Gene expression is altered after bisphenol A exposure in human fetal oocytes in vitro

Brieño‐Enríquez, Miguel A.; Reig-Viader, Rita; Cabero, L.; Torán, Núria; Martínez, Flavio; Roig, Ignasi; Caldés, Montserrat Garcia

doi:10.1093/molehr/gar074

Cited by 69 publications

(37 citation statements)

References 64 publications

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“…Additionally, previous studies have also demonstrated that BPA exposure impairs the double-strand break repair machinery, increases the number of homologous recombination protein RAD-51 foci in late pachytene, 14 elevates mismatch repair-related MLH1 foci, 9, 15 and upregulates the expression of genes involved in DSB generation (Spo11), signaling (H2AX), and repair (RPA, BML). 36 These results suggest that exposure to a low dose of BPA may lead to the persistence of mDSBs by inhibiting their repair, although high doses of BPA have been reported to be genotoxic. 37 Subsequently, these unresolved mDSBs in pachytene spermatocytes result in the disruption of meiotic progression and chromosome abnormalities, such as asynapsis, chromosomal aberrations, and interrupted regions of SYCP3 staining, as also demonstrated by previous studies.…”

Section: Discussionmentioning

confidence: 87%

Exposure to bisphenol A disrupts meiotic progression during spermatogenesis in adult rats through estrogen-like activity

et al. 2013

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The effect of bisphenol A (BPA) on the reproductive system is highly debated but has been associated with meiotic abnormalities. However, evidence is lacking with regard to the mechanisms involved. In order to explore the underlying mechanisms of BPA-induced meiotic abnormalities in adult male rats, we exposed 9-week-old male Wistar rats to BPA by gavage at 0, 2, 20 or 200 μg/kg body weight (bw)/day for 60 consecutive days. 17β-Estradiol (E2) was administered at 10 μg/kg bw/day as the estrogenic positive control. Treatments with 200 μg/kg bw/day of BPA and E2 significantly decreased sperm counts and inhibited spermiation, characterized by an increase in stage VII and decrease in stage VIII in the seminiferous epithelium. This was concomitant with a disruption in the progression of meiosis I and the persistence of meiotic DNA strand breaks in pachytene spermatocytes,and the ataxia–telangiectasia-mutated and checkpoint kinase 2 signal pathway was also activated; Eventually, germ cell apoptosis was triggered as evaluated by terminal dUTP nick-end labeling assay and western blot for caspase 3. Using the estrogen receptor (ER) antagonist ICI 182780, we determined that ER signaling mediated BPA-induced meiotic disruption and reproductive impairment. Our results suggest that ER signaling-mediated meiotic disruption may be a major contributor to the molecular events leading to BPA-related male reproductive disorders. These rodent data support the growing association between BPA exposure and the rapid increase in the incidence of male reproductive disorders.

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Section: Discussionmentioning

confidence: 87%

Exposure to bisphenol A disrupts meiotic progression during spermatogenesis in adult rats through estrogen-like activity

et al. 2013

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“…Brieño-Enriquez et al (2011, 2012) reported that BPA (1–30 μM) increased oocyte degeneration by impairing meiotic progression in cultured human fetal oocytes and that, similar to mouse studies, human fetal oocytes that progressed to prophase exhibited increased levels of recombination (MLH1 foci) and gene expression changes. BPA also increased methylation errors in differentially methylated regions of maternally imprinted genes of oocytes in cultured preantral follicles of C57/BL6xCBA/Ca mice (Trapphoff et al 2013).…”

Section: Early Oogenesis and Ovarian Follicle Formationmentioning

confidence: 77%

Bisphenol A and Reproductive Health: Update of Experimental and Human Evidence, 2007–2013

Peretz

Vrooman

Ricke

et al. 2014

Environ Health Perspect

467

301

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Background: In 2007, an expert panel reviewed associations between bisphenol A (BPA) exposure and reproductive health outcomes. Since then, new studies have been conducted on the impact of BPA on reproduction.Objective: In this review, we summarize data obtained since 2007, focusing on a) findings from human and animal studies, b) the effects of BPA on a variety of reproductive end points, and c) mechanisms of BPA action.Methods: We reviewed the literature published from 2007 to 2013 using a PubMed search based on keywords related to BPA and male and female reproduction.Discussion: Because BPA has been reported to affect the onset of meiosis in both animal and in vitro models, interfere with germ cell nest breakdown in animal models, accelerate follicle transition in several animal species, alter steroidogenesis in multiple animal models and women, and reduce oocyte quality in animal models and women undergoing in vitro fertilization (IVF), we consider it an ovarian toxicant. In addition, strong evidence suggests that BPA is a uterine toxicant because it impaired uterine endometrial proliferation, decreased uterine receptivity, and increased implantation failure in animal models. BPA exposure may be associated with adverse birth outcomes, hyperandrogenism, sexual dysfunction, and impaired implantation in humans, but additional studies are required to confirm these associations. Studies also suggest that BPA may be a testicular toxicant in animal models, but the data in humans are equivocal. Finally, insufficient evidence exists regarding effects of BPA on the oviduct, the placenta, and pubertal development.Conclusion: Based on reports that BPA impacts female reproduction and has the potential to affect male reproductive systems in humans and animals, we conclude that BPA is a reproductive toxicant.Citation: Peretz J, Vrooman L, Ricke WA, Hunt PA, Ehrlich S, Hauser R, Padmanabhan V, Taylor HS, Swan SH, VandeVoort CA, Flaws JA. 2014. Bisphenol A and reproductive health: update of experimental and human evidence, 2007–2013. Environ Health Perspect 122:775–786; http://dx.doi.org/10.1289/ehp.1307728

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“…In connected studies it has been demonstrated that the exposure of human oocytes to BPA is linked to up-regulation of genes involved in meiotic processes connected to double strand breaks repair progression (Brieno-Enriquez et al 2012). A non-linear response to BPA doses on the incidence of MII oocytes with aligned chromosomes has also been determined (Machtinger et al 2013).…”

Section: Influences Of Bpa On Reproduction Of Femalesmentioning

confidence: 99%

Bisphenol S instead of bisphenol A: a story of reproductive disruption by regretable substitution - a review

Žalmanová¹,

Hošková²,

Nevoral³

et al. 2016

Czech J. Anim. Sci.

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A range of substances that are released into the environment, foodstuffs and drinking water as a result of human activity were originally considered relatively harmless, and it was only later that their adverse effects were discovered. In general the use of such substances is currently restricted, and they are often replaced by other substances. This applies also in the case of a range of endocrine disruptors. These substances have the capacity to disturb the balance of physiological functions of the organism on the level of hormonal regulation, and their pleiotropic spectrum of effects is very difficult to predict. Endocrine disruptors include the currently intensively studied bisphenol A (BPA), a prevalent environmental pollutant and contaminant of both water and foodstuffs. BPA has a significantly negative impact on human health, particularly on the regulation mechanisms of reproduction, and influences fertility. The ever increasingly stringent restriction of the industrial production of BPA is leading to its replacement with analogues, primarily with bisphenol S (BPS), which is not subject to these restrictions and whose impacts on the regulation of reproduction have not yet been exhaustively studied. However, the limited number of studies at disposal indicates that BPS may be at least as harmful as BPA. There is therefore a potential danger that the replacement of BPA with BPS will become one of the cases of regrettable substitution, in which the newly used substances manifest similar or even worse negative effects than the substances which they have replaced. The objective of this review is to draw attention to ill-advised replacements of endocrine disruptors with substances whose effects are not yet tested, and which may represent the same risks for the environment, for the reproduction of males and females, and for human health as have been demonstrated in the case of the originally used substances.

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Gene expression is altered after bisphenol A exposure in human fetal oocytes in vitro

Cited by 69 publications

References 64 publications

Exposure to bisphenol A disrupts meiotic progression during spermatogenesis in adult rats through estrogen-like activity

Exposure to bisphenol A disrupts meiotic progression during spermatogenesis in adult rats through estrogen-like activity

Bisphenol A and Reproductive Health: Update of Experimental and Human Evidence, 2007–2013

Bisphenol S instead of bisphenol A: a story of reproductive disruption by regretable substitution - a review

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