My project was a mechanistic study to determine the disposition and toxicity effects of Cadmium on wild-type and Bcrp-null mice following acute exposure. Tissues were analyzed after 24 hours post administration of 5.5 mg/kg CdCl2 to confirm what is stated in the literature. Indeed, loss of the bcrp transporter in mice led to an increase in hepatic and renal cadmium accumulation and to an enhancement in expression of stress- and injury-related genes.