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

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. This prompted the present study in which the effects of vitamin D deficiency on Cd intoxication were investigated in ovariectomized (OX) female rats. The effects of vitamin D deficiency on cadmium (Cd) intoxication were investigated in ovariectomized (OX) female rats. We administrated a low concentration of Cd chloride intravenously to OX female rats that were fed a vitamin D deficient diet (< 0.3 IU/g) or a normal diet (3 IU/g) 5 days a week for up to 50 weeks. The vitamin D deficient diet decreased serum concentrations of active and inactive forms of vitamin D, but did not affect the metabolism of the kidney or bone. Cd treatment alone induced a decrease in serum concentrations of vitamin D as well as renal dysfunction, renal anemia and abnormal bone metabolism. Osteoporosis with osteomalacia, tubular nephropathy, fibrous osteitis 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 IID by itself, but enhanced the toxicity of Cd in regard to osteoporosis with osteomalacia, renal tubular nephropathy and renal anemia.