Xanthine oxidase is an enzyme that metabolizes nitrogen compounds called purines. It is produced in the liver and can be released into the blood when the liver is damaged. A deficiency of XO can lead to xanthinuria, while overactivity can cause hyperuricemia. XO inhibitors are prescribed to avoid gout, kidney stones, and kidney failure.
Xanthine oxidase (XO or XOA) is an enzyme that catalyzes the chain reactions of oxidizing hypoxanthine to xanthine and oxidizing xanthine to uric acid and hydrogen peroxide (H2O2). Oxidation requires the addition of oxygen and water. This process is important because it explains how humans can metabolize nitrogen compounds called purines.
When xanthine oxidase, a type of xanthine oxidoreductase (XOR), undergoes a reversible process called sulfhydryl oxidation, it becomes xanthine dehydrogenase. In the sulfhydryl oxidation, a sulfur-containing organic compound is used instead of water. Xanthine dehydrogenase can also catalyze the oxidation of purines. Substrates for this enzyme include xanthine, nicotinamide adenine dinucleotide, and water.
As an enzyme, xanthine oxidase is classified as a protein. It is mainly produced and found in the liver. When the liver is damaged, liver cells release xanthine oxidase into the blood. Therefore, when a doctor suspects that a patient has a liver problem, a blood test for this enzyme may be ordered.
The molecular weight of this enzyme is 270,000 units. Its catalytic action is due to the presence of two molybdenum atoms, eight iron atoms and two flavin molecules. It contains the metals molybdenum and iron, so xanthine oxidase is also classified in the group of metalloproteins.
A deficiency of XO or its relatives can lead to a condition called xanthinuria. When this enzyme is missing, xanthine accumulates in the blood. High unresolved xanthine concentrations can eventually overload the kidneys and lead to kidney failure. This condition does not yet have a definitive treatment. However, affected people are advised to avoid foods high in purines, such as meat and pulses, and to drink plenty of water to support the kidneys.
Alternatively, a person could have insufficient xanthine oxidase due to molybdenum or iron mineral deficiencies. In this case, nutritional supplementation is usually implemented. Molybdenum can be administered in the form of sodium molybdate or ammonia molybdate. Iron can be supplied in the form of iron compounds, such as ferrous sulfate and ferrous gluconate.
When a person consumes too many purines or when the body’s xanthine oxidase is overactive, excessive levels of uric acid can be produced, leading to a condition called hyperuricemia. Too much uric acid in the body can lead to gout, kidney stones, and kidney failure. To avoid these consequences, people with hyperuricemia are advised to reduce their intake of purine-rich foods and are prescribed XO inhibitors. Examples of XO inhibitors are allopurinol, oxipurinol and febuxostat.
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