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  • 1 Friedrich Schiller University of Jena Institute of Nutrition and Environment Dornburger Str. 24 D-07743 Jena Germany
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In animals and man, molybdenum has been recognized as an essential component of the enzymes xanthine oxidase, aldehyde oxidase and sulphite oxidase. Nutritional molybdenum deficiencies in animals have been produced in experiments with goats and a molybdenum-poor diet (growth depression, decrease in conception rate, poor foetal survival rate). In practice, the molybdenum supply to animals and humans meets the requirements (animals < 100 μg kg −1 /feed dry matter, man 25 μg/day). The essentiality of molybdenum and sulphite oxidase in man was documented by more than 100 patients who lacked the enzyme function, either as the result of a defect in genetic coding, or of a genetic deficiency in the molybdenum cofactor and a molybdenum deficiency during parenteral nutrition.Molybdenum toxicity (molybdenosis) in animals primarily affects ruminants (cattle). It is manifested by diarrhea, anorexia, depigmentation of hair, neurological disturbances and premature death. Molybdenum interacts with copper, and some symptoms of molybdenum toxicity are similar to those of copper deficiency. Only few data are available concerning toxicity to humans.

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