Alterations of signal transduction pathways involved in 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced malignant transformation of human cells in culture

Yang, Jihoon

doi:10.1016/s0045-6535(98)00003-4

Cited by 2 publications

(1 citation statement)

References 24 publications

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“…In this context, many researchers have focused on the connection between TCDD effect and PKC signaling. However, the effect of TCDD on this system is quite controversial; for example, while some researchers have reported the TCDD-produced activation of PKC pathways (Hanneman et al, 1996;Bagchi et al, 1997;Kim et al, 2007), other groups have argued that TCDD has a negative effect (Zorn et al, 1995;Yang, 1998). It has also been reported that both negative and positive effects emerge depending on the experimental conditions (Weber et al, 1994(Weber et al, , 1996.…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2011

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-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.

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