title: The effect of intravenous iron on oxidative stress in hemodialysis patients at various levels of vitamin C.
abstract: OBJECTIVE
  Vitamin C levels decrease during hemodialysis (HD), which deteriorates antioxidant defense. Vitamin C may also act pro-oxidatively, via reduction in Fe(III). We sought to determine whether intravenous iron (Fe(iv))-induced oxidative stress differs in HD patients with low and physiological vitamin C levels and whether intravenous vitamin C (C(iv)) administration during HD would change the response to Fe(iv).
  
  
  METHODS
  Twenty patients with vitamin C deficiency (median 15.7 micromol/l, range 8.0-22.7) received Fe(iv) (100 mg iron sucrose between 150 and 180 min of HD). After 4 weeks of oral supplementation, the levels of vitamin C were comparable with those of controls (60.1 micromol/l, range 47.4-70.9). Patients were subsequently treated with (1) Fe(iv), (2) Fe(iv) and continuous 2 mg/min C(iv) throughout HD, (3) saline (S), and (4) S+C(iv). Plasma thiobarbituric acid reacting substances (TBARS) and vitamin C were assessed before, during and after FE(iv)(S), and 15, 30 and 60 min after infusion.
  
  
  RESULTS
  Fe(iv) induced a comparable rise in TBARS in patients with vitamin C deficiency (before Fe(iv), 1.9 micromol/l, range 1.4-1.9; after Fe(iv), 2.6 micromol/l, range 2.3-2.9; p < 0.01) and in those with normal vitamin C (before Fe(iv), 1.9 micromol/l, range 1.7-2.1; after Fe(iv), 2.6 micromol/l, range 2.5-2.9; p < 0.01). Fe(iv)+C(iv) resulted in a greater increase in TBARS (after Fe(iv), 3.1 micromol/l, range 2.8-3.2) compared with Fe(iv) (p < 0.01).
  
  
  CONCLUSIONS
  Iron sucrose-induced oxidative stress is comparable in HD patients with vitamin C deficiency and in those with normal vitamin C. We documented a pro-oxidative effect of vitamin C during Fe(iv)+C(iv) administration.
authors.affiliation: Department of Medicine I, Charles University, Medical School and Teaching Hospital Pilsen, Pilsen, Czech Republic. eiselt@fnplzen.cz
authors.forename: Jaromír
authors.initials: J
authors.lastname: Eiselt
authors.forename: Jaroslav
authors.initials: J
authors.lastname: Racek
authors.forename: Karel
authors.initials: K
authors.lastname: Opatrný
authors.forename: Ladislav
authors.initials: L
authors.lastname: Trefil
authors.forename: Pavel
authors.initials: P
authors.lastname: Stehlík
mesh_terms: D000284:Administration, Oral; D000368:Aged; D000975:Antioxidants / Q000008:administration & dosage / Q000032:analysis*; D001205:Ascorbic Acid / Q000008:administration & dosage / Q000097:blood*; D001206:Ascorbic Acid Deficiency / Q000097:blood* / Q000188:drug therapy / Q000209:etiology; D005260:Female; D005290:Ferric Compounds / Q000008:administration & dosage*; D000077605:Ferric Oxide, Saccharated; D005937:Glucaric Acid; D006801:Humans; D007262:Infusions, Intravenous; D015227:Lipid Peroxidation / Q000187:drug effects; D008297:Male; D008875:Middle Aged; D018384:Oxidative Stress / Q000187:drug effects*; D006435:Renal Dialysis / Q000009:adverse effects; D017392:Thiobarbituric Acid Reactive Substances / Q000032:analysis
chemical_list: D000975:Antioxidants; D005290:Ferric Compounds; D017392:Thiobarbituric Acid Reactive Substances; D000077605:Ferric Oxide, Saccharated; D001205:Ascorbic Acid; D005937:Glucaric Acid