HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Atanasova, B. D Articles by Simpson, R. J Search for Related Content PubMed PubMed Citation Articles by Atanasova, B. D Articles by Simpson, R. J Agricola Articles by Atanasova, B. D Articles by Simpson, R. J

Duodenal ascorbate and ferric reductase in human iron deficiency^1,2,3

¹ From the Department of Clinical Laboratory and Clinical Immunology, Medical University, Sofia, Bulgaria; the Division of Life Sciences, King's College London, London; the Gastrointestinal Laboratory, The Rayne Institute, St Thomas' Hospital, London; and the Department of Medicine, GKT School of Medicine, King's College, London

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.

Design: 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.

Key Words: Iron absorption • iron nutrition • vitamin C

This article has been cited by other articles:

				G. O. Latunde-Dada, R. J. Simpson, and A. T. McKie Duodenal Cytochrome B Expression Stimulates Iron Uptake by Human Intestinal Epithelial Cells J. Nutr., June 1, 2008; 138(6): 991 - 995. [Abstract] [Full Text] [PDF]