Molybdenum is an essential trace mineral in humans that forms a compound known as molybdopterin that is required as a cofactor for the metalloenzymes xanthine oxidase, xanthine dehydrogenase, sulphite oxidase and aldehyde oxidase. Deficiency has been recorded in only one case in the medial literature with the symptoms reversing upon administration of a molybdenum supplement. Genetic deficiency of molybdopterin also results in the same symptoms as dietary deficiency and include abnormalities in the metabolism of uric acid, xanthine and sulphite. Research (here) has estimated that the daily requirement of molybdenum is ≈25µg/d which appears to be easily achievable in a normal mixed diet. The UK RDA for molybdenum is set at 50µg/d which is based on studies modelling positive and negative molybdenum balance. Intakes of up to 1500µg/d appear to be non-toxic but when toxicity does occur it manifests as gout due to increase xanthine dehydrogenase activity.
Research1 has investigated the safety of molybdenum in a clinical study involving 4 healthy men who were fed molybdenum intakes of 22, 72, 121, 467 and 1490µg/d for 24 days each. Exercise was taken under supervision and subjects were fed a low molybdenum diet with a multivitamin tablet to standardise their nutrient intakes. The kinetics of molybdenum was assessed by feeding 100Mo and infusing 97Mo during the study and measuring the concentrations in faeces and urine. As the intake of molybdenum was increased, the excretion from urine increased, suggesting that molybdenum is conserved at lower intakes, that turnover is low and that excess molybdenum is excreted in the urine. The absorption of molybdenum was estimated to be ≈88 to 93% during the study with the most efficient absorption occurring at the highest intakes. No toxicity from molybdenum was detected even at the highest intakes
At the lowest intake of molybdenum, the faeces and urine accounted for 41% and 59% of the total molybdenum excretion, respectively. Faecal elimination dropped as intakes increased and urinary elimination increased such that at the highest intake faecal elimination was just 6% and urinary excretion was 94% of total. The data collected from the first 6 days showing a positive molybdenum balance suggested that the normal diet contained more than the 22 µg/d contained in the study. As the study progressed the excess molybdenum was excreted and molybdenum balance then became negative at the earlier, lower intakes. Molybdenum is well absorbed, possibly through passive means, which would explain the more efficient absorption at higher doses. Only 0.2 to 0.4% of the infused molybdenum was excreted into the faeces, suggesting that molybdenum flux through bile is not an important route of elimination.
RdB
