The Effects of a Vitamin D-deficient Diet on Chronic Cadmium Exposure in Rats

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Itai-itai disease (IID) of humans is one of the most severe forms of chronic Cadmium (Cd) intoxication occurring mainly in post-menopausal women and is characterized by osteoporosis with osteomalacia, renal tubular disorder, and renal anemia. Some researchers insist the major cause of IID is not Cd but malnutrition, especially hypovitaminosis D. We administrated a low concentration of Cd chloride intravenously to OX female rats that were fed a vitamin D deficient diet or a normal diet for 50 weeks. The vitamin D deficient diet decreased serum concentration of vitamin D, but did not affect the metabolism of the kidney or bone. Cd treatment alone induced a decrease in serum concentration of vitamin D as well as renal dysfunction, renal anemia and abnormal bone metabolism. Osteoporosis with osteomalacia, tubular nephropathy, fibrous osteodystrophy and bone marrow hyperplasia occurred following Cd treatment. In rats treated with Cd and administered a vitamin D deficient diet, the toxic effects of Cd on kidney, bone and hematopoiesis were enhanced in comparison to rats treated with the Cd and a normal diet. The present experiment demonstrated that hypovitaminosis D did not evoke morphologic features of IID in humans but did enhance the Cd-induced toxicity in the rat model of this disease.
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