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Effect of Lead Ingestion on Functions of Vitamin D and its Metabolites¹

Connie M. Smith^*, Hector F. DeLuca^*, Yoko Tanaka^* and Kathryn R. Mahaffey

^* Department of Biochemistry, College of Agricultural and Life Sciences, University of Wisconsin-Madison, Madison, WI 53706 Division of Nutrition, Food and Drug Administration, 1090 Tusculum Ave., Cincinnati, OH 45226

A study of the effect of ingestion of lead on the metabolism and function of vitamin D was carried out in rats fed diets varying in calcium and phosphorus content. The ingestion of 0.82% lead as lead acetate suppressed plasma levels of 1,25-dihydroxycholecalciferol in rats fed either a low phosphorus or a low calcium diet while it had no effect on this parameter in rats fed either a high calcium diet or a normal phosphorus diet. Most important, the ingestion of lead totally blocked the intestinal calcium transport response to cholecalciferol, 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol. On the other hand, the ingestion of lead acetate had no influence on the mobilization of calcium from bone, the elevation of serum inorganic phosphorus and in the mineralization of rachitic bone in the same animals. Thus by the feeding of 0.82% lead as the acetate, the physiologic responses to vitamin D and its metabolites in intestine and bone could be separated. Although the effect of 0.82% lead on the intestinal responses to vitamin D and its metabolites was greatest in animals fed a low calcium or a low phosphorus diet, it was present with all diets tested.

KEY WORDS: • lead • vitamin D • cholecalciferol

¹ Supported in part by FDA contract no. RFP 223-77-2166, program project grant no. AM-14881 from the National Institutes of Health and the Harry Steenbock Research Fund of the Wisconsin Alumni Research Foundation.

Manuscript received 13 January 1981.

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