Loading…
Oral ferrous sulfate supplements increase the free radical-generating capacity of feces from healthy volunteers
Most dietary iron remains unabsorbed and hence may be available to participate in Fenton-driven free radical generation in conjunction with the colonic microflora, leading to the production of carcinogens or direct damage to colonocytes. Our aims were to measure the proportion of fecal iron availabl...
Saved in:
Published in: | The American journal of clinical nutrition 1999-02, Vol.69 (2), p.250 |
---|---|
Main Authors: | , , , |
Format: | Article |
Language: | English |
Subjects: | |
Online Access: | Get full text |
Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
Summary: | Most dietary iron remains unabsorbed and hence may be available to participate in Fenton-driven free radical generation in conjunction with the colonic microflora, leading to the production of carcinogens or direct damage to colonocytes.
Our aims were to measure the proportion of fecal iron available to participate in free radical generation and to determine the effect of an oral supplement of ferrous sulfate on free radical generation.
Eighteen healthy volunteers recorded their food intake and collected fecal samples before, during, and after 2 wk of supplementation (19 mg elemental Fe/d). Total, free, and weakly chelated fecal iron were measured and free radical production was determined by using an in vitro assay with dimethyl sulfoxide as a free radical trap.
Fecal iron increased significantly during the period of supplementation and returned to baseline within 2 wk. The concentration of weakly bound iron in feces (approximately 1.3% of total fecal iron) increased from 60 micromol/L before to 300 micromol/L during supplementation, and the production of free radicals increased significantly (approximately 40%). Higher-carbohydrate diets were associated with reduced free radical generation.
Unabsorbed dietary iron may increase free radical production in the colon to a level that could cause mucosal cell damage or increased production of carcinogens. |
---|---|
ISSN: | 0002-9165 1938-3207 |