Membrane potential dependence of Fe(III) uptake by mouse duodenum |
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Authors: | K B Raja R J Simpson T J Peters |
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Affiliation: | Department of Clinical Biochemistry, King's College School of Medicine and Dentistry, London, U.K. |
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Abstract: | Intestinal iron uptake by mouse duodenal fragments is inhibited in the absence of oxygen and glucose from the incubation medium and by a variety of metabolic inhibitors. The mechanism of energy coupling to iron uptake is, however, unclear. In vitro experiments using duodenal fragments showed Fe3+ uptake to be markedly inhibited, in a reversible fashion, by the replacement of incubation medium Na+ by K+. Addition of phloridzin to the medium failed to affect iron uptake, suggesting that the above effect was not a consequence of reduced glucose uptake. Substitution of Na+ by Rb+ also potently reduced duodenal iron uptake. Replacement of medium NaCl by either mannitol or choline chloride had no significant effect on Fe3+ uptake, thus excluding the possibility of the Fe3+ uptake process being Na+-dependent. Similar observations were made with duodenal fragments from animals with enhanced Fe3+ absorption, due to chronic hypoxia. Valinomycin (1-5 microM) increased the uptake of both glucose and Fe3+. Higher concentrations (22.5 microM) of the ionophore were inhibitory. In vivo studies (tied-off segments) using Rb+-containing medium confirmed the inhibitory effects of univalent cations on Fe3+ absorption. Enhanced absorption of Fe3+ was also demonstrable in vivo, with low concentrations of valinomycin and nigericin added to the luminal medium. These observations suggest that the Fe3+ uptake process may be dependent on the brush-border membrane potential. |
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