title: Steroid sex hormones and macrophage function: modulation of reactive oxygen intermediates and nitrite release.
abstract: OBJECTIVE
  In general, females have a more active immune response than do males. The effects of female sex hormones on lymphocytes have been studied extensively but their effects on macrophages are poorly understood.
  
  
  METHODS
  In this study, peritoneal macrophages (M phi) obtained from male rats were treated in vitro with estradiol (E2), progesterone (P), testosterone (TS), or hydrocortisone (HC) and their effects on superoxide, hydrogen peroxide, and nitrite release determined.
  
  
  RESULTS
  At concentrations between 10(-10) and 10(-9) M, female and male sex hormones had no significant effect on superoxide release but, at concentrations above or below that range, these hormones stimulated the release of these reactive oxygen intermediates (ROI). In contrast, M phi treated with HC generally exhibited either unaltered or reduced ROI release.
  
  
  CONCLUSIONS
  These findings suggest that female sex hormones regulate ROI release by M phi in a manner not entirely shared by other steroid hormones. At most concentrations used, E2, P, TS, and HC significantly inhibited nitrite release by M phi. However, with 10(-10) M of E2 or 10(-9)M of P, nitrite release by M phi was not affected. In the presence of anti-TNF antibody, the amounts of superoxide and hydrogen peroxide release were moderately reduced but nitrite release was dramatically inhibited. The sensitivity of M phi to variations in the concentrations of female sex hormones may contribute to gender-related differences in the immune response.
authors.affiliation: Department of Anatomy and Cell Biology, University of Illinois at Chicago.
authors.forename: T C
authors.initials: TC
authors.lastname: Chao
authors.forename: P J
authors.initials: PJ
authors.lastname: Van Alten
authors.forename: R J
authors.initials: RJ
authors.lastname: Walter
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D004958:Estradiol / Q000494:pharmacology; D012739:Gonadal Steroid Hormones / Q000494:pharmacology*; D006854:Hydrocortisone / Q000494:pharmacology; D006861:Hydrogen Peroxide / Q000378:metabolism; D017737:Macrophages, Peritoneal / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D009573:Nitrites / Q000378:metabolism*; D011374:Progesterone / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D017382:Reactive Oxygen Species / Q000378:metabolism*; D013481:Superoxides / Q000378:metabolism; D013739:Testosterone / Q000494:pharmacology; D013755:Tetradecanoylphorbol Acetate / Q000494:pharmacology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology; D015054:Zymosan / Q000494:pharmacology
chemical_list: D012739:Gonadal Steroid Hormones; D009573:Nitrites; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D013481:Superoxides; D013739:Testosterone; D011374:Progesterone; D004958:Estradiol; D015054:Zymosan; D006861:Hydrogen Peroxide; D013755:Tetradecanoylphorbol Acetate; D006854:Hydrocortisone