Physiological transport of zinc

Aiken, Simon Piers (1989) Physiological transport of zinc. University of Southampton, Doctoral Thesis.

Abstract

The form of zinc that is transported into cells has not yet been identified. The hypothesis that zinc may be transported as a zinc-hisitidine complex has been examined. Uptake of 65-Zn was studied in vitro using rate erythrocytes. Uptake was stimulated by L-histidine (500μM-10mM), but D-histidine inhibited uptake. The effect of L-histidine was sodium-dependent and temperature-dependent, but was DIDS-insensitive. These results are consistent with histidine-linked zinc transport. Another zinc-binding amino acid, L-cysteine, inhibited uptake. Uptake was not affected by L-alanine (100μM-10mM). L-hisitdine also stimulated efflux of 65-Zn from erythrocytes. The distribution of 65-Zn was studied in vivo using rats infused with L-histidine. Infusion for 6 hours (plasma concentrations 2-3.5mM), beginning 48 hours after 65-Zn administration, did not alter activities of 65-Zn in a variety of tissues. However, 65-Zn activity in liver was higher than for control rats. Tissue activity per unit weight (as a proportion of the injected dose) was increased in ileum, skin, bone and muscle from rats injected intravenously during L-histidine infusion. Tissue activity in erythrocytes, liver, spleen and brain was decreased by L-histidine. Infusion of D-histidine produced the same effects. Therefore, these in vivo results do not support the hypothesis of histidine-linked zinc transport. The results show that histidine can affect zinc distribution in animals. However, the mechanism is unclear. Calculation of ionic zinc concentrations in infused rats suggested that ionic zinc transport was not a likely explanation for the in vivo results. It is suggested that some other form of zinc may be transported into tissues. The alteration of zinc status by histidine in humans is discussed, with particular reference to disturbances of zinc physiology during pregnancy.

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