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Dietary Iron Levels and Hypoxia Independently affect Iron Absorption in Mice^1,2,

Department of Clinical Biochemistry, King's College School of Medicine and Dentistry, London SE5 9PJ UK

The effect of dietary iron levels on the hypoxic response of iron absorption was investigated by feeding mice diets of different iron composition and determining iron absorption. Eight groups of mice were fed a purified diet consisting of casein, corn oil and sucrose with vitamins and iron-free mineral supplements. Groups A–D were fed a nonpurified diet until 6 wk old and then switched to purified diet for 4 d. Groups E–H were fed purified diet for 4 wk from weaning. Groups C, D, G and H were exposed to hypoxia (53.3 kPa) for the last 3 d of the study. Groups A, C, E and G received the low iron purified diet (<1 mg iron per kg); the other groups received the same diet supplemented with 62 mg/kg iron as FeCl₃·6H₂O. Hypoxic exposure raised iron absorption (P < 0.001) by a similar proportion (2.5- to 5.0-fold) in all mice but did not affect duodenal nonheme iron levels. Low iron diet feeding raised iron absorption but reduced duodenal and liver nonheme iron levels. In a second experiment, mice fed nonpurified diet were divided into four groups and exposed to normal atmosphere or hypoxia (53.3 kPa) with or without dosing with 100 µg iron by stomach tube 1 h before determining iron absorption. There was no effect of iron dosing on iron absorption at either pressure. The data suggest that the control of iron absorption by tissue oxygen acts through a mechanism independent of the control exerted by dietary or mucosal iron levels.

KEY WORDS: • mice • iron deficiency • iron • intestinal absorption • dietary iron

¹ This is a contribution from the King's College Centre for the Study of Metals in Biology and Medicine.

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 reprint requests should be addressed at Department of Clinical Biochemistry, King's College School of Medicine and Dentistry, Bessemer Rd., London SE5 9PJ UK.

Manuscript received 6 December 1995. Revision accepted 3 April 1996.

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