Oral cadmium chloride intoxication in mice: effects of dose on tissue damage, intestinal absorption and relative organ distribution.

The acute toxicity of soluble cadmium salts has almost exclusively been studied experimentally after parenteral exposures, where acute mortality is caused by hepatic necrosis. This report describes an alternative experimental model using oral exposure. A single oral toxic dose of CdCl2 to mice induced toxic gastroenteritis; subsequent hepatic and renal lesions were also observed. Whole-body gamma-counting after a single oral toxic 109CdCl2 dose to mice showed a dose-dependent delay of the fecal excretion of non-absorbed cadmium. This delay was absent when a low, non-toxic dose was administered. This effect is most likely due to decreased peristalsis and, at higher doses, intestinal atony due to oral cadmium toxicity. After fecal elimination of non-absorbed cadmium, the residual body burden of cadmium expressed as percent of initial dose reflects the fractional intestinal cadmium absorption due to slow reexcretion of absorbed cadmium. The fractional absorption increased with increasing doses of cadmium. The relative cadmium deposition in brain, testes and intestines decreased with increasing dose, whereas the relative liver deposition increased with dose. The delayed fecal elimination and increased fractional absorption of cadmium may significantly contribute to the development of both local and systemic toxicity in oral cadmium intoxication.