Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P47989 (xanthine oxidase)
 8,633 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A sensitive and precise assay of guanase was based on the conversion of 14C-guanine to uric acid in the presence of excess xanthine oxidase. The enzyme was entirely soluble in rat tissues and no inhibitors of it were detected. The most active tissues were red blood cells, lung and lactating mammary gland, with more than twice the activity of liver. The contained blood could account for the low activity in adult skeletal muscle and some other tissues. All fetal tissues examined were without activity. Activity in mammary gland rose fourfold during lactation and dropped precipitously during involution, with a secondary rise associated in time with the loss of cells from the gland. Reticulocytes present normally and after hemorrhagic anemia appeared to account for substantially all of the high guanase activity in red blood cells. The guanase level could be used to predict the degree of reticulocytosis in rats within confidence limits of +/- 0.2%. The virtual absence of guanase in human red cells was confirmed, even in bloods containing elevated reticulocyte numbers.
 ...
PMID:Guanase in reticulocytes and other rat tissues. 72 38

The rise in plasma uric acid (UA) in chronic renal failure (CRF) is quite limited. This may be due to either increased extrarenal excretion, diminished biosynthesis, and/or enhanced degradation of uric acid. The intestinal flux studies revealed a striking modification of urate transport from no net flux to a net secretory flux in the jejunum and from a basal net absorptive to a net secretory flux in the colon of CRF animals. In addition, CRF animals showed a marked reduction in hepatic, renal, and enteric tissue xanthine oxidase activity and no significant change in tissue uricase activity. The correction of anemia with erythropoietin did not significantly alter the plasma concentration or urinary excretion of urate. Thus, enhanced enteric excretion and depressed production of uric acid (reduced xanthine oxidase activity) may account for the lack of significant hyperuricemia in CRF.
 ...
PMID:Effect of chronic experimental renal insufficiency on urate metabolism. 858 4

This study was designed to focus on the potential stress that xanthine oxidase could produce in copper-deficient rats fed fructose. Fructose consumption results in an excess production of uric acid due to an increased degradation of nucleotides. The enzyme xanthine oxidase catalyzes the oxidation of both hypoxanthine and xanthine. During the oxidation process free radicals are generated, which in turn, induce lipid peroxidation and premature death. Allopurinol -- a competitive inhibitor of xanthine oxidase -- could alleviate the combined effects of fructose feeding and copper deficiency. Twenty-five male rats were fed for 4 weeks from weaning a copper-deficient or adequate diet containing fructose. Twelve rats were given a daily oral dose of 5 mg allopurinol/100 g b.wt. Two copper-deficient rats that were not treated with allopurinol died prematurely during the fourth week of the study. No mortality occurred in the group of copper-deficient rats that had been treated with allopurinol. Anemia was alleviated by allopurinol, which in turn, could be responsible for improved growth rate. Allopurinol was effective in inhibiting xanthine oxidase activity in vivo as measured by the dramatic reduction of uric acid production. Lipid peroxidation, however, was not affected by allopurinol. It is concluded that the beneficial effects of allopurinol in copper deficiency do not appear to be related to prevention of oxygen radicals, but rather, to the protection against the catabolic destruction of purines, which in turn, increases nucleotide pool.
 ...
PMID:Allopurinol, an inhibitor of xanthine oxidase, reduces uric acid levels and modifies the signs associated with copper deficiency in rats fed fructose. 890 1

This study reports that lawsone (2-hydroxy-1,4-naphthoquinone) undergoes redox cycling in the presence of the hypoxanthine/xanthine oxidase system. The rate of cytochrome c reduction obtained in the presence of 80 microM lawsone was almost three times the rate of cytochrome c reduction measured in its absence. This increase in the rate of cytochrome c reduction was partially inhibited by superoxide dismutase, suggesting the involvement of O(2)(.-) in this process. It is remarkable to note that, even though lawsone is considered to be a non-redox-cycling quinone in vitro, this quinone was shown to be more toxic in vivo in rats than menadione, causing haemolytic anemia of an oxidative nature and renal damage. The view that this quinone is a non-redox-cycling quinone was based on the inability of one-electron-transferring flavoenzymes such as NADPH-cytochrome c reductase to reduce this naphthoquinone. Our finding that lawsone, like menadione, undergoes redox cycling in the presence of the hypoxanthine/xanthine oxidase system could explain the observed oxidative damage of tissues inflicted by this quinone in rats in vivo. Such an observation therefore reconciles the in vivo toxicity results of this naphthoquinone with those of in vitro experiments.
 ...
PMID:Evidence for redox cycling of lawsone (2-hydroxy-1,4-naphthoquinone) in the presence of the hypoxanthine/xanthine oxidase system. 1288 2

Iron is one of the most important essential metal ions of which significance is well known for ages. This element is a key moiety of several enzymes in iron containing heme or nonheme form and transfer and storage protein, hemoglobin and myoglobin. Several membrane carriers of iron have already been identified. The redox state of iron is determined by xanthine oxidase, cytochromes and Hp or ceruloplasmin and ferroxidase activity of apo-ferritin, respectively. Some vitamins (C, B2-, B3-, B6-, B12) play also a role in the metabolism of iron. The iron content of cells of the organs is well regulated by the iron homeostasis. Iron has a significant role in the immune system by producing oxygen containing free radicals. Anaemia induced by iron deficiency may cause a challenge concerns for pregnant women, babies and adolescent, primarily.
 ...
PMID:[Physiologic and pathologic role of iron in the human body. Iron deficiency anemia in newborn babies]. 1550 4

Dang-Gui-Shao-Yao-San (DGSYS) is a mixture of medicinal herbs, which has long been used in traditional Chinese medicine for treating anemia and ovulary disorders. Its preparation comprises Angelicae sinensis (Oliv.) Diels, Ligustucum chuanxiong Hort, Paeonia lactiflora pall, Poria cocos (Schw.) Wolf, Atractylodis macrocephala Koidz and Alisma orientalis (Sam.) Juzep. The present study examined the anti-superoxide formation, free radical scavenging and anti-lipid peroxidation activities of DGSYS by xanthine oxidase inhibition, cytochrome C system with superoxide anion released by the fMLP or PMA activating pathway in human neutrophils, and FeCl2 ascorbic acid-induced lipid peroxidation effects on lipids in rat liver homogenate, respectively. DGSYS showed anti-superoxide formation and free radical scavenging activity in a concentration-dependent manner. It also inhibited PMA- but not fMLP-induced superoxide anion released from human neutrophils. These antioxidant actions of DGSYS showed beneficial cytoprotective effects against lipid peroxidation in rat liver homogenate, human platelet aggregation induced by arachidonic acid (AA) and adenosine diphosphate (ADP) and mitomycin C-mediated hemolytic in human erythrocytes.
 ...
PMID:Antioxidant and antiplatelet effects of dang-gui-shao-yao-san on human blood cells. 1626 87

Gout is a metabolic disorder of purine metabolism that results in crystallization of uric acid in the form of monosodium urate crystals, affects 8.3 million Americans and is the most common cause of inflammatory arthritis in adults. Urate lowering therapy is the mainstay of treatment for chronic gout. Initial treatments of choice in gout include allopurinol, a purine analog which inhibits xanthine oxidase and decreases the production of uric acid as well as probenecid which increases the urinary excretion of uric acid. However, 3% of patients will fail these treatments. In 2010, pegloticase, a recombinant urate oxidase conjugated to polyethylene glycol, was approved for these patients. Pegloticase has been shown to rapidly normalize plasma uric acid values, resolve tophi and improve quality of life in these patients. Hereby we present a case of a 50-year-old African male admitted to the hospital with symptomatic anemia 1 week after pegloticase infusion. He was found to have glucose-6-phosphate dehydrogenase deficiency, predisposing him to hemolytic anemia. Hereby we discuss his clinical course, and suggest glucose-6-phosphate dehydrogenase deficiency screening prior to pegloticase infusion.
 ...
PMID:Pegloticase Induced Hemolytic Anemia in a Patient With G6PD Deficiency. 3230 Apr 19

Allopurinol is a xanthine oxidase inhibitor used in management of chronic gout. It acts by reducing the amount of uric acid by inhibiting purine metabolism. A middle-aged hypertensive female who was on allopurinol for 7 months presented with generalized weakness and exertional dyspnea. Investigations revealed pancytopenia: normocytic normochromic anemia (Hb-3.2g/dL, TLC-3400/mm3) and severe thrombocytopenia (Platelets-1000/mm3) with mild hepatosplenomegaly and grade 2 medico renal disease with normal cardiac status. Nutritional, hemolytic and infective causes were ruled out. She was transfused with fresh whole blood, platelets, administered empirical antibiotics and started on steroids. Initially, she responded to treatment but later developed an episode of convulsions with anuria and succumbed to leukopenic sepsis secondary to hypo/aplastic anemia probably due to allopurinol. Allopurinol is used extensively in the management of chronic gout and is well tolerated due to its safety profile. But we here report a case of allopurinol induced aplastic anemia leading to the demise of a patient. Allopurinol though safe needs careful monitoring.
 ...
PMID:Allopurinol: Sorrow to the marrow. 3275 32