also depended on the specific hormone ligand used. The results signify the importance of the regulatory mechanisms interposed between transcription and translation and raise the possibility that BPA could act to influence nuclear hormone receptor levels independently of ligand-receptor interaction.}, year = {2016}, eissn = {1588-2705}, pages = {497-513}, orcid-numbers = {Tóth, István/0000-0002-0168-4753} } @article{MTMT:1918146, title = {Bisphenol A prevents the synaptogenic response to estradiol in hippocampus and prefrontal cortex of ovariectomized nonhuman primates}, url = {https://m2.mtmt.hu/api/publication/1918146}, author = {Leranth, C and Hajszán, Tibor and Szigeti-Buck, K and Bober, J and MacLusky, NJ}, doi = {10.1073/pnas.0806139105}, journal-iso = {P NATL ACAD SCI USA}, journal = {PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA}, volume = {105}, unique-id = {1918146}, issn = {0027-8424}, abstract = {Exposure measurements from several countries indicate that humans are routinely exposed to low levels of bisphenol A (BPA), a synthetic xenoestrogen widely used in the production of polycarbonate plastics. There is considerable debate about whether this exposure represents an environmental risk, based on reports that BPA interferes with the development of many organs and that it may alter cognitive functions and mood. Consistent with these reports, we have previously demonstrated that BPA antagonizes spine synapse formation induced by estrogens and testosterone in limbic brain areas of gonadectomized female and male rats. An important limitation of these studies, however, is that they were based on rodent animal models, which may not be representative of the effects of human BPA exposure. To address this issue, we examined the influence of continuous BPA administration, at a daily dose equal to the current U.S. Environmental Protection Agency's reference safe daily limit, on estradiol-induced spine synapse formation in the hippocampus and prefrontal cortex of a nonhuman primate model. Our data indicate that even at this relatively low exposure level, BPA completely abolishes the synaptogenic response to estradiol. Because remodeling of spine synapses may play a critical role in cognition and mood, the ability of BPA to interfere with spine synapse formation has profound implications. This study is the first to demonstrate an adverse effect of BPA on the brain in a nonhuman primate model and further amplifies concerns about the widespread use of BPA in medical equipment, and in food preparation and storage.}, year = {2008}, eissn = {1091-6490}, pages = {14187-14191} } @article{MTMT:1920765, title = {The environmental estrogen bisphenol a inhibits estradiol-induced hippocampal synaptogenesis}, url = {https://m2.mtmt.hu/api/publication/1920765}, author = {MacLusky, NJ and Hajszán, Tibor and Leranth, C}, doi = {10.1289/ehp.7633}, journal-iso = {ENVIRON HEALTH PERSP}, journal = {ENVIRONMENTAL HEALTH PERSPECTIVES}, volume = {113}, unique-id = {1920765}, issn = {0091-6765}, abstract = {Bisphenol A (BPA) is an estrogenic chemical that is widely used in the manufacture of plastics and epoxy resins. Because BPA leaches out of plastic food and drink containers, as well as the BPA-containing plastics used in dental prostheses and sealants, considerable potential exists for human exposure to this compound. In this article we show that treatment of ovariectomized rats with BPA dose-dependently inhibits the estrogen-induced formation of dendritic spine synapses on pyramidal neurons in the CA1 area of the hippocampus. Significant inhibitory effects of BPA were observed at a dose of only 40 mu g/kg, below the current U.S. Environmental Protection Agency reference daily limit for human exposure. Because synaptic remodeling has been postulated to contribute to the rapid effects of estrogen on hippocampus-dependent memory, these data suggest that environmental BPA exposure may interfere with the development and expression of normal sex differences in cognitive function, via inhibition of estrogen-dependent hippocampal synapse formation. It may also exacerbate the impairment of hippocampal function observed during normal aging, as endogenous estrogen production declines.}, year = {2005}, eissn = {1552-9924}, pages = {675-679} }