Impairment of microsomal calcium sequestration activity upon superoxide dismutase depletion in rat liver.

We have studied the Ca2+-accumulation activity of microsomal vesicles isolated from the liver of rats held for from 2 to 8 weeks on a copper-deficient diet. With this treatment that deeply modifies fatty acid composition, microsomal membranes show progressively lower Ca2+ sequestration. The activity can be fully restored upon physiological copper supply to the depleted animals. The determination of kinetic parameters of microsomal Ca2+ uptake shows that copper deficiency affects mainly the apparent velocity, leaving unaffected the apparent affinity of the pump for Ca2+. Many similarities were found between this model and the Morris hepatomas with different growth rate. The data support the hypothesis that the oxidative stress imposed on the cell by the loss of superoxide dismutase can influence many cell features, with different implications in the regulation of several biological and biochemical functions.