title: Duodenal ascorbate and ferric reductase in human iron deficiency.
abstract: BACKGROUND
  The first step in iron absorption requires the reduction of ferric iron to ferrous iron, a change that is catalyzed by duodenal ferric reductase. Iron deficiency is associated with high iron absorption, high ferric reductase activity, and high duodenal ascorbate concentrations in experimental animals, but it is not known whether a relation between reductase and ascorbate is evident in humans.
  
  
  OBJECTIVE
  The objective of the study was to assess the relation between ferric reductase activity in human duodenal biopsy specimens and ascorbate concentrations in iron-replete and iron-deficient subjects.
  
  
  METHODS
  Patients and control subjects were overnight-fasted adults presenting sequentially for upper gastrointestinal endoscopic investigation. Ferric reductase activity in duodenal biopsy specimens was assayed by using nitroblue tetrazolium. Ascorbate was assayed in duodenal biopsy specimens and plasma.
  
  
  RESULTS
  Iron-deficient patients had significantly higher reductase activity (n = 6-9; P < 0.05) and duodenal (n = 20; P < 0.001) and plasma (n = 6; P < 0.001) ascorbate concentrations than did control subjects. Incubation of biopsy specimens with dehydroascorbate (to boost cellular ascorbate) increased reductase activity in the tissues that initially had normal activity (n = 9; P < 0.01) but inhibited reductase activity in the tissues that already had high reductase activity (n = 13; P < 0.001).
  
  
  CONCLUSIONS
  Iron deficiency in humans is associated with increased duodenal ascorbate concentrations. This finding suggests that increased reductase activity is partly due to an increase in this substrate for duodenal cytochrome b reductase 1.
authors.affiliation: Department of Clinical Laboratory and Clinical Immunology, Medical University, Sofia, Bulgaria.
authors.forename: Bisera D
authors.initials: BD
authors.lastname: Atanasova
authors.forename: Andy Cy
authors.initials: AC
authors.lastname: Li
authors.forename: Ingvar
authors.initials: I
authors.lastname: Bjarnason
authors.forename: Kamen N
authors.initials: KN
authors.lastname: Tzatchev
authors.forename: Robert J
authors.initials: RJ
authors.lastname: Simpson
mesh_terms: D000328:Adult; D000368:Aged; D000975:Antioxidants / Q000378:metabolism; D001205:Ascorbic Acid / Q000097:blood*; D016022:Case-Control Studies; D004386:Duodenum / Q000201:enzymology* / Q000473:pathology; D038181:FMN Reductase / Q000378:metabolism* / Q000502:physiology; D005260:Female; D006801:Humans; D007408:Intestinal Absorption; D007501:Iron / Q000493:pharmacokinetics; D000090463:Iron Deficiencies; D008297:Male; D008875:Middle Aged
chemical_list: D000975:Antioxidants; D007501:Iron; D038181:FMN Reductase; C023903:ferric citrate iron reductase; D001205:Ascorbic Acid