Intrauterine Exposure to Paracetamol and Aniline Impairs Female Reproductive Development by Reducing Follicle Reserves and Fertility.
Identifieur interne : 001B82 ( PubMed/Checkpoint ); précédent : 001B81; suivant : 001B83Intrauterine Exposure to Paracetamol and Aniline Impairs Female Reproductive Development by Reducing Follicle Reserves and Fertility.
Auteurs : Jacob Bak Holm [Oman] ; Severine Mazaud-Guittot [France] ; Niels Banhos Danneskiold-Sams E [Danemark] ; Clementine Chalmey [France] ; Benjamin Jensen [Danemark] ; Mette Marie N Rreg Rd [Danemark] ; Cecilie Hurup Hansen [Danemark] ; Bjarne Styrishave [Danemark] ; Terje Svingen [Danemark] ; Anne Marie Vinggaard [Danemark] ; Holger Martin Koch [Allemagne] ; Josephine Bowles ; Peter Koopman ; Bernard Jégou [France] ; Karsten Kristiansen [Danemark] ; David M Bjerg Kristensen [Oman]Source :
- Toxicological sciences : an official journal of the Society of Toxicology [ 1096-0929 ] ; 2016.
Descripteurs français
- KwdFr :
- Acétaminophène (toxicité), Animaux, Dérivés de l'aniline (toxicité), Effets différés de l'exposition prénatale aux facteurs de risque (), Effets différés de l'exposition prénatale aux facteurs de risque (anatomopathologie), Effets différés de l'exposition prénatale aux facteurs de risque (physiopathologie), Femelle, Follicule ovarique (), Follicule ovarique (embryologie), Fécondité (), Grossesse, Mâle, Souris de lignée C57BL, Système génital de la femme (embryologie), Système génital de la femme (malformations), Âge gestationnel.
- MESH :
- anatomopathologie : Effets différés de l'exposition prénatale aux facteurs de risque.
- embryologie : Follicule ovarique, Système génital de la femme.
- malformations : Système génital de la femme.
- physiopathologie : Effets différés de l'exposition prénatale aux facteurs de risque.
- toxicité : Acétaminophène, Dérivés de l'aniline.
- Animaux, Effets différés de l'exposition prénatale aux facteurs de risque, Femelle, Follicule ovarique, Fécondité, Grossesse, Mâle, Souris de lignée C57BL, Âge gestationnel.
English descriptors
- KwdEn :
- Acetaminophen (toxicity), Aniline Compounds (toxicity), Animals, Female, Fertility (drug effects), Genitalia, Female (abnormalities), Genitalia, Female (embryology), Gestational Age, Male, Mice, Inbred C57BL, Ovarian Follicle (drug effects), Ovarian Follicle (embryology), Pregnancy, Prenatal Exposure Delayed Effects (chemically induced), Prenatal Exposure Delayed Effects (pathology), Prenatal Exposure Delayed Effects (physiopathology).
- MESH :
- chemical , toxicity : Acetaminophen, Aniline Compounds.
- abnormalities : Genitalia, Female.
- chemically induced : Prenatal Exposure Delayed Effects.
- drug effects : Fertility, Ovarian Follicle.
- embryology : Genitalia, Female, Ovarian Follicle.
- pathology : Prenatal Exposure Delayed Effects.
- physiopathology : Prenatal Exposure Delayed Effects.
- Animals, Female, Gestational Age, Male, Mice, Inbred C57BL, Pregnancy.
Abstract
Studies report that fetal exposure to paracetamol/acetaminophen by maternal consumption can interfere with male reproductive development. Moreover, recent biomonitoring data report widespread presence of paracetamol in German and Danish populations, suggesting exposure via secondary (nonpharmaceutical) sources, such as metabolic conversion from the ubiquitous industrial compound aniline. In this study, we investigated the extent to which paracetamol and aniline can interfere with female reproductive development. Intrauterine exposure to paracetamol by gavage of pregnant dams resulted in shortening of the anogenital distance in adult offspring, suggesting that fetal hormone signaling had been disturbed. Female offspring of paracetamol-exposed mothers had ovaries with diminished follicle reserve and reduced fertility. Fetal gonads of exposed animals had also reduced gonocyte numbers, suggesting that the reduced follicle count in adults could be due to early disruption of germ cell development. However, ex vivo cultures of ovaries from 12.5 days post coitum fetuses showed no decrease in proliferation or expression following exposure to paracetamol. This suggests that the effect of paracetamol occurs prior to this developmental stage. Accordingly, using embryonic stem cells as a proxy for primordial germ cells we show that paracetamol is an inhibitor of cellular proliferation, but without cytotoxic effects. Collectively, our data show that intrauterine exposure to paracetamol at levels commonly observed in pregnant women, as well as its precursor aniline, may block primordial germ cell proliferation, ultimately leading to reduced follicle reserves and compromised reproductive capacity later in life.
DOI: 10.1093/toxsci/kfv332
PubMed: 26732887
Affiliations:
- Allemagne, Danemark, France, Oman
- Hovedstaden, Région Bretagne
- Copenhague, Rennes
- Université de Rennes 1
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pubmed:26732887Le document en format XML
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<author><name sortKey="Mazaud Guittot, Severine" sort="Mazaud Guittot, Severine" uniqKey="Mazaud Guittot S" first="Severine" last="Mazaud-Guittot">Severine Mazaud-Guittot</name>
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<author><name sortKey="Chalmey, Clementine" sort="Chalmey, Clementine" uniqKey="Chalmey C" first="Clementine" last="Chalmey">Clementine Chalmey</name>
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<author><name sortKey="Hansen, Cecilie Hurup" sort="Hansen, Cecilie Hurup" uniqKey="Hansen C" first="Cecilie Hurup" last="Hansen">Cecilie Hurup Hansen</name>
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<author><name sortKey="Styrishave, Bjarne" sort="Styrishave, Bjarne" uniqKey="Styrishave B" first="Bjarne" last="Styrishave">Bjarne Styrishave</name>
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<author><name sortKey="Svingen, Terje" sort="Svingen, Terje" uniqKey="Svingen T" first="Terje" last="Svingen">Terje Svingen</name>
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<author><name sortKey="Vinggaard, Anne Marie" sort="Vinggaard, Anne Marie" uniqKey="Vinggaard A" first="Anne Marie" last="Vinggaard">Anne Marie Vinggaard</name>
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<author><name sortKey="Koch, Holger Martin" sort="Koch, Holger Martin" uniqKey="Koch H" first="Holger Martin" last="Koch">Holger Martin Koch</name>
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<wicri:noRegion>44789 Bochum</wicri:noRegion>
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<author><name sortKey="Bowles, Josephine" sort="Bowles, Josephine" uniqKey="Bowles J" first="Josephine" last="Bowles">Josephine Bowles</name>
<affiliation><nlm:affiliation>Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD 4072, Australia; and.</nlm:affiliation>
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</affiliation>
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<author><name sortKey="Koopman, Peter" sort="Koopman, Peter" uniqKey="Koopman P" first="Peter" last="Koopman">Peter Koopman</name>
<affiliation><nlm:affiliation>Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD 4072, Australia; and.</nlm:affiliation>
<wicri:noCountry code="subField">Australia; and</wicri:noCountry>
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<term>Aniline Compounds (toxicity)</term>
<term>Animals</term>
<term>Female</term>
<term>Fertility (drug effects)</term>
<term>Genitalia, Female (abnormalities)</term>
<term>Genitalia, Female (embryology)</term>
<term>Gestational Age</term>
<term>Male</term>
<term>Mice, Inbred C57BL</term>
<term>Ovarian Follicle (drug effects)</term>
<term>Ovarian Follicle (embryology)</term>
<term>Pregnancy</term>
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<term>Prenatal Exposure Delayed Effects (pathology)</term>
<term>Prenatal Exposure Delayed Effects (physiopathology)</term>
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<term>Animaux</term>
<term>Dérivés de l'aniline (toxicité)</term>
<term>Effets différés de l'exposition prénatale aux facteurs de risque ()</term>
<term>Effets différés de l'exposition prénatale aux facteurs de risque (anatomopathologie)</term>
<term>Effets différés de l'exposition prénatale aux facteurs de risque (physiopathologie)</term>
<term>Femelle</term>
<term>Follicule ovarique ()</term>
<term>Follicule ovarique (embryologie)</term>
<term>Fécondité ()</term>
<term>Grossesse</term>
<term>Mâle</term>
<term>Souris de lignée C57BL</term>
<term>Système génital de la femme (embryologie)</term>
<term>Système génital de la femme (malformations)</term>
<term>Âge gestationnel</term>
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</keywords>
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<term>Ovarian Follicle</term>
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<term>Système génital de la femme</term>
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<term>Ovarian Follicle</term>
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<front><div type="abstract" xml:lang="en">Studies report that fetal exposure to paracetamol/acetaminophen by maternal consumption can interfere with male reproductive development. Moreover, recent biomonitoring data report widespread presence of paracetamol in German and Danish populations, suggesting exposure via secondary (nonpharmaceutical) sources, such as metabolic conversion from the ubiquitous industrial compound aniline. In this study, we investigated the extent to which paracetamol and aniline can interfere with female reproductive development. Intrauterine exposure to paracetamol by gavage of pregnant dams resulted in shortening of the anogenital distance in adult offspring, suggesting that fetal hormone signaling had been disturbed. Female offspring of paracetamol-exposed mothers had ovaries with diminished follicle reserve and reduced fertility. Fetal gonads of exposed animals had also reduced gonocyte numbers, suggesting that the reduced follicle count in adults could be due to early disruption of germ cell development. However, ex vivo cultures of ovaries from 12.5 days post coitum fetuses showed no decrease in proliferation or expression following exposure to paracetamol. This suggests that the effect of paracetamol occurs prior to this developmental stage. Accordingly, using embryonic stem cells as a proxy for primordial germ cells we show that paracetamol is an inhibitor of cellular proliferation, but without cytotoxic effects. Collectively, our data show that intrauterine exposure to paracetamol at levels commonly observed in pregnant women, as well as its precursor aniline, may block primordial germ cell proliferation, ultimately leading to reduced follicle reserves and compromised reproductive capacity later in life.</div>
</front>
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<DateCreated><Year>2016</Year>
<Month>02</Month>
<Day>26</Day>
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<DateCompleted><Year>2016</Year>
<Month>12</Month>
<Day>13</Day>
</DateCompleted>
<DateRevised><Year>2016</Year>
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<Day>30</Day>
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<Month>Mar</Month>
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<Title>Toxicological sciences : an official journal of the Society of Toxicology</Title>
<ISOAbbreviation>Toxicol. Sci.</ISOAbbreviation>
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<ArticleTitle>Intrauterine Exposure to Paracetamol and Aniline Impairs Female Reproductive Development by Reducing Follicle Reserves and Fertility.</ArticleTitle>
<Pagination><MedlinePgn>178-89</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1093/toxsci/kfv332</ELocationID>
<Abstract><AbstractText>Studies report that fetal exposure to paracetamol/acetaminophen by maternal consumption can interfere with male reproductive development. Moreover, recent biomonitoring data report widespread presence of paracetamol in German and Danish populations, suggesting exposure via secondary (nonpharmaceutical) sources, such as metabolic conversion from the ubiquitous industrial compound aniline. In this study, we investigated the extent to which paracetamol and aniline can interfere with female reproductive development. Intrauterine exposure to paracetamol by gavage of pregnant dams resulted in shortening of the anogenital distance in adult offspring, suggesting that fetal hormone signaling had been disturbed. Female offspring of paracetamol-exposed mothers had ovaries with diminished follicle reserve and reduced fertility. Fetal gonads of exposed animals had also reduced gonocyte numbers, suggesting that the reduced follicle count in adults could be due to early disruption of germ cell development. However, ex vivo cultures of ovaries from 12.5 days post coitum fetuses showed no decrease in proliferation or expression following exposure to paracetamol. This suggests that the effect of paracetamol occurs prior to this developmental stage. Accordingly, using embryonic stem cells as a proxy for primordial germ cells we show that paracetamol is an inhibitor of cellular proliferation, but without cytotoxic effects. Collectively, our data show that intrauterine exposure to paracetamol at levels commonly observed in pregnant women, as well as its precursor aniline, may block primordial germ cell proliferation, ultimately leading to reduced follicle reserves and compromised reproductive capacity later in life.</AbstractText>
<CopyrightInformation>© The Author 2016. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Holm</LastName>
<ForeName>Jacob Bak</ForeName>
<Initials>JB</Initials>
<AffiliationInfo><Affiliation>*Laboratory of Genomics and Molecular Biomedicine, Department of Biology, University of Copenhagen, 2100 Copenhagen, Denmark; david@moebjerg.com.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Mazaud-Guittot</LastName>
<ForeName>Severine</ForeName>
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</AffiliationInfo>
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<Initials>NB</Initials>
<AffiliationInfo><Affiliation>*Laboratory of Genomics and Molecular Biomedicine, Department of Biology, University of Copenhagen, 2100 Copenhagen, Denmark;</Affiliation>
</AffiliationInfo>
</Author>
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<ForeName>Mette Marie</ForeName>
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</AffiliationInfo>
</Author>
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<ForeName>Cecilie Hurup</ForeName>
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<AffiliationInfo><Affiliation>Toxicology Laboratory, Department of Pharmacy, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark;</Affiliation>
</AffiliationInfo>
</Author>
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<Initials>B</Initials>
<AffiliationInfo><Affiliation>Toxicology Laboratory, Department of Pharmacy, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark;</Affiliation>
</AffiliationInfo>
</Author>
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<Initials>T</Initials>
<AffiliationInfo><Affiliation>Division of Diet, Disease Prevention and Toxicology, National Food Institute, Technical University of Denmark, 2860 Søborg, Denmark;</Affiliation>
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<ForeName>Josephine</ForeName>
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<AffiliationInfo><Affiliation>Institute for Molecular Bioscience, The University of Queensland, Brisbane, QLD 4072, Australia; and.</Affiliation>
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<AffiliationInfo><Affiliation>*Laboratory of Genomics and Molecular Biomedicine, Department of Biology, University of Copenhagen, 2100 Copenhagen, Denmark;</Affiliation>
</AffiliationInfo>
</Author>
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<ForeName>David Møbjerg</ForeName>
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