| Literature DB >> 25449418 |
Chae Kwan Lee1, Sung Goo Kang2, Jong Tae Lee1, Soo-Woong Lee3, Jeong Ho Kim1, Dae Hwan Kim4, Byung Chul Son1, Kun Hyung Kim1, Chun Hui Suh1, Se Yeong Kim1, Yeong Beom Park5.
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.Entities:
Keywords: Fetal growrh retardation; PFOS; Placenta; Placental lactogen; Prolactin-like protein
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Year: 2014 PMID： 25449418 DOI： 10.1016/j.mce.2014.10.026
Source DB: PubMed Journal: Mol Cell Endocrinol ISSN： 0303-7207 Impact factor: 4.102