scholarly journals The effects of allopurinol, uric acid, and inosine administration on xanthine oxidoreductase activity and uric acid concentrations in broilers

2012 ◽  
Vol 91 (11) ◽  
pp. 2895-2903 ◽  
Author(s):  
T. Settle ◽  
M.D. Carro ◽  
E. Falkenstein ◽  
W. Radke ◽  
H. Klandorf
Keyword(s):  
Uric Acid ◽  
Xanthine Oxidoreductase ◽  
Oxidoreductase Activity

scholarly journals Effect of NADH on hypoxanthine hydroxylation by native NAD+-dependent xanthine oxidoreductase of rat liver, and the possible biological role of this effect

1981 ◽  
Vol 200 (3) ◽  
pp. 597-603 ◽  
Author(s):  
Z W Kamiński ◽  
M M Jezewska
Keyword(s):  
Uric Acid ◽  
Rat Liver ◽  
Time Course ◽  
De Novo ◽  
Xanthine Oxidoreductase ◽  
Reaction Sequence ◽  
Oxidoreductase Activity ◽  
Dependent Activity ◽  
Sepharose 4B

The course of the reaction sequence hypoxanthine leads to xanthine leads to uric acid, catalysed by the NAD+-dependent activity of xanthine oxidoreductase, was investigated under conditions either of immediate oxidation of the NADH formed or of NADH accumulation. The enzymic preparation was obtained from rat liver, and purified 75-fold (as compared with the 25000 g supernatant) on a 5′-AMP-Sepharose 4B column; in this preparation the NAD+-dependent activity accounted for 100% of total xanthine oxidoreductase activity. A spectrophotometric method was developed for continuous measurements of changes in the concentrations of the three purines involved. The time course as well as the effects of the concentrations of enzyme and of hypoxanthine were examined. NADH produced by the enzyme lowered its activity by 50%, resulting in xanthine accumulation and in decreases of uric acid formation and of hypoxanthine utilization. The inhibition of the Xanthine oxidoreductase NAD+-dependent activity by NADH is discussed as a possible factor in the regulation of IMP biosynthesis by the ‘de novo’ pathway or (from unchanged hypoxanthine) by ther salvage pathway.

scholarly journals Xanthine oxidoreductase activity is associated with serum uric acid and glycemic control in hemodialysis patients

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Ayumi Nakatani ◽  
Shinya Nakatani ◽  
Eiji Ishimura ◽  
Takayo Murase ◽  
Takashi Nakamura ◽  
...  
Keyword(s):  
Uric Acid ◽  
Glycemic Control ◽  
Serum Uric Acid ◽  
Hemodialysis Patients ◽  
Xanthine Oxidoreductase ◽  
Oxidoreductase Activity

scholarly journals Plasma Xanthine Oxidoreductase Activity Associated with Glycemic Control in Patients with Pre-Dialysis Chronic Kidney Disease

2021 ◽  
pp. 1-9
Author(s):  
Shinya Nakatani ◽  
Eiji Ishimura ◽  
Takayo Murase ◽  
Takashi Nakamura ◽  
Ayumi Nakatani ◽  
...  
Keyword(s):  
Uric Acid ◽  
Glycemic Control ◽  
Multiple Regression ◽  
Plasma Glucose ◽  
Hemoglobin A1c ◽  
Cross Sectional Study ◽  
Xanthine Oxidoreductase ◽  
Oxidoreductase Activity ◽  
Cross Sectional ◽  
Increased Risk

<b><i>Introduction:</i></b> Xanthine oxidoreductase (XOR) activity plays an important role as a pivotal source of reactive oxygen species, which is associated with cardiovascular disease (CVD) events. Patients with CKD have increased risk of CVD events. In the present study, factors associated with plasma XOR activity in pre-dialysis CKD patients were investigated. <b><i>Methods:</i></b> In this cross-sectional study, plasma XOR activity in 118 pre-dialysis CKD patients (age 68 [57–75] years; 64 males, 26 with diabetes mellitus [DM]) was determined using a newly established highly sensitive assay based on (<sup>13</sup>C<sub>2</sub>,<sup>15</sup>N<sub>2</sub>) xanthine and liquid chromatography/triple quadrupole mass spectrometry. <b><i>Results:</i></b> Plasma glucose, hemoglobin A1c, and estimated glomerular filtration (eGFR) were significantly and positively correlated with plasma logarithmically transformed XOR (ln-XOR) activity. In multiple regression analyses, eGFR and hemoglobin A1c or plasma glucose were significantly, independently, and positively associated with plasma ln-XOR activity after adjusting for several confounders. Plasma XOR activity was significantly higher in CKD patients with (<i>n</i> = 26) than in those without (<i>n</i> = 92) DM (62.7 [32.3–122] vs. 25.7 [13.4–45.8] pmol/h/mL, <i>p</i> &#x3c; 0.001). A total of 38 patients were taking uric acid-lowering drugs. Multiple regression analysis of CKD patients not administered uric acid-lowering drugs (<i>n</i> = 80) showed no significant association between eGFR and plasma ln-XOR activity. In contrast, association between glycemic control and plasma ln-XOR activity was significant even in CKD patients without uric acid-lowering drug treatment. <b><i>Conclusions:</i></b> These results indicate the importance of glycemic control in CKD patients in regard to decreased XOR, possibly leading to a decrease in CVD events.

scholarly journals Unexpected high plasma xanthine oxidoreductase activity in female subjects with low levels of uric acid

2018 ◽  
Vol 65 (11) ◽  
pp. 1083-1092 ◽  
Author(s):  
Masato Furuhashi ◽  
Kazuma Mori ◽  
Marenao Tanaka ◽  
Takuto Maeda ◽  
Megumi Matsumoto ◽  
...  
Keyword(s):  
Uric Acid ◽  
High Plasma ◽  
Xanthine Oxidoreductase ◽  
Oxidoreductase Activity ◽  
Low Levels ◽  
Female Subjects

scholarly journals Alcohol abuse is associated with enhanced pulmonary and systemic xanthine oxidoreductase activity

2017 ◽  
Vol 313 (6) ◽  
pp. L1047-L1057 ◽  
Author(s):  
Mehdi A. Fini ◽  
Jeanette Gaydos ◽  
Alicia McNally ◽  
Vijaya Karoor ◽  
Ellen L. Burnham
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Nlrp3 Inflammasome ◽  
Human Subjects ◽  
Xanthine Oxidoreductase ◽  
Healthy Human ◽  
Oxidoreductase Activity ◽  
Pyrin Domain ◽  
Molecular Pattern ◽  
Cox 2

Acute respiratory distress syndrome (ARDS) is a common and devastating disorder. Alcohol use disorders (AUDs) increase ARDS risk and worsen outcomes through mechanisms that may include enhancement of pulmonary oxidative stress. Alcohol consumption increases activity of the enzyme xanthine oxidoreductase (XOR) that contributes to production of both reactive oxygen species (ROS) and uric acid, a damage-associated molecular pattern. These by-products have the potential to modulate proinflammatory pathways, such as those involving cyclooxygenase (COX)-2, and to activate the nucleotide-binding domain, leucine-rich-containing family, pyrin-domain containing-3 (NLRP3) inflammasome. We sought to determine if pulmonary and systemic XOR activity was altered by AUDs. Bronchoscopy with bronchoalveolar lavage (BAL) and blood sampling was performed in otherwise healthy human subjects with AUDs and controls. Uric acid in epithelial-lining fluid, derived from BAL, was substantially higher among individuals with AUDs and did not normalize after 7 days of abstinence; serum uric acid did not differ across groups. XOR enzyme activity in fresh BAL cells and serum was significantly increased in subjects with AUDs. XOR protein in BAL cells from AUD subjects was increased in parallel with COX-2 expression, and furthermore, mRNA expression of NLRP3 inflammasome components was sustained in LPS-stimulated BAL cells from AUD subjects in conjunction with increased IL-1β. Our data suggest that AUDs augment pulmonary and systemic XOR activity that may contribute to ROS and uric acid generation, promoting inflammation. Further investigations will be necessary to determine if XOR inhibition can mitigate alcohol-associated pulmonary oxidative stress, diminish inflammation, and improve ARDS outcomes.

New insights into purine metabolism in metabolic diseases: role of xanthine oxidoreductase activity

2020 ◽  
Vol 319 (5) ◽  
pp. E827-E834 ◽  
Author(s):  
Masato Furuhashi
Keyword(s):  
Adipose Tissue ◽  
Uric Acid ◽  
Metabolic Diseases ◽  
Tissue Injury ◽  
Human Adipose Tissue ◽  
Purine Metabolism ◽  
Xanthine Oxidoreductase ◽  
Oxidoreductase Activity ◽  
Atp Production

Xanthine oxidoreductase (XOR) consists of two different forms, xanthine dehydrogenase and xanthine oxidase (XO), and is a rate-limiting enzyme of uric acid production from hypoxanthine and xanthine. Uric acid is the end product of purine metabolism in humans and has a powerful antioxidant effect. The lack of ascorbic acid, known as vitamin C, in hominoids has been thought to cause a compensatory increase in uric acid as an antioxidant by unfunctional gene mutation of uricase to a pseudogene. Because XO is involved in an increase in reactive oxygen species (ROS) by generating superoxide and hydrogen peroxide, inadequate activation of XOR promotes oxidative stress-related tissue injury. Plasma XOR activity is associated with obesity, smoking, liver dysfunction, hyperuricemia, dyslipidemia, insulin resistance, and adipokines, indicating a novel biomarker of metabolic disorders. However, XOR activity in adipose tissue is low in humans unlike in rodents, and hypoxanthine is secreted from human adipose tissue. The concentration of hypoxanthine, but not xanthine, is independently associated with obesity in a general population, indicating differential regulation of hypoxanthine and xanthine. Treatment with an XOR inhibitor can decrease uric acid for preventing gout, reduce production of XO-related ROS, and promote reutilization of hypoxanthine and ATP production through the salvage pathway. It has recently been suggested that discontinuation of an XOR inhibitor causes adverse cardiovascular outcomes as XOR inhibitor withdrawal syndrome, possibly due to cardiac disturbance of conduction and contraction by reduced ATP production. New insights into purine metabolism, including the role of XOR activity in the past 5 yr, are mainly discussed in this review.

scholarly journals Old drug, new indication: Olsalazine sodium reduced serum uric acid levels in mice via inhibiting xanthine oxidoreductase activity

2017 ◽  
Vol 135 (3) ◽  
pp. 114-120 ◽  
Author(s):  
Yanfen Niu ◽  
Hongjian Li ◽  
Lihui Gao ◽  
Hua Lin ◽  
Hsiangfu Kung ◽  
...  
Keyword(s):  
Uric Acid ◽  
Serum Uric Acid ◽  
Xanthine Oxidoreductase ◽  
Oxidoreductase Activity
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