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Summary: Iron is a vital element for almost all living organisms. In mammals iron is taken by the intestinal epithelium, primarily in the duodenum. The initial step of absorption involves the reduction of ferric to ferrous iron both in gastric lumen and at the brush-border apical membrane. Reductase activity is increased by factors physiologically stimulating iron absorption, such as iron deficiency and chronic hypoxia. Ascorbic acid (Vitamin C) has long been known to enhance absorption of dietary iron in humans as shown by several nutritional/dietetic studies. This effect has been ascribed to lumenal reduction and solubilization of iron. Recent molecular cloning of the mammalian duodenal brush-border reductase activity has provided evidence that ascorbate may play an intracellular role in determining iron absorption rates. Previously, ascorbate concentrations have been determined in duodenum, but only in normal subjects and there is no evidence on how duodenal ascorbate alters in relation to intestinal iron absorption. The aim of this study is to examine mucosal and plasma levels of ascorbate and dehydroascorbate in normal subjects and patients with iron deficiency that is known to be a stimulator for iron absorption. Duodenal biopsies were homogenized in 5% metaphosphoric acid using single burst homogeniser. Tissue and plasma ascorbate levels were assayed by ferrozine spectrophotometric method. Blood was taken from each subject to assess the iron status. The analyses of human samples revealed increased duodenal (p <0.001, n = 20) and plasma (p <0.001, n = 6) ascorbate levels in patients with iron deficiency. These findings support an important intracellular role of ascorbic acid in human dietary iron absorption.

Duodenal mucosal and plasma ascorbate levels of patients with iron deficiency