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Endocrinology. Molybdenum deficiency refers to the clinical consequences of inadequate intake of molybdenum in the diet. The amount of molybdenum required is relatively small, and molybdenum deficiency usually does not occur in natural settings. [1] However, it can occur in individuals receiving parenteral nutrition. [2][3]
Molybdenum deficiency symptoms in most plants are associated with a build-up of nitrate in the affected plant part. This is a result of poor nitrate reductase activity. Symptoms include: [ 1][ 2] premature germination of maize grain. In legumes, inhibition of N 2 fixation may lead to pale, yellowing, nitrogen-deficient plants.
Since pure molybdenum deficiency from this cause occurs primarily in adults, the neurological consequences are not as marked as in cases of congenital cofactor deficiency. [104] A congenital molybdenum cofactor deficiency disease, seen in infants, is an inability to synthesize molybdenum cofactor, the heterocyclic molecule discussed above that ...
Since pure molybdenum deficiency from this cause occurs primarily in adults, the neurological consequences are not as marked as in cases of congenital cofactor deficiency. [28] A congenital molybdenum cofactor deficiency disease, seen in infants, is an inability to synthesize molybdenum cofactor, the heterocyclic molecule discussed above that ...
Molybdenum cofactor deficiency is a rare human disease in which the absence of molybdopterin – and consequently its molybdenum complex, commonly called molybdenum cofactor – leads to accumulation of toxic levels of sulphite and neurological damage. Usually this leads to death within months of birth, due to the lack of active sulfite oxidase.
Molybdenum is part of the nitrate reductase enzyme (needed for the reduction of nitrate) and the nitrogenase enzyme (required for biological nitrogen fixation). [10] Reduced productivity as a result of molybdenum deficiency is usually associated with the reduced activity of one or more of these enzymes.
For example, legumes host molybdenum-containing nitrogenase, but animals do not. Many animals rely on hemoglobin (Fe) for oxygen transport, but plants do not. Fertilizers are often tailored to address mineral deficiencies in particular soils. Examples include molybdenum deficiency, manganese deficiency, zinc deficiency, and so on.
Type I xanthinuria can be caused by a deficiency of xanthine oxidase, which is an enzyme necessary for converting xanthine to uric acid. [2] Type II xanthinuria and molybdenum cofactor deficiency lack one or two other enzyme activities in addition to xanthine oxidase. [3]