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Iron Status Affects Aluminum Uptake and Transport by Caco-2 Cells^1,2,

Department of Medicine and Center for Excellence in Cancer Research, Louisiana State University Medical Center, Shreveport, LA 71130

To study the cell biology of aluminum uptake and transport in intestinal epithelia, an in vitro system based on intestine-derived Caco-2 cells grown in bicameral chambers was used. Aluminum was offered on the apical surface of Caco-2 cell monolayers as either aluminum citrate, aluminum lactate or aluminum nitrilotriacetate at 1:2 molar ratios, and the aluminum uptake into the cells and transport into the basal chamber were measured. The kinetics of cellular uptake of aluminum were different for the three chelators, although with all three chelators a final cellular concentration of 50 nmol/mg cell protein was achieved. The total transport of aluminum into the basal chamber was greater for aluminum citrate and aluminum nitrilotriacetate than for aluminum lactate, suggesting that the chelator may direct aluminum into compartments from which aluminum is more easily transported. The iron status of the Caco-2 cells significantly affected both cellular uptake and transport of aluminum. Both irondepleted and iron-overloaded cells exhibited significantly lower aluminum transport than cells of normal iron status. Aluminum loading of the Caco-2 cells had adverse effects on ⁵⁹Fe²⁺ and ⁵⁹Fe³⁺ transport compared with that of normal cells. These findings suggest that the Caco-2 cell line grown in bicameral chambers provides a model for studying aluminum transport, that aluminum uptake and transport to the basal chamber were affected by the chelator used, and that aluminum uptake and transport pathways are similar to those of iron.

KEY WORDS: • intestine • aluminum • iron • transport • Caco-2 cells

¹ Supported in part by grants DK-41279 from the National Institutes of Health, the Center for Excellence in Cancer Research, Treatment and Education, Louisiana State University Medical Center, the American Cancer Society Institutional Research Grant 171-B, and Widener University, Chester, PA.

² The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

³ To whom correspondence and reprint requests should be addressed.

⁴ Current address: Department of Biology, Widener University, Chester, PA 19013.

Manuscript received 23 July 1993. Revision accepted 9 March 1994.

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