Bisphenol A exposure in utero disrupts early oogenesis in the mouse

Martha Susiarjo; Terry J Hassold; Edward Freeman; Patricia A Hunt

doi:10.1371/journal.pgen.0030005

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Bisphenol A exposure in utero disrupts early oogenesis in the mouse

Journal article

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Bisphenol A exposure in utero disrupts early oogenesis in the mouse

Martha Susiarjo, Terry J Hassold, Edward Freeman and Patricia A Hunt

PLoS genetics, Vol.3(1), pp.e5-0070

01/12/2007

DOI: https://doi.org/10.1371/journal.pgen.0030005

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https://hdl.handle.net/2376/109396

PMID: 17222059

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Abstract

MutL Protein Homolog 1

Chromosomes, Mammalian - genetics

Fetus - metabolism

Fetus - pathology

Aneuploidy

Metaphase - drug effects

Chromosome Segregation - drug effects

Estrogen Receptor beta - deficiency

Oocytes - cytology

Meiosis - drug effects

Crossing Over, Genetic - drug effects

Pachytene Stage - drug effects

Oocytes - drug effects

Recombination, Genetic - genetics

Female

Oogenesis - drug effects

Nuclear Proteins - genetics

Phenols - pharmacology

Benzhydryl Compounds

Chromosomes, Mammalian - drug effects

Mice, Knockout

Fetus - drug effects

Pregnancy

Animals

Adaptor Proteins, Signal Transducing - genetics

Mice

Recombination, Genetic - drug effects

Estrogen plays an essential role in the growth and maturation of the mammalian oocyte, and recent studies suggest that it also influences follicle formation in the neonatal ovary. In the course of studies designed to assess the effect of the estrogenic chemical bisphenol A (BPA) on mammalian oogenesis, we uncovered an estrogenic effect at an even earlier stage of oocyte development--at the onset of meiosis in the fetal ovary. Pregnant mice were treated with low, environmentally relevant doses of BPA during mid-gestation to assess the effect of BPA on the developing ovary. Oocytes from exposed female fetuses displayed gross aberrations in meiotic prophase, including synaptic defects and increased levels of recombination. In the mature female, these aberrations were translated into an increase in aneuploid eggs and embryos. Surprisingly, we observed the same constellation of meiotic defects in fetal ovaries of mice homozygous for a targeted disruption of ERbeta, one of the two known estrogen receptors. This, coupled with the finding that BPA exposure elicited no additional effects in ERbeta null females, suggests that BPA exerts its effect on the early oocyte by interfering with the actions of ERbeta. Together, our results show that BPA can influence early meiotic events and, importantly, indicate that the oocyte itself may be directly responsive to estrogen during early oogenesis. This raises concern that brief exposures during fetal development to substances that mimic or antagonize the effects of estrogen may adversely influence oocyte development in the exposed female fetus.

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Title: Bisphenol A exposure in utero disrupts early oogenesis in the mouse
Creators: Martha Susiarjo - Department of Genetics, Case Western Reserve University, Cleveland, Ohio, United States of America
Terry J Hassold
Edward Freeman
Patricia A Hunt
Publication Details: PLoS genetics, Vol.3(1), pp.e5-0070
Academic Unit: Molecular Biosciences, School of
Publisher: United States
Identifiers: 99900547231501842
Language: English
Resource Type: Journal article