Vanadium Pentoxide V2O5 manufacturers--Benren Alloy Co.Ltd

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Molybdenum is a constituent of the enzymes xanthine oxidase, sulfite oxidase, and aldehyde oxidase. Among other reactions, xanthine oxidase catalyzes conversion of xanthine and hypoxanthine to uric acid; sulfite oxidase converts sulfite to sulfate; and aldehyde oxidase detoxifies a variety of harmful organic molecules (such as aldehydes into acids
In animals, diet induced molybdenum deficiency has been produced experimentally with tungstate(tungstate trioxide,tungstic acid ). The deficiency symptoms are characterized by decreased weight gain, food consumption, and life expectancy and deranged microbiological processes in the rumen. Renal xanthine calculi have been reported in sheep grazing on low-molybdenum pasture
In humans, molybdenum deficiency resulting from prolonged TPN support has been reported in literature. The deficiency syndrome included tachycardia, tachypnea, headache, night blindness, nausea, vomiting, central scotomas, culminating in generalized edema, lethargy, disorientation, and coma. The biochemical changes associated with the syndrome were: hypermethioninemia, hypouricemia, hypouricosuria, low urinary excretion of inorganic sulfate and elevated urinary excretion of Thiosulfate. Supplementation of TPN solutions with Molybdenum has been reported to alleviate the symptoms and normalize the biochemical abnormalities.
This product contains aluminum that may be toxic. Aluminum may reach toxic levels with prolonged parenteral administration if kidney function is impaired. Premature neonates are particularly at risk because their kidneys are immature, and they require large amounts of calcium and phosphate solutions, which contain aluminum.
As molybdenum is excreted in urine and bile, Molybdenum supplements may need to be adjusted, reduced, or omitted in renal dysfunction and bile duct obstruction.

Molybdenum metabolism has been reported to be inversely related to copper, sulfate ions, tungsten, methionine, and cysteine.