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Nutrient Physiology, Metabolism, and Nutrient-Nutrient Interactions

Bioactive Dietary Polyphenolic Compounds Reduce Nonheme Iron Transport across Human Intestinal Cell Monolayers^1,2

³ Department of Nutritional Sciences, Pennsylvania State University, University Park, PA 16802 and ⁴ Nutrition and Metabolism Center, Children's Hospital, Oakland Research Institute, Oakland, CA 94609

There is persuasive epidemiological evidence that regular intake of dietary bioactive polyphenolic compounds promotes human health. Because dietary polyphenolic compounds have a wide range of effects in vivo and vitro, including chelation of metals such as iron, it is prudent to test whether the regular consumption of bioactive polyphenolic components impair the utilization of dietary iron. We examined the influence of the dietary polyphenols (-) -epigallocatechin-3-gallate (EGCG) and grape seed extract (GSE) on transepithelial iron transport in Caco-2 intestinal cells. The range of EGCG and GSE concentrations used in this study was within physiological levels and did not affect the integrity of differentiated Caco-2 cell monolayers. Both EGCG and GSE decreased (P < 0.001) transepithelial iron transport. However, apical iron uptake was increased (P < 0.001) by the addition of EGCG and GSE. The increased uptake of iron might be due in part to the reducing activity of EGCG and GSE. Both EGCG and GSE reduced 15% of the applied Fe³⁺ to Fe²⁺ in the uptake buffer. Despite the increased cellular levels of ⁵⁵Fe, the transfer of iron across the basolateral membrane of the enterocyte was extremely low, indicating that basolateral exit via ferroportin-1 was impaired, possibly through formation of a nontransportable polyphenol-iron complex. Our data show that polyphenols inhibit nonheme iron absorption by reducing basolateral iron exit rather than by decreasing apical iron import in intestinal cells.

^* To whom correspondence should be addressed. E-mail: ouh1{at}psu.edu.

Manuscript received 22 February 2008. Initial review completed 30 April 2008. Revision accepted 9 July 2008.