Exposure of mouse oocytes to bisphenol A causes meiotic arrest but not aneuploidy

Eichenlaub-Ritter U, Vogt E, Cukurcam S, Sun F, Pacchierotti F, Parry J (2008)
MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS 651(1-2): 82-92.

Journal Article | Published | English

No fulltext has been uploaded

Author
; ; ; ; ;
Abstract
Mouse oocytes isolated from large antral follicles were exposed to a wide range of concentrations of bisphenol A (BPA) during maturation in vitro (50 ng/ml to 10 mu g/ml BPA in medium). Exposure to high concentrations of BPA (10 mu g/ml) affected spindle formation, distribution of pericentriolar material and chromosome alignment on the spindle (termed congression failure), and caused a significant meiotic arrest. However, BPA did not increase hyperploidy at meiosis II at any tested concentration. Some but not all meiosis I arrested oocytes had MAD2-positive foci at centromeres of chromosomes in bivalents, suggesting that they had failed to pass the spindle checkpoint control. In a second set of experiments prepubertal mice were exposed sub-chronically for 7 days to low BPA by daily oral administration, followed by in vitro maturation of the denuded oocytes to metaphase II in the absence of BPA, as this treatment protocol was previously reported to induce chromosome congression failure and therefore suspected to cause aneuploidy in oocytes. The sub-chronic exposure subtly affected spindle morphology and oocyte maturation. However, as with the exposure in vitro, there was no evidence that low BPA doses increased hyperploidy at meiosis II. In conclusion, the data suggest that mouse oocytes from mice respond to BPA-induced disturbances in spindle formation by induction of meiotic arrest. This response might result from an effective checkpoint mechanism preventing the occurrence of chromosome malsegregation and aneuploidy. Low chronic BPA exposure in vivo as such does not appear to pose a risk for induction of errors in chromosome segregation at first meiosis in mouse oocytes. Additional factors besides BPA may have caused the high rate of congression failure and the temporary increase in hyperploidy in mouse metaphase II oocytes reported previously. (c) 2007 Elsevier B.V. All rights reserved.
Publishing Year
ISSN
PUB-ID

Cite this

Eichenlaub-Ritter U, Vogt E, Cukurcam S, Sun F, Pacchierotti F, Parry J. Exposure of mouse oocytes to bisphenol A causes meiotic arrest but not aneuploidy. MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS. 2008;651(1-2):82-92.
Eichenlaub-Ritter, U., Vogt, E., Cukurcam, S., Sun, F., Pacchierotti, F., & Parry, J. (2008). Exposure of mouse oocytes to bisphenol A causes meiotic arrest but not aneuploidy. MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS, 651(1-2), 82-92.
Eichenlaub-Ritter, U., Vogt, E., Cukurcam, S., Sun, F., Pacchierotti, F., and Parry, J. (2008). Exposure of mouse oocytes to bisphenol A causes meiotic arrest but not aneuploidy. MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS 651, 82-92.
Eichenlaub-Ritter, U., et al., 2008. Exposure of mouse oocytes to bisphenol A causes meiotic arrest but not aneuploidy. MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS, 651(1-2), p 82-92.
U. Eichenlaub-Ritter, et al., “Exposure of mouse oocytes to bisphenol A causes meiotic arrest but not aneuploidy”, MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS, vol. 651, 2008, pp. 82-92.
Eichenlaub-Ritter, U., Vogt, E., Cukurcam, S., Sun, F., Pacchierotti, F., Parry, J.: Exposure of mouse oocytes to bisphenol A causes meiotic arrest but not aneuploidy. MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS. 651, 82-92 (2008).
Eichenlaub-Ritter, Ursula, Vogt, Edgar, Cukurcam, Suna, Sun, Fengyun, Pacchierotti, Francesca, and Parry, Jim. “Exposure of mouse oocytes to bisphenol A causes meiotic arrest but not aneuploidy”. MUTATION RESEARCH-GENETIC TOXICOLOGY AND ENVIRONMENTAL MUTAGENESIS 651.1-2 (2008): 82-92.
This data publication is cited in the following publications:
This publication cites the following data publications:

32 Citations in Europe PMC

Data provided by Europe PubMed Central.

Bisphenol-A and Female Infertility: A Possible Role of Gene-Environment Interactions.
Huo X, Chen D, He Y, Zhu W, Zhou W, Zhang J., Int J Environ Res Public Health 12(9), 2015
PMID: 26371021
Preimplantation Exposure to Bisphenol A and Triclosan May Lead to Implantation Failure in Humans.
Yuan M, Bai MZ, Huang XF, Zhang Y, Liu J, Hu MH, Zheng WQ, Jin F., Biomed Res Int 2015(), 2015
PMID: 26357649
Exposure to low-dose bisphenol A impairs meiosis in the rat seminiferous tubule culture model: a physiotoxicogenomic approach.
Ali S, Steinmetz G, Montillet G, Perrard MH, Loundou A, Durand P, Guichaoua MR, Prat O., PLoS ONE 9(9), 2014
PMID: 25181051
Exposure to bisphenol A results in a decline in mouse spermatogenesis.
Zhang GL, Zhang XF, Feng YM, Li L, Huynh E, Sun XF, Sun ZY, Shen W., Reprod. Fertil. Dev. 25(6), 2013
PMID: 22951085
Oocyte developmental competence and embryo development: impact of lifestyle and environmental risk factors.
Varghese AC, Ly KD, Corbin C, Mendiola J, Agarwal A., Reprod. Biomed. Online 22(5), 2011
PMID: 21388885

69 References

Data provided by Europe PubMed Central.

Gender difference in serum bisphenol A levels may be caused by liver UDP-glucuronosyltransferase activity in rats.
Takeuchi T, Tsutsumi O, Nakamura N, Ikezuki Y, Takai Y, Yano T, Taketani Y., Biochem. Biophys. Res. Commun. 325(2), 2004
PMID: 15530427
Biotransformations of bisphenol A in a mammalian model: answers and new questions raised by low-dose metabolic fate studies in pregnant CD1 mice.
Zalko D, Soto AM, Dolo L, Dorio C, Rathahao E, Debrauwer L, Faure R, Cravedi JP., Environ. Health Perspect. 111(3), 2003
PMID: 12611660
Potent estrogenic metabolites of bisphenol A and bisphenol B formed by rat liver S9 fraction: their structures and estrogenic potency.
Yoshihara S, Mizutare T, Makishima M, Suzuki N, Fujimoto N, Igarashi K, Ohta S., Toxicol. Sci. 78(1), 2004
PMID: 14691209
Estrogen and bisphenol A disrupt spontaneous [Ca(2+)](i) oscillations in mouse oocytes.
Mohri T, Yoshida S., Biochem. Biophys. Res. Commun. 326(1), 2005
PMID: 15567167
Signaling from the membrane via membrane estrogen receptor-alpha: estrogens, xenoestrogens, and phytoestrogens.
Watson CS, Bulayeva NN, Wozniak AL, Finnerty CC., Steroids 70(5-7), 2005
PMID: 15862819
Effects of nitric oxide synthase inhibitors on porcine oocyte meiotic maturation.
Tao Y, Xie H, Hong H, Chen X, Jang J, Xia G., Zygote 13(1), 2005
PMID: 15984155
Association between spindle assembly checkpoint expression and maternal age in human oocytes.
Steuerwald N, Cohen J, Herrera RJ, Sandalinas M, Brenner CA., Mol. Hum. Reprod. 7(1), 2001
PMID: 11134360
Age-associated alteration of gene expression patterns in mouse oocytes.
Hamatani T, Falco G, Carter MG, Akutsu H, Stagg CA, Sharov AA, Dudekula DB, VanBuren V, Ko MS., Hum. Mol. Genet. 13(19), 2004
PMID: 15317747
Effects of endocrine disrupters on the oocytes and embryos of farm animals.
Brevini TA, Cillo F, Antonini S, Gandolfi F., Reprod. Domest. Anim. 40(4), 2005
PMID: 16008759
Toxicokinetics of bisphenol A in female DA/Han rats after a single i.v. and oral administration.
Upmeier A, Degen GH, Diel P, Michna H, Bolt HM., Arch. Toxicol. 74(8), 2000
PMID: 11097379
Polo-box motif targets a centrosome regulator, RanGTPase.
Jang YJ, Ji JH, Ahn JH, Hoe KL, Won M, Im DS, Chae SK, Song S, Yoo HS., Biochem. Biophys. Res. Commun. 325(1), 2004
PMID: 15522227
Polo-like kinase 1 creates the tension-sensing 3F3/2 phosphoepitope and modulates the association of spindle-checkpoint proteins at kinetochores.
Ahonen LJ, Kallio MJ, Daum JR, Bolton M, Manke IA, Yaffe MB, Stukenberg PT, Gorbsky GJ., Curr. Biol. 15(12), 2005
PMID: 15964272
Bisphenol A binds to protein disulfide isomerase and inhibits its enzymatic and hormone-binding activities.
Hiroi T, Okada K, Imaoka S, Osada M, Funae Y., Endocrinology 147(6), 2006
PMID: 16543366
Bisphenol A exposure in utero disrupts early oogenesis in the mouse.
Susiarjo M, Hassold TJ, Freeman E, Hunt PA., PLoS Genet. 3(1), 2007
PMID: 17222059

Export

0 Marked Publications

Open Data PUB

Web of Science

View record in Web of Science®

Sources

PMID: 18096426
PubMed | Europe PMC

Search this title in

Google Scholar