title: Reactive oxygen species stimulate prostaglandin F2 alpha production in human endometrial stromal cells in vitro.
abstract: BACKGROUND
  The present study was undertaken to investigate the effect of reactive oxygen species on prostaglandin F2 alpha (PGF2 alpha) production by human endometrial stromal cells (ESC).
  
  
  RESULTS
  Isolated ESC were incubated with hydrogen peroxide, which induces lipid peroxidation. Hydrogen peroxide increased both intracellular and medium concentrations of PGF2 alpha (P < 0.01). A time course study showed that hydrogen peroxide significantly increased PGF2 alpha concentrations in the medium after 6 h incubation (P < 0.01), after which no further increase was observed. To study whether the increase in PGF2 alpha production caused by hydrogen peroxide was mediated by cyclooxygenase, ESC were incubated with indomethacin (0.5 microg/ml), an inhibitor of cyclooxygenase, in the presence of hydrogen peroxide. Indomethacin significantly blocked the increases in PGF2 alpha production caused by hydrogen peroxide (P < 0.01). Hydrogen peroxide also increased PGF2 alpha production by decidualized ESC (P < 0.01), induced by the incubation with medroxyprogesterone acetate (10(-6) mol/l) and oestradiol (10(-8) mol/l).
  
  
  CONCLUSIONS
  Reactive oxygen species stimulate PGF2 alpha production in ESC, suggesting that they might influence endometrial function by regulating PGF2 alpha production.
authors.affiliation: Department of Obstetrics and Gynecology, Yamaguchi University School of Medicine, Minamikogushi 1-1-1, Ube 755-8505, Japan. obgyn@po.cc.yamaguchi-u.ac.jp
authors.forename: N
authors.initials: N
authors.lastname: Sugino
authors.forename: A
authors.initials: A
authors.lastname: Karube-Harada
authors.forename: S
authors.initials: S
authors.lastname: Kashida
authors.forename: S
authors.initials: S
authors.lastname: Takiguchi
authors.forename: H
authors.initials: H
authors.lastname: Kato
mesh_terms: D000328:Adult; D002478:Cells, Cultured; D016861:Cyclooxygenase Inhibitors / Q000494:pharmacology; D003656:Decidua / Q000166:cytology / Q000378:metabolism; D015237:Dinoprost / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D004717:Endometrium / Q000166:cytology / Q000378:metabolism*; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology; D007213:Indomethacin / Q000494:pharmacology; D008054:Lipid Peroxides / Q000096:biosynthesis; D017258:Medroxyprogesterone Acetate / Q000494:pharmacology; D009994:Osmolar Concentration; D016877:Oxidants / Q000494:pharmacology; D011451:Prostaglandin-Endoperoxide Synthases / Q000502:physiology; D017382:Reactive Oxygen Species / Q000494:pharmacology*; D017154:Stromal Cells / Q000378:metabolism*; D013997:Time Factors
chemical_list: D016861:Cyclooxygenase Inhibitors; D008054:Lipid Peroxides; D016877:Oxidants; D017382:Reactive Oxygen Species; D004958:Estradiol; D015237:Dinoprost; D006861:Hydrogen Peroxide; D017258:Medroxyprogesterone Acetate; D011451:Prostaglandin-Endoperoxide Synthases; D007213:Indomethacin