title: Changes in serum and renal vitamin E levels in deoxycorticosterone acetate-salt hypertensive rats.
abstract: BACKGROUND
  Hypertension is an important risk factor for the progression of chronic renal disease, which may result in the development of end-stage renal disease. Since reactive oxygen species are implicated in the induction of hypertension, antioxidants have been used to reduce blood pressure and renal impairment in animal models and in human hypertension. However, the available data are not conclusive.
  
  
  METHODS
  To investigate oxidative stress in hypertension, we evaluated renal and serum vitamin E levels as the most effective antioxidant to reduce lipid peroxidation by high-performance liquid chromatography among rats subjected to deoxycorticosterone acetate (DOCA)-salt treatment for 4 weeks. Renal levels of malondialdehyde (MDA) as a marker of cell lipid peroxidation were also assayed in treated rats. Systolic blood pressure (SBP) was measured in conscious rats by the tail-cuff method using a PowerLab/4sp data acquisition system.
  
  
  RESULTS
  SBP increased significantly in DOCA-salt-treated rats compared to the sham group after 4 weeks of treatment. Serum vitamin E levels were significantly lower and renal MDA concentrations significantly higher in treated compared to sham rats. However, renal vitamin E levels were also significantly higher among treated compared to sham rats.
  
  
  CONCLUSIONS
  Decreased plasma vitamin E levels and increased renal MDA levels show systemic and local oxidative stress in DOCA-salt-treated rats. However, the higher renal vitamin E level suggested a local compensatory mechanism. Vitamin E administration might be appropriate, as significant decreases in vitamin E levels were observed in the serum of DOCA-salt-treated rats.
authors.affiliation: Department of Physiology, School of Medicine, The School of Public Health, Tehran University of Medical Sciences, Tehran, Iran.
authors.forename: B
authors.initials: B
authors.lastname: Seifi
authors.forename: M
authors.initials: M
authors.lastname: Kadkhodaee
authors.forename: M
authors.initials: M
authors.lastname: Zahmatkesh
authors.forename: F
authors.initials: F
authors.lastname: Golab
authors.forename: E
authors.initials: E
authors.lastname: Bakhshi
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism; D003900:Desoxycorticosterone / Q000494:pharmacology*; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000139:chemically induced / Q000150:complications / Q000378:metabolism*; D007674:Kidney Diseases / Q000209:etiology; D007676:Kidney Failure, Chronic / Q000209:etiology; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012965:Sodium Chloride / Q000494:pharmacology; D014810:Vitamin E / Q000097:blood / Q000378:metabolism*
chemical_list: D000975:Antioxidants; D014810:Vitamin E; D003900:Desoxycorticosterone; D012965:Sodium Chloride