Molybdenum is not reported in healthy humans but deficiency has been observed in patients undergoing prolonged total parental nutrition.
As molybdenum functions only in the form of the molybdenum cofactor in humans, any disturbance of molybdenum cofactor metabolism can disrupt the function of all molybdoenzymes.
Molybdenum enzymes play an important role in catalyzing redox reactions that characteristically involve oxygen transfer.
In this case there is a deficiency of three enzymes namely sulphite oxidase, xanthine oxidase and aldehydes oxidase.
The disorder is genetically inherited from the parents in an autosomal recessive fashion.
Individuals suffering from molybdenum cofactor deficiency only exhibit sulfite oxidase deficiency.
Excess amount of sulfites are toxic to the nervous system, and consequently signs of molybdenum deficiency caused by this are headache, rapid breathing and heart rate, nausea and vomiting, acute asthma attacks, visual problems, disorientation, and finally coma.
Deficiency of molybdenum
