title: In utero perfluorooctane sulfonate exposure causes low body weights of fetal rats: A mechanism study.
abstract: OBJECTIVE
  The objective of the present study is to investigate the mechanism of perfluorooctane sulfonate-induced low body weight of fetus by analysis of glucocorticoid metabolizing enzyme 11β-hydroxysteroid dehydrogenase 2 and gene expression profiling of the placenta after in utero PFOS exposure.
  
  
  METHODS
  Pregnant Sprague-Dawley dams were gavaged with 0, 5, and 20 mg/kg body weight PFOS daily from gestational day 12-18. On gestational day 18, pregnant dams were euthanized, placentas, and fetuses were collected.
  
  
  METHODS
  Body weights of fetuses and placentas were measured, the corticosterone levels in fetal serum, and 11β-hydroxysteroid dehydrogenase 2 as well as the placental gene profiling were analyzed.
  
  
  RESULTS
  20 mg/kg PFOS significantly reduced fetal body weight and placental weight. Both 5 and 20 mg/kg PFOS increased fetal serum corticosterone levels. PFOS potently inhibited placental 11β-hydroxysteroid dehydrogenase 2 activity. Of 21,910 genes, 45 genes were significantly downregulated ≥2 fold by 20 mg/kg PFOS, including extracellular matrix (Slpi and Pi16), growth factors and hormones (Trh and Pdf), ion transporters (Aqp1, S100a4, and Abp1), signal transducers (Kap and Ampd3), and structural constituents (A2m and Des).
  
  
  CONCLUSIONS
  PFOS exposure may alter placental development and function, causing intrauterine growth restriction via inhibiting placental 11β-hydroxysteroid dehydrogenase 2.
authors.affiliation: The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China.
authors.forename: Xiaoheng
authors.initials: X
authors.lastname: Li
authors.affiliation: The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China.
authors.forename: Leping
authors.initials: L
authors.lastname: Ye
authors.affiliation: The Population Council & the Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
authors.forename: Yufei
authors.initials: Y
authors.lastname: Ge
authors.affiliation: The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China.
authors.forename: Kaiming
authors.initials: K
authors.lastname: Yuan
authors.affiliation: Heilongjiang Key Laboratory of Anti-fibrosis Biotherapy, Mudanjiang Medical University, Heilongjiang 157011, PR China.
authors.forename: Yufei
authors.initials: Y
authors.lastname: Zhang
authors.affiliation: Department of Oncology, The Affiliated Taizhou Municipal Hospital, Taizhou University, 381 Zhongshan East Road, Jiaojiang District, Taizhou City, Zhejiang Province, 318000, PR China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Liang
authors.affiliation: The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China.
authors.forename: Jia
authors.initials: J
authors.lastname: Wei
authors.affiliation: The Population Council & the Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.
authors.forename: Connie
authors.initials: C
authors.lastname: Zhao
authors.affiliation: The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China.
authors.forename: Qing-Quan
authors.initials: QQ
authors.lastname: Lian
authors.affiliation: The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China. Electronic address: wzzxq@wzhealth.com.
authors.forename: Xueqiong
authors.initials: X
authors.lastname: Zhu
authors.affiliation: The Second Affiliated Hospital & Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, Zhejiang 325027, China; The Population Council & the Rockefeller University, 1230 York Avenue, New York, NY 10065, USA. Electronic address: r_ge@yahoo.com.
authors.forename: Ren-Shan
authors.initials: RS
authors.lastname: Ge
mesh_terms: D042842:11-beta-Hydroxysteroid Dehydrogenases / Q000037:antagonists & inhibitors / Q000378:metabolism; D017738:Alkanesulfonic Acids / Q000378:metabolism / Q000633:toxicity*; D000818:Animals; D005260:Female; D005317:Fetal Growth Retardation / Q000139:chemically induced* / Q000235:genetics; D020567:Fetal Weight / Q000187:drug effects*; D005466:Fluorocarbons / Q000378:metabolism / Q000633:toxicity*; D005786:Gene Expression Regulation / Q000187:drug effects; D008431:Maternal-Fetal Exchange; D010920:Placenta / Q000187:drug effects* / Q000378:metabolism; D011247:Pregnancy; D051381:Rats; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction / Q000187:drug effects; D013851:Thinness / Q000139:chemically induced* / Q000473:pathology
chemical_list: D017738:Alkanesulfonic Acids; D005466:Fluorocarbons; C076994:perfluorooctane sulfonic acid; D042842:11-beta-Hydroxysteroid Dehydrogenases
keywords: 11β-hydroxysteroid dehydrogenase 2; Gene expression; Glucocorticoid; PFOS; Perfluoroalkylated substances; Placenta