Zinc cellular traffic: physiopathological considerations

Zinc cellular traffic is reviewed in both influx and efflux stages. Zinc influx happens through three different modalities: 1) anionic exchange channels, with the metal cotransported in complex form with anions, often as anionic monovalent complex (Zn [HCO3)2Cl]. Bicarbonate-ions, chloro-ions and thiocyanate-ions can stimulate zinc << uptake >>, while phosphate and sulphate-ions are inhibitory. 2) facilitated diffusion through amino acids which, by passing into cells, carry zinc (particularly cysteine and histidine) with them. 3) transferrin receptor route, very important for cellular uptake of iron and zinc. Various mitogenic factors cause increased synthesis of transferrin receptors and increase of metal uptake. Zinc efflux happens through zinc/calcium exchange (zinc efflux coupled with calcium influx). Calcium is then expelled from cells by means of calcium pump (with energy consumption), regulated by membrane Ca-ATPase. Impairment of this ionic exchange process may cause an intracellular accumulation (as may be seen in SHR rats).