2,3,7,8-Tetrachlorodibenzo-p-dioxin potentially attenuates the gene expression of pituitary gonadotropin β-subunits in a fetal age-specific fashion: A comparative study using cultured pituitaries

Tomoki Takeda, Midori Yamamoto, Masaru Himeno, Shinji Takechi, Tadatoshi Yamaguchi, Takumi Ishida, Yuji Ishii, Hideyuki Yamada

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Our previous studies have demonstrated that maternal exposure to 2,3,7,8-tetrachlorodibenzo- p-dioxin (TCDD) causes a reduction in gonadotropin biosynthesis in the fetal pituitary, resulting in the attenuated expression of steroidogenic proteins in the fetal gonads and the impairment of sexual behaviors in adulthood. However, the mechanism of the attenuation remains unknown. To address this issue, we investigated whether TCDD affects the pituitary production of gonadotropins, using cultured pituitary. In the absence of gonadotropin-releasing hormone (GnRH), a regulator of gonadotropin biosynthesis, TCDD did not affect the expression of gonadotropin mRNAs both in fetal and postnatal pituitaries. On the other hand, in the presence of GnRH, TCDD interfered with the synthesis of gonadotropin β-subunit mRNAs only in the fetal pituitary. A protein kinase C (PKC) activator (phorbol 12-myristate 13-acetate) and a PKA activator (8-bromoadenosine-3' 5'-cyclic monophosphate) induced the expression of gonadotropin mRNAs in the fetal pituitary. Among the subunits, only the induction of β-subunit was reduced by TCDD treatment. These results suggest that TCDD reduces gonadotropin biosynthesis via damage to GnRH-stimulated PKC and PKA signaling in a β-subunit- and fetal age-specific manner.

Original languageEnglish
Pages (from-to)221-229
Number of pages9
JournalJournal of Toxicological Sciences
Volume36
Issue number2
DOIs
Publication statusPublished - Apr 2011

All Science Journal Classification (ASJC) codes

  • Toxicology

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