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Programming of metabolic effects in C57BL/6JxFVB mice by in utero and lactational exposure to perfluorooctanoic acid.
van Esterik, J C J; Bastos Sales, L; Dollé, M E T; Håkansson, H; Herlin, M; Legler, J; van der Ven, L T M.
Afiliación
  • van Esterik JC; Center for Health Protection, National Institute for Public Health and the Environment (RIVM), PO Box 1, 3720 BA, Bilthoven, The Netherlands.
  • Bastos Sales L; Department of Chemistry and Biology, Institute for Environmental Studies (IVM), VU University, De Boelelaan 1085, 1081 HV, Amsterdam, The Netherlands.
  • Dollé ME; Department of Chemistry and Biology, Institute for Environmental Studies (IVM), VU University, De Boelelaan 1085, 1081 HV, Amsterdam, The Netherlands.
  • Håkansson H; Center for Health Protection, National Institute for Public Health and the Environment (RIVM), PO Box 1, 3720 BA, Bilthoven, The Netherlands.
  • Herlin M; Institute of Environmental Medicine, Karolinska Institutet, P.O. Box 210, SE-171 77, Stockholm, Sweden.
  • Legler J; Institute of Environmental Medicine, Karolinska Institutet, P.O. Box 210, SE-171 77, Stockholm, Sweden.
  • van der Ven LT; Department of Chemistry and Biology, Institute for Environmental Studies (IVM), VU University, De Boelelaan 1085, 1081 HV, Amsterdam, The Netherlands.
Arch Toxicol ; 90(3): 701-15, 2016 Mar.
Article en En | MEDLINE | ID: mdl-25827101
Perfluorooctanoic acid (PFOA) is known to cause developmental toxicity and is a suggested endocrine disrupting compound (EDC). Early life exposure to EDCs has been implicated in programming of the developing organism for chronic diseases later in life. Here we study perinatal metabolic programming by PFOA using an experimental design relevant for human exposure. C57BL/6JxFVB hybrid mice were exposed during gestation and lactation via maternal feed to seven low doses of PFOA at and below the NOAEL used for current risk assessment (3-3000 µg/kg body weight/day). After weaning, offspring were followed for 23-25 weeks without further exposure. Offspring showed a dose-dependent decrease in body weight from postnatal day 4 to adulthood. Growth under high fat diet in the last 4-6 weeks of follow-up was increased in male and decreased in female offspring. Both sexes showed increased liver weights, hepatic foci of cellular alterations and nuclear dysmorphology. In females, reductions in perigonadal and perirenal fat pad weights, serum triglycerides and cholesterol were also observed. Endocrine parameters, such as glucose tolerance, serum insulin and leptin, were not affected. In conclusion, our study with perinatal exposure to PFOA in mice produced metabolic effects in adult offspring. This is most likely due to disrupted programming of metabolic homeostasis, but the assayed endpoints did not provide a mechanistic explanation. The BMDL of the programming effects in our study is below the current point of departure used for calculation of the tolerable daily intake.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Efectos Tardíos de la Exposición Prenatal / Lactancia / Caprilatos / Fluorocarburos Tipo de estudio: Risk_factors_studies Límite: Animals / Pregnancy Idioma: En Revista: Arch Toxicol Año: 2016 Tipo del documento: Article País de afiliación: Países Bajos Pais de publicación: Alemania
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Efectos Tardíos de la Exposición Prenatal / Lactancia / Caprilatos / Fluorocarburos Tipo de estudio: Risk_factors_studies Límite: Animals / Pregnancy Idioma: En Revista: Arch Toxicol Año: 2016 Tipo del documento: Article País de afiliación: Países Bajos Pais de publicación: Alemania