1887

Abstract

Zn uptake by was biphasic. The first phase was independent of metabolic energy, consisting of adsorption to the cell surface, and followed a Freundlich isotherm. The second phase was dependent on metabolic energy, ATPase activity and the transmembrane proton gradient, and consisted of uptake into the cell. Energy-dependent uptake showed Michaelis-Menten kinetics with a of 3·7μ-Zn and a of 1·6 nmol min per 10 cells at Zn concentrations below 80 μm but deviated at higher concentrations. K and Mg inhibited energy-dependent Zn uptake while Na and Ca did not. The effect of heavy metals was complex and included both inhibition and stimulation of Zn uptake. K efflux accompanied Zn uptake at all Zn concentrations but there was no simple stoichiometric relationship between the two. Toxic effects of Zn such as inhibition of H efflux and K uptake and reduction of viability were observed at all Zn concentrations and toxicity appeared to be a major factor in K efflux. Toxicity also affected the kinetics of Zn uptake, being a major cause of deviation from Michaelis-Menten kinetics. Zn was compartmented within the cell: 56 % of the total intracellular pool was in the soluble vacuolar fraction, 39 % was bound to insoluble components and only 5 % was found in the cytosol. Isolated yeast vacuoles possessed an ATP-dependent Zn uptake system whose properties were consistent with a Zn/H antiport.

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1987-03-01
2022-01-17
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