Bisphenol A acts differently from and independently of thyroid hormone in suppressing thyrotropin release from the bullfrog pituitary

Miyoko Kaneko, Reiko Okada, Kazutoshi Yamamoto, Masahisa Nakamura, Gilberto Mosconi, Alberta M. Polzonetti-Magni, Sakae Kikuyama*

*Corresponding author for this work

    Research output: Contribution to journalArticlepeer-review

    37 Citations (Scopus)


    The objective of this investigation was to ascertain whether bisphenol A (BPA), which has a structural resemblance to thyroid hormone (TH), acts as a TH agonist or antagonist in terms of affecting the release of thyrotropin (TSH). To this end, we exposed adult bullfrog (Rana catesbeiana) pituitary cells to BPA and/or TH in the presence or absence of corticotropin-releasing factor (CRF), which is known to have a potent TSH-releasing activity in amphibians. BPA (10-9-10-4 M) did not affect the basal release of TSH. However, it suppressed CRF-inducible TSH release at 10-4 M, but not at 10-5 M. Triiodothyronine (T3) at 10-7 M and l-thyroxine (T4) at 10-6 M also suppressed the CRF-inducible release of TSH. The combination of T3 (10-7 M) or T4 (10-6 M) with BPA (10-4 M) had an additive effect in suppressing TSH release. A comparison of the suppressive effects of BPA and T3 on the release of TSH following the addition of actinomycin D or cycloheximide to the culture medium revealed that both of the latter compounds blocked T3-inducible but not BPA-inducible suppression of TSH release. The results indicate that the mechanism of action of BPA is different from that of T3 in that T3 action involves RNA and protein synthesis, whereas BPA action does not involve either of these processes. Furthermore, BPA was found to suppress the thyrotropin-releasing hormone-inducible release of both prolactin (PRL) and TSH. Our results suggest that BPA acts not only as a blocker of TSH secretagogues but also as a blocker of a PRL secretagogue at the pituitary level. Estradiol affected neither the release of TSH nor the release of PRL in the presence or absence of their secretagogues, suggesting that the suppression of the release of TSH and PRL caused by BPA may not be derived from its estrogenic activity.

    Original languageEnglish
    Pages (from-to)574-580
    Number of pages7
    JournalGeneral and Comparative Endocrinology
    Issue number3
    Publication statusPublished - 2008 Feb 1


    • Bisphenol A
    • Endocrine disruptor
    • Negative feedback
    • Thyroid hormone (TH)
    • Thyrotropin (TSH)

    ASJC Scopus subject areas

    • Endocrinology


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