Abstract
One and 24 h after the administration of 63NiCl2 and 63Ni(CO)4 to mice, 63Ni was present in association with both particulate and soluble cellular constituents in the lung, liver and kidney. After disruption of the cellular organeles by sonication, a considerable part of the 63Ni was still bound to the cellular fragments. Sephadex G-75 chromatography of the cytosol of the lung showed that the largest proportion of 63Ni was eluted in the void volume and a smaller proportion was present in the salt volume. In the kidney, the proportions were reversed. Twenty-four h after the injection of 63NiCl2, an intermediate 63Ni-containing peak, with an estimated MW of .apprx. 30,000, was found in the lung and the kidney. In the liver of 63NiCl2-injected mice, most of the Ni was recovered in the void volume, a lesser amount in the salt volume. There was no evidence that 63Ni was bound to metallothionein (induced by Cd-pretreatment) or to superoxide dismutase in the studied tissues. Pretreatments with non-labeled NiCl2 did not alter the elution profiles. In serum, most 63Ni was present in association with albumin. Gel-chromatograms of red blood-cell hemolysates from 63Ni(CO)4-injected mice showed 63Ni at an elution volume corresponding to Hb, but 63Ni-binding ligands with higher and lower MW were also present.

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