Abstract
Intravenous administration of 63Ni 2+ (as 63NiCl 2) together with potassium ethylxanthate resulted in highly increased levels of 63Ni 2+ in several tissues of mice in comparison with animals given 63Ni 2+ alone. However, this effect was not observed when 63Ni 2+ and potassium ethylxanthate were given orally. Sodium diethyldithiocarbamate was active in increasing 63Ni 2+ concentrations after both intravenous and oral administration. Both ethylxanthate and diethylthiocarbamate can form highly lipophilic complexes with nickel and a facilitated penetration of these complexes through the cellular membranes of the tissues probably explains the increased uptake of the metal. Xanthates are unstable at acid pH and degradation in the acid milieu of the stomach probably underlies the lack of effect at oral administration.
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