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achieved in animals, despite major reduction in the activity of these molybdoenzymes. Rather, molybdenum essentiality is based on a genetic defect that prevents sulfite oxidase synthesis. Because sulfite is not oxidized to sulfate, severe neurological damage leading to early death occurs with this inborn error of metabolism (Johnson, 1997). Further support for an essential metabolic role for molybdenum relates to amino acid intolerance in a patient who received long-term total parenteral nutrition without molybdenum (Abumrad et al., 1981). The intolerance, which was probably due to abnormal sulfur amino acid metabolism, was reversed with intravenous repletion of ammonium molybdate.

Physiology of Absorption, Metabolism, and Excretion

The high efficiency of molybdenum absorption over an extensive range of intakes suggests that molybdenum absorption is a passive (nonmediated) process. The competitive inhibition of molybdenum uptake by sulfate that has been observed in rat intestines suggests a carrier may be involved. The mechanism of molybdenum absorption (transcellular or paracellular transport) and the location(s) within the gastrointestinal tract responsible for absorption have not been studied (Nielsen, 1999). Molybdenum concentrations in whole blood vary widely but average about 5 nmol/L (Versieck et al., 1978). Protein-bound molybdenum constitutes between 83 and 97 percent of the total molybdenum in erythrocytes. Potential plasma molybdenum transport proteins include α-macroglobulin. Molybdenum retention may be conserved in part through formation of the molybdopterin complex. Urinary excretion is a direct reflection of the dietary molybdenum intake level (Turnlund et al., 1995a, 1995b). Stable isotope studies showing molybdenum retention at low molybdenum intakes and rapid excretion at high intakes suggest that the kidney is the primary site of molybdenum homeostatic regulation. However, widely different oral test doses of molybdenum, between 22 and 1,490 μg/day, resulted in only a small difference in absorption of 88 and 93 percent, respectively. The source of fecal molybdenum is not clear, but could include biliary molybdenum (Nielsen, 1999).

Clinical Effects of Inadequate Intake

Molybdenum deficiency has not been observed in healthy people. A severe metabolic defect, molybdenum cofactor deficiency, had been identified in 47 patients by 1993. The disease results in defi-



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