Nickel mobilization by sodium diethyldithiocarbamate in nickel-carbonyl-treated mice.

Whole-body autoradiography and liquid scintillation counting were used to study the effect of sodium diethyldithiocarbamate on the tissue disposition of 63nickel in mice exposed to 63nickel carbonyl by inhalation or intraperitoneally. The sodium diethyldithiocarbamate markedly affected the disposition of the 63nickel in several tissues. Diethyldithiocarbamate forms lipophilic chelates with many metals, including nickel, and the mobilization of the 63nickel is probably due to a redistribution in the tissues of the complex formed. In the lung--the principal target tissue for nickel carbonyl--a decrease was observed, and this may be the reason for the beneficial effect of sodium diethyldithiocarbamate in nickel carbonyl intoxications. In mice which were exposed to 63nickel carbonyl by inhalation, the level of 63nickel in the brain was very high and the sodium diethyldithiocarbamate reduced this labelling. Intraperitoneal injections of 63nickel carbonyl resulted in a low labelling of the brain, and in this instance an increased brain radioactivity was induced by the sodium diethyldithiocarbamate. This observation can probably be explained by an affinity of the lipophilic nickel-diethyldithiocarbamate complex for the lipid-rich brain tissue.