title: Effect of oestrogen on reactive oxygen species production in the aortas of ovariectomized Dahl salt-sensitive rats.
abstract: OBJECTIVE
  In the present study, we examined whether ovariectomy increases reactive oxygen species (ROS) and the expression of nicotinamide adenine dinucleotide phosphate, reduced form (NADPH) oxidase and modulates the scavenger enzymes for ROS in the aortas of Dahl salt-sensitive (DSS) rats fed a high salt diet.
  
  
  METHODS
  DSS female rats were ovariectomized and fed a high salt diet (8% NaCl), or a high salt diet plus oestrogen supplement for 4 weeks. Urinary levels of hydrogen peroxide (H2O2) were measured by using 2',7'-dichlorofluorescein. The expression of an NADPH oxidase subunit p22phox, extracellular superoxide dismutase (ecSOD), glutathione peroxidase (GPx)1, GPx4 and monocyte chemoattractant protein 1 (MCP-1) messenger RNA was assessed by reverse transcription-polymerase chain reaction. The expression of MCP-1, and macrophage infiltration were examined by immunohistochemical analysis.
  
  
  RESULTS
  Ovariectomy increased superoxide production and the expression of NADPH oxidase subunit p22phox mRNA and protein in the aortas of DSS rats fed a high salt diet. In contrast, ovariectomy reduced the expression of ecSOD mRNA and protein and the expression of GPx1 and GPx4 mRNA in the aorta. Ovariectomy increased MCP-1 mRNA and protein expression and ED1-positive cells in the aorta.
  
  
  CONCLUSIONS
  Ovariectomy leads to an amplification of oxidative stress in DSS rats fed a high salt diet synergistically by an increase in the ROS-generating system and a decrease in the ROS-eliminating system, as shown in the increase in superoxide production and the urinary excretion of H2O2. Oestrogen supplementation counteracted these alterations, showing how oestrogen is antioxidative.
authors.affiliation: Department of Cardiovascular Physiology, Faculty of Medicine, Kagawa University, 1750-1 Ikenobe, Miki-Kita, Kagawa 761-0793, Japan.
authors.forename: Ling
authors.initials: L
authors.lastname: Zhang
authors.forename: Shigemoto
authors.initials: S
authors.lastname: Fujii
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Kosaka
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism; D018932:Chemokine CCL2 / Q000378:metabolism; D004195:Disease Models, Animal; D015536:Down-Regulation; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D005979:Glutathione Peroxidase / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000652:urine*; D019255:NADPH Oxidases / Q000378:metabolism; D010052:Ovariectomy; D018384:Oxidative Stress / Q000187:drug effects* / Q000502:physiology; D051381:Rats; D020303:Rats, Inbred Dahl; D017382:Reactive Oxygen Species / Q000378:metabolism*; D017673:Sodium Chloride, Dietary; D013482:Superoxide Dismutase / Q000378:metabolism; D015854:Up-Regulation; D000094765:Glutathione Peroxidase GPX1
chemical_list: D018932:Chemokine CCL2; D004967:Estrogens; D017382:Reactive Oxygen Species; D017673:Sodium Chloride, Dietary; D006861:Hydrogen Peroxide; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D019255:NADPH Oxidases; C515768:Cyba protein, rat; D000094765:Glutathione Peroxidase GPX1; C000722069:Gpx1 protein, rat