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Abstract
The aim of this study was to determine the bioavailability and adverse effects of cadmium (Cd) and copper (Cu) on hibernating Egyptian toads and whether ascorbic acid (vitamin C) blocked Cd- and Cu-induced effects during hibernation. The oxidative status of liver, kidney, and intestine of Bufo regularis to Cd, Cu, and/or a combination of both metals administered orally for 2 weeks was determined. In the protection studies, vitamin C was given for 1 h prior to administration of Cu, Cd, and/or metal combination for 2 weeks. Treatment with Cu, Cd, and a combination of both metals produced a reduction in red blood count cells and hemoglobin content, while white blood count cells showed an increase in numbers during these treatments. After 2 weeks exposure, Cd and Cu increased significantly in all the tissues studied. Cu storage presented the following sequence: liver > intestine > kidney. Cd storage presented the following sequence: intestine > kidney > liver. When exposed to both metals, Cu and Cd storage presented the following sequence: liver > intestine > kidney. Histopathological examination of the liver revealed marked alterations including loss of hepatic cell architecture, and some cells exhibited distinct cytoplasmic vacuoles. The majority of blood vessels exhibited a marked dilatation and congestion with infiltration of blood cells, prominent hyperemia of hepatic veins, and significant proliferation of bile ductules. Histopathological changes in the kidney showed destruction and degeneration of both renal tubule cells and glomerular with infiltration of leukocytes and inflammatory cells. Histopathological alterations in the intestine were restricted to the innermost mucosal epithelium with marked degeneration of the villi and submucosa and an extensive fragmentation of mucosal epithelium as well as atrophy of goblet cells. The administration of vitamin C 1 h prior to administration of Cd, Cu, and metal combination did not protect against hepatic, renal, and intestinal damage. However, parental vitamin C given alone increased tissue toxicity.