Abstract
Arsenic, mercury, and thallium all inhibited the pulmonary excretion of volatile selenium compounds by rats injected with subacute doses of sodium selenite. Lead had no effect on selenium volatilization. Mercury increased the retention of selenium in the blood, kidneys, and spleen; thallium increased the retention of selenium in the kidneys and liver. The biliary excretion of selenium was stimulated severalfold by the administration of arsenic, but not by mercury, thallium, or lead. Arsenic improved the growth of rats chronically poisoned by selenium, largely prevented the liver damage caused by selenium, and decreased the amount of selenium retained in the tissues. Neither thallium nor mercury protected against chronic selenosis.
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