A review of mechanisms controlling ovulation with implications for the anovulatory effects of polychlorinated dibenzo-p-dioxins in rodents

Petroff, Brian K.; Roby, Katherine F.; Gao, Xin; Son, Deok Soo; Williams, S. Janette; Johnson, Donald C.; Rozman, Karl K.; Terranova, Paul F.

doi:10.1016/s0300-483x(00)00367-x

Cited by 61 publications

(33 citation statements)

References 85 publications

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“…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.…”

Section: Discussionmentioning

confidence: 99%

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

Jung

Park

et al. 2010

Endocr J

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2,3,7,8-tetrachlorodibenzo-p-dioxin(TCDD or dioxin) is regarded as an endocrine-disrupting chemical with the ability to disrupt reproductive systems [1,2]. A single high dose of TCDD induces abortion, alters sexual behavior, decreases spermatogenesis and diminishes fertility [3][4][5][6]. In the rat, TCDD compromises ovarian follicular development and function including a premature transition to reproductive senescence [5] and a disruption of estrous cyclicity with prolonged periods of diestrus [7]. An acute prepubertal exposure to TCDD in intact and hypophysectomized rats reduces ovulation directly by blocking the follicular rupture and indirectly by blocking the luteinizing hormone (LH) surge [8][9][10]. reduces ovulation rate in rats. The present study was to investigate whether TCDD alters the progression of cell cycle, and thus resulting in the blockade of ovulation in gonadotropin-primed, immature rats. The ovulation rate and ovarian weight were reduced in intact rats given TCDD (32 µg/kg BW in corn oil) by gavage one day before pregnant mare's serum gonadotropin (PMSG; 5 IU/rat) injection. Flow cytometry demonstrated that the percentage of granulosa cells in S-phase was increased at 24 h following PMSG treatment, but declined at 8 h following hCG treatment in corn oil-treated rats. Interestingly, the number of S-phase cells in TCDD-treated rats was reduced 24 and 48 h following PMSG treatment. TCDD, however, increased the percentage of cells in G2/M-phase at 24 h following PMSG treatment. TCDD inhibited the mRNA levels of Cdk2 at 0 h and 24 h, and cyclin D2 at 24 h and 48 h following PMSG treatment. Protein levels of aryl hydrocarbon receptor in granulosa cells were elevated in TCDD-treated rats at 12 h and 24 h following PMSG treatment. The present study indicates that TCDD reduces S-phase cells and inhibits levels of Cdk2 and cyclin D2 at 24 h following PMSG treatment, implying the ovulation-inhibiting action of TCDD may be exerted through the attenuation of cell cycle progression via AhR-mediated cascade.Key words: Dioxin, AhR, Ovary, Cell cycleAlthough it is apparent that TCDD affects follicular maturation and ovulation, the mechanisms that underlie these reproductive toxicities are poorly understood. It is generally accepted that TCDD action is mediated by the aryl hydrocarbon receptor (AhR)-signaling cascade, a transcription factor whose natural ligand remains unknown [11,12]. 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]. Moreover, TCDD decreases the expression of Cyp17 in human lu...

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Section: Discussionmentioning

confidence: 99%

“…A single high dose of TCDD induces abortion, alters sexual behavior, decreases spermatogenesis and diminishes fertility [3][4][5][6]. In the rat, TCDD compromises ovarian follicular development and function including a premature transition to reproductive senescence [5] and a disruption of estrous cyclicity with prolonged periods of diestrus [7].…”

mentioning

confidence: 99%

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

Jung

Park

et al. 2010

Endocr J

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“…The subject of the molecular actions of polyhalogenated arylhydrocarbons, such as polychlorinated dibenzo-p-dioxins (PCDDs; dioxins) and polychlorinated biphenyls (PCBs) on female reproduction has been reviewed previously (Petroff et al 2001. Therefore, this section focuses on recent findings on the ability of these chemicals to reduce the availability of ovarian hormones as a mechanism for ovarian endocrine disruption.…”

Section: Polyhalogenated Arylhydrocarbonsmentioning

confidence: 99%

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

Craig¹,

Wang²,

Flaws³

2011

Reproduction

225

123

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Endocrine-disrupting chemicals (EDCs) are exogenous agents with the ability to interfere with processes regulated by endogenous hormones. One such process is female reproductive function. The major reproductive organ in the female is the ovary. Disruptions in ovarian processes by EDCs can lead to adverse outcomes such as anovulation, infertility, estrogen deficiency, and premature ovarian failure among others. This review summarizes the effects of EDCs on ovarian function by describing how they interfere with hormone signaling via two mechanisms: altering the availability of ovarian hormones, and altering binding and activity of the hormone at the receptor level. Among the chemicals covered are pesticides (e.g. dichlorodiphenyltrichloroethane and methoxychlor), plasticizers (e.g. bisphenol A and phthalates), dioxins, polychlorinated biphenyls, and polycyclic aromatic hydrocarbons (e.g. benzo[a]pyrene).

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“…Other studies showed that TCDD distributed at the CNS exerts neurotoxicological effects: a high TCDD dose (10 mg/kg) administered to rats was shown to reduce LH secretion and the number of ova at ovulation (Petroff et al 2001). Exposure to TCDD at 15 mg/kg was reported to decrease the neuropeptide Y level in the arcuate nucleus (Fetissov et al 2004) that is presumably involved in ovulation (Estrada et al 2003) and the sexual maturation of the hypothalamus (Kalra & Kalra 2004).…”

Section: Figurementioning

confidence: 99%

Perinatal exposure of female rats to 2,3,7,8-tetrachlorodibenzo-p-dioxin induces central precocious puberty in the offspring

Kakeyama

Sone

Tohyama

2008

Journal of Endocrinology

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Exposure to 2,3,7, during the fetal and neonatal periods has been indicated to alter the development of the offspring later in life. In this study, we determined whether perinatal exposure to a low dose of TCDD affects the onset of puberty in the female offspring of Long-Evans hooded rats. On day 15 of gestation, pregnant female rats were administered TCDD by gavage at a single dose of 0 (vehicle), 200, or 800 ng/kg b.w. In the female offspring born to dams administered with TCDD at either 200 or 800 ng/kg b.w., the vaginal opening and first estrus occurred w4-7 days earlier than in the offspring born to vehicle-treated animals. The ovarian weight gain was also accelerated following exposure to TCDD in a dose-dependent manner. We next examined the ovarian compensatory hypertrophy (OCH) as an indicator of the maturation of the LH/GnRH-generating system in the pituitary and the hypothalamus. Exposure to TCDD accelerated the onset of OCH in the female offspring in a dose-dependent manner. In particular, in the offspring born to the dams exposed to TCDD at 800 ng/kg b.w., hypertrophy, which is characterized by hyperovulation and a marked increase in the weight of the remaining ovary after hemi-ovariectomy, was observed on postnatal days 27-30, which was 10 days earlier than in the offspring born to the vehicle-treated dams. These results indicate that perinatal exposure to a low dose of TCDD induces precocious puberty, including early maturation of the hypothalamic-pituitary axis, the gonads and genitals, in female Long-Evans hooded rats.

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A review of mechanisms controlling ovulation with implications for the anovulatory effects of polychlorinated dibenzo-p-dioxins in rodents

Cited by 61 publications

References 85 publications

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

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

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

Perinatal exposure of female rats to 2,3,7,8-tetrachlorodibenzo-p-dioxin induces central precocious puberty in the offspring

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