Cited by 101Per- and polyfluoroalkyl substances researchEffects and risks of endocrine disrupting chemicalsHypothalamic control of reproductive hormones

The mammary gland is a sensitive pubertal target in CD-1 and C57Bl/6 mice following perinatal perfluorooctanoic acid (PFOA) exposure

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Tucker, Deirdre K., Macon, Madisa B., Strynar, Mark J., Dagnino, Sonia, Andersen, Erik, Fenton, Suzanne E.·2015·Reproductive Toxicology

Abstract

Perfluorooctanoic acid (PFOA) is a developmental toxicant in mice, with varied strain outcomes depending on dose and period of exposure. The impact of PFOA on female mouse pubertal development at low doses (≤1mg/kg) has yet to be determined. Therefore, female offspring from CD-1 and C57Bl/6 dams exposed to PFOA, creating serum concentrations similar to humans, were examined for pubertal onset, including mammary gland development. Pups demonstrated a shorter PFOA elimination half-life than that reported for adult mice. Prenatal exposure to PFOA caused significant mammary developmental delays in female offspring in both strains. Delays started during puberty and persisted into young adulthood; severity was dose-dependent. Also an evaluation of female serum hormone levels and pubertal timing onset revealed no effects of PFOA compared to controls in either strain. These data suggest that the mammary gland is more sensitive to early low level PFOA exposures compared to other pubertal endpoints, regardless of strain.

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Crossref · 10.1016/j.reprotox.2014.12.002

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  • Female mice exposed to PFOA during a critical period of fetal development experienced significant delays in mammary gland development, a measure of pubertal progress.

    “Female mice exposed to PFOA during a critical period of fetal development experienced significant delays in mammary gland development, a measure of pubertal progress.32”

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References 50 · Cited by 101

Research works printed but not linked: 44

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Authors
Tucker, D. K., Macon, M. B., Strynar, M. J., Dagnino, S., Andersen, E., & Fenton, S. E.
Affiliations
  • University of North Carolina at Chapel Hill (US)
  • Environmental Protection Agency (US)
  • National Institutes of Health (US)
Corresponding author
Fenton, Suzanne E.
Venue
Reproductive Toxicology
Publisher
Elsevier BV
Published
2015-07
Volume
54
Pages
26-36
ISSN
0890-6238 (ISSN-L)
OpenAlex
W1965185429
Cited by
101
References
50
Citations by year
2026: 3 · 2025: 5 · 2024: 13 · 2023: 9 · 2022: 9 · 2021: 15 · 2020: 12 · 2019: 6 · 2018: 10 · 2017: 9 · 2016: 6 · 2015: 3 · 2014: 1
FWCI
4.82
Type
journal article
Language
en
Open access
Locations
  • Reproductive Toxicology (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
  • Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
  • UNC Libraries
Funders
  • NIH
  • NIEHS
Topics
  • Physical Sciences › Environmental Science › Environmental Chemistry › Per- and polyfluoroalkyl substances research
  • Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
  • Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
Keywords
perfluorooctanoic acid, mammary gland development, puberty onset, perinatal exposure, developmental toxicity, ICR mice, C57BL/6 mice, strain differences, serum hormone levels, female offspring, low-dose exposure
MeSH terms
Age Factors, Animals, Body Burden, Caprylates, Dose-Response Relationship, Drug, Environmental Pollutants, Female, Fluorocarbons, Gestational Age, Liver, Mammary Glands, Animal, Mice, Inbred C57BL, Pregnancy, Prenatal Exposure Delayed Effects, Risk Factors, Risk Assessment, Maternal Exposure, Sexual Development

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