Alteration in ovarian gene expression in response to 2,3,7,8-tetrachlorodibenzo-p-dioxin: reduction of cyclooxygenase-2 in the blockage of ovulation

A non-hormonal model for emergency contraception: prostaglandin synthesis inhibitor effects on luteal function and lifespan, a pilot study

“…Perhaps the daily administration of treatment drug in our study influenced ovulation differently than intermittent treatment. Other animal and human studies have demonstrated that PTGS2 inhibitors can prevent or delay follicle rupture which would lead to a longer menstrual cycle and a hormone profile similar to what we found [13][14][15][16][17][18][19]. Additionally, as recent studies utilizing non-human primates found that the levels of PTGS2 and microsomal prostaglandin E2 (PGE2) synthase (necessary for PGE2 synthesis) as well as the PGE2 receptor subtype 3 (PTGER3) increase during luteal development [20], one can hypothesize that blocking PTGS2 activity should delay or reduce luteal development.…”

Attenuation of cell cycle progression by 2,3,7,8-tetrachlorodibenzo-p-dioxin eliciting ovulatory blockade in gonadotropin-primed immature rats

“…Although several studies demonstrate the inhibitory effect of TCDD on ovulation in the rat [3,[7][8][9][10]16], how TCDD exerts its action has not been clarified. The present findings demonstrate that, via AhR-mediated cascade, TCDD inhibits the progression of cell cycle exploring the mechanism through which TCDD mediates the blockade of ovulation.…”

“…Since the presence of AhR has been reported in the ovary [13][14][15], TCDD could directly act at the ovary to disrupt critical cellular signals via AhR-mediated alterations in gene transcription, thereby contributing to the observed impairment of follicular maturation and ovulation. TCDD administration to immature rats primed with gonadotropins inhibits ovarian Ptgs2 expression [16], a requisite gene for ovulation [17]. TCDD stimulates Cyp1a1 and Cyp1b1 expression in rat granulosa cells, thereby reducing estrogen secretion by catalyzing estrogen metabolism [18,19].…”

Endocrine-disrupting chemicals in ovarian function: effects on steroidogenesis, metabolism and nuclear receptor signaling

“…In the porcine ovary, TCDD (32 pg/ml) induces the expression of AHR in granulosa, but not theca cells (Wojtowicz et al 2005). In the rat ovary, TCDD (32 mg/kg) inhibits ovulation by suppressing the expression of prostaglandinendoperoxide synthase 2 (PTGS2, also known as cyclooxygenase-2 (COX-2)), a critical ovulation factor, via the AHR signaling pathway (Mizuyachi et al 2002).…”