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Effects of perfluorooctane sulfuric acid on placental PRL-family hormone production and fetal growth retardation in mice.

Abstract
Perfluorooctane sulfuric acid (PFOS) is a persistent organic pollutant, causes fetal growth retardation but the mechanism is still unclear. This study focused on PFOS-induced toxicity such as placental trophoblast cell histopathological changes, endocrine function (i.e., prolactin (PRL)-family hormone production) and subsequent fetal growth retardation in mice. Maternal body weight gain, placental and fetal weights were significantly decreased in proportion to PFOS dosage. Placental efficiency (fetal weight/placental weight) was significantly reduced dose-dependently. Necrotic changes were observed in PFOS-treated placental tissues, and the area of injury increased dose-dependently. Finally, mRNA levels and maternal serum concentrations of the PRL-family hormones (mPL-II, mPLP-Cα, mPLP-K) were significantly reduced dose-dependently. In addition, the changing pattern between PRL-family hormone concentrations and fetal body weight was positively correlated. These results suggest that gestational PFOS treatment induces placental histopathological changes and disruption of endocrine function, finally may lead to fetal growth retardation in mice.
AuthorsChae Kwan Lee, Sung Goo Kang, Jong Tae Lee, Soo-Woong Lee, Jeong Ho Kim, Dae Hwan Kim, Byung Chul Son, Kun Hyung Kim, Chun Hui Suh, Se Yeong Kim, Yeong Beom Park
JournalMolecular and cellular endocrinology (Mol Cell Endocrinol) Vol. 401 Pg. 165-72 (Feb 05 2015) ISSN: 1872-8057 [Electronic] Ireland
PMID25449418 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2014 Elsevier Ireland Ltd. All rights reserved.
Chemical References
  • Alkanesulfonic Acids
  • Fluorocarbons
  • Pit1 protein, mouse
  • Placental Hormones
  • Transcription Factor Pit-1
  • Prolactin
  • perfluorooctane sulfonic acid
Topics
  • Alkanesulfonic Acids (toxicity)
  • Animals
  • Body Weight (drug effects)
  • Embryo, Mammalian
  • Female
  • Fetal Growth Retardation (chemically induced, metabolism, pathology)
  • Fluorocarbons (toxicity)
  • Gene Expression Regulation, Developmental (drug effects)
  • Mice
  • Placental Hormones (blood, genetics)
  • Pregnancy
  • Prolactin (blood, genetics)
  • Transcription Factor Pit-1 (genetics)
  • Trophoblasts (drug effects, pathology)

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