Effects of selected endocrine disruptors on meiotic maturation, cumulus expansion, synthesis of hyaluronan and progesterone by porcine oocyte–cumulus complexes

Mlynarčíková, Alžbeta Bujňáková; Nagyová, Eva; Ficková, M; Scsuková, Soňa

doi:10.1016/j.tiv.2008.12.017

Cited by 84 publications

(54 citation statements)

References 39 publications

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“…Specifically, between 48 and 72 h, PCB 153 decreased progesterone secretion, but after 72 h, it induced a dose-dependent increase in progesterone secretion (Augustowska et al 2001). A later study in the same in vitro model evaluated the effects of PCBs 153, 118, 180, and 138, and showed that congeners 153 (8 mg/ml), 118 (3 mg/ml), and 180 (3 mg/ml) increased E 2 secretion, while congener 138 (8 mg/ml) increased testosterone secretion (Mlynarcíková et al 2009). Although various studies have described the ability of PCBs to alter ovarian steroidogenesis, the molecular mechanisms underlying these alterations remain to be determined.…”

Section: Polyhalogenated Arylhydrocarbonsmentioning

confidence: 97%

“…Another study with porcine granulosa cells showed that, depending on the dose given, BPA increased basal (1 mM) and FSHinduced (10 mM) progesterone production, while it inhibited (1-100 mM) FSH-induced E 2 production (Mlynarcíková et al 2005). Furthermore, BPA (100 mM) decreased progesterone production, decreased expansion of cumulus cells and inhibited oocyte maturation in porcine oocyte-cumulus complexes (Mlynarcíková et al 2009). BPA treatment (40-100 mM) decreased aromatase mRNA and protein, and reduced E 2 production by primary human granulosa cells and a human ovarian granulosa-like tumor cell line (Kwintkiewicz et al 2010).…”

Section: Plasticizers: Bisphenol a And Phthalatesmentioning

confidence: 98%

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

Craig¹,

Wang²,

Flaws³

2011

Reproduction

230

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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Section: Polyhalogenated Arylhydrocarbonsmentioning

confidence: 97%

Section: Plasticizers: Bisphenol a And Phthalatesmentioning

confidence: 98%

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

Craig¹,

Wang²,

Flaws³

2011

Reproduction

230

123

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“…These doses are approximately equivalent to 0.492-49.2 lM, which encompass the doses ranging from 0.2 to 20 lg/ ml. The concentrations of DEHP and MEHP selected in these experiments have also been determined to be clinically relevant [20,52,[57][58][59]. Importantly, plasma concentrations of DEHP and MEHP in healthy women have been reported to be 0.18 lg/ml and 0.58 lg/ml, respectively, and peritoneal fluid concentrations of DEHP and MEHP in these women were reported to be 0.46 lg/ml and 0.37 lg/ml, respectively, which encompasses the lower selected concentrations [60].…”

Section: Introductionmentioning

confidence: 99%

Mono(2-Ethylhexyl) Phthalate Accelerates Early Folliculogenesis and Inhibits Steroidogenesis in Cultured Mouse Whole Ovaries and Antral Follicles1

Hannon

Brannick

Wang

et al. 2015

Biology of Reproduction

113

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Humans are ubiquitously exposed to di(2-ethylhexyl) phthalate (DEHP), which is an environmental toxicant present in common consumer products. DEHP potentially targets the ovary through its metabolite mono(2-ethylhexyl) phthalate (MEHP). However, the direct effects of MEHP on ovarian folliculogenesis and steroidogenesis, two processes essential for reproductive and nonreproductive health, are unknown. The present study tested the hypotheses that MEHP directly accelerates early folliculogenesis via overactivation of phosphatidylinositol 3-kinase (PI3K) signaling, a pathway that regulates primordial follicle quiescence and activation, and inhibits the synthesis of steroid hormones by decreasing steroidogenic enzyme levels. Neonatal ovaries from CD-1 mice were cultured for 6 days with vehicle control, DEHP, or MEHP (0.2-20 lg/ml) to assess the direct effects on folliculogenesis and PI3K signaling. Further, antral follicles from adult CD-1 mice were cultured with vehicle control or MEHP (0.1-10 lg/ml) for 24-96 h to establish the temporal effects of MEHP on steroid hormones and steroidogenic enzymes. In the neonatal ovaries, MEHP, but not DEHP, decreased phosphatase and tensin homolog levels and increased phosphorylated protein kinase B levels, leading to a decrease in the percentage of germ cells and an increase in the percentage of primary follicles. In the antral follicles, MEHP decreased the mRNA levels of 17alpha-hydroxylase-17,20-desmolase, 17beta-hydroxysteroid dehydrogenase, and aromatase leading to a decrease in testosterone, estrone, and estradiol levels. Collectively, MEHP mediates the effect of DEHP on accelerated folliculogenesis via overactivating PI3K signaling and inhibits steroidogenesis by decreasing steroidogenic enzyme levels.

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“…The incidence is higher with the poisonous material accumulating during maternal aging. Bisphenol A (BPA) is a typical endocrine disruptor and it is a man-made substance existing in our ordinary life, which is widely used in polycarbonate plastics and epoxy resins manufacturing and production of cans containing food, beverages, and dental sealants (79). The possible relationship between female meiotic defects and BPA was found accidentally based on the observation of the sudden increase of meiotic abnormalities, including aneuploidy, in oocytes from mice exposed to damaged plastic caging materials (39).…”

Section: Environmental Factors Affect Chromosome Segregation Mainly Tmentioning

confidence: 99%

Why is Chromosome Segregation Error in Oocytes Increased With Maternal Aging?

2011

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It is well documented that female fertility is decreased with advanced maternal age due to chromosome abnormality in oocytes. Increased chromosome missegregation is mainly caused by centromeric cohesion reduction. Other factors such as weakened homologous recombination, improper spindle organization, spindle assembly checkpoint (SAC) malfunction, chromatin epigenetic changes, and extra-oocyte factors may also cause chromosome errors.

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Effects of selected endocrine disruptors on meiotic maturation, cumulus expansion, synthesis of hyaluronan and progesterone by porcine oocyte–cumulus complexes

Cited by 84 publications

References 39 publications

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

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

Mono(2-Ethylhexyl) Phthalate Accelerates Early Folliculogenesis and Inhibits Steroidogenesis in Cultured Mouse Whole Ovaries and Antral Follicles1

Why is Chromosome Segregation Error in Oocytes Increased With Maternal Aging?

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