Xanthine oxidase (XO or XOA) is an enzyme that catalyzes the chain reactions of hypoxanthine oxidizing to xanthine and xanthine oxidizing to uric acid and hydrogen peroxide (H2O2). Oxidation requires the addition of oxygen and water. This process is important because it explains how humans are able to metabolize nitrogen compounds called purines.
When xanthine oxidase, a type of xanthine oxidoreductase (XOR), undergoes a reversible process called sulfhydryl oxidation, it becomes converted to xanthine dehydrogenase. In sulfhydryl oxidation, a sulfur-containing organic compound is used rather than water. Xanthine dehydrogenase is also able to catalyze the oxidation of purines. The 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 located in the liver. When the liver is damaged, the hepatic cells release xanthine oxidase into the blood. Therefore, when a doctor suspects that a patient has a liver problem, a blood assay for this enzyme might be requested.
This enzyme’s molecular weight is 270,000 units. Its catalytic action is because of 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 under the group of metalloproteins.
A deficiency of XO or its relatives can lead to a condition called xanthinuria. When this enzyme is lacking, xanthine accumulates in the blood. Unresolved high concentrations of xanthine can eventually overload the kidneys and result in kidney failure. This condition has no definite treatment yet. People who are affected, however, are advised to forego high-purine foods, such as meat and legumes, and to drink lots of water to help the kidneys.
Alternatively, a person might have insufficient xanthine oxidase because of molybdenum or iron mineral deficiencies. In this case, nutritional supplementation is usually implemented. Molybdenum can be delivered in the form of sodium molybdate or ammonia molybdate. Iron can be delivered in the form of iron compounds, such as ferrous sulfate and ferrous gluconate.
When a person consumes too much 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 renal failure. To avoid these consequences, people who have hyperuricemia are advised to cut down their intake of purine-rich foods and are prescribed XO inhibitors. Examples of XO inhibitors are allopurinol, oxypurinol and febuxostat.
