DIFFERENCES IN PROPERTIES OF XANTHINE DEHYDROGENASE AND XANTHINE OXIDASE

1991 ◽  
pp. 885-894
Author(s):  
Takeshi Nishino
2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1057.1-1057
Author(s):  
S. Bedina ◽  
A. Trofimenko ◽  
E. Mozgovaya ◽  
M. Mamus ◽  
S. Spitsina

Background:Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by the presence of rheumatoid factor (RF) and anticitrulline autoantibodies. Recent evidences suggest that impairment of neutrophil extracellular traps (NETs) could exert substantial influence on RA pathogenesis. The production of NETs depends heavily on the ROS generation. One of its mechanisms is xanthine oxidoreductase (XOR) mediated degradation of purine metabolites. Analysis of pro-oxidant activity of the enzymatic complex XOR and its constituents, xanthine oxidase (XO) and xanthine dehydrogenase (XDG), is an issue of considerable interest in this context.Objectives:Evaluation of XO and XDG activities in RF-positive and RF-negative RA using both plasma and lysed lymphocyte samples.Methods:The research was carried out in agreement with the WMA Declaration of Helsinki principles. Diagnosis of RA had been verified using ACR/EULAR 2010 criteria. Enzymatic activities in plasma and lymphocytes were measured spectrophotometrically and expressed as nmol/min/ml. Enzymatic activities in lymphocytes were also normalized to 1×107 cells/ml. Statististical tests were selected in line with common guidelines. Differences were considered significant when p<0.05. Reference ranges were calculated as means ±2SD.Results:75 adult RA patients (52 females and 23 males, mean age 43.9±0.97 years, mean disease duration 8.5±0.3 years) from the rheumatology unit of Volgograd Clinical Emergency Hospital #25 as well as 35 healthy controls were included in the study. RF-positive RA and RF-negative RA were observed in 49 (65.3%) and 26 (34.7%) patients, respectively. Reference ranges for plasma and lymphocyte XO activities were 2.60-3.96 and 14.2-27.8 nmol/min/ml, respectively. Similar ranges for XDG activities were 4.49-5.93 and 22.5-40.7 nmol/min/ml, respectively. Enzymatic profile of RA patients is characterized by significantly increased XO activity in plasma and decreased XO and XDG activities in lymphocytes (р<0.001). XO activity is increased (p<0.001), XDG activity is decreased (p<0.001) in blood plasma of patients with RF-negative RA, while the activity of both enzymes is decreased in lymphocytes (p<0.001). XO activity (p<0.001) and XDG activity (p<0.05) is increased in blood plasma, XO activity and XDG activity are decreased (p<0.001) in lymphocytes of patients with RF-positive RA. Plasma XO and XDG activities are also higher, and lymphocyte XO and XDG activities are lower in patients with RF-positive RA than in patients with RF-negative RA (р<0.001).Conclusion:Our study revealed the relationship between enzyme parameters and rheumatoid factor presence. More pronounced changes in the enzyme activities were observed in patients with RF-positive RA. These results demonstrate that activation of the xanthine oxidase/xanthine dehydrogenase enzyme complex is an substantial factor of induction and continuation of the autoimmune rheumatoid inflammation.Disclosure of Interests:None declared


1994 ◽  
Vol 56 (2) ◽  
pp. 162-167 ◽  
Author(s):  
Riley Rees ◽  
Del Smith ◽  
Ti Dong Li ◽  
Belinda Cashmer ◽  
Warren Garner ◽  
...  

1988 ◽  
Vol 254 (5) ◽  
pp. G753-G760 ◽  
Author(s):  
T. G. McKelvey ◽  
M. E. Hollwarth ◽  
D. N. Granger ◽  
T. D. Engerson ◽  
U. Landler ◽  
...  

Previous studies have proposed and supported a role for the proteolytic, irreversible conversion of xanthine dehydrogenase to xanthine oxidase (XO) in postischemic injury in a wide variety of organs. A second mechanism of conversion, due to sulfhydryl modification and reversible with dithiothreitol (DTT), is potentially important but has not been well investigated. In this study rat liver and kidney were found to produce significant amounts of DTT-reversible XO during normothermic global ischemia. Formation of reversible XO precedes that of irreversible XO by approximately 0.5 h with a strong correlation (r = 0.92) existing between the rate of irreversible XO formation and the concentration of reversible XO. The formation of reversible XO is preceded by a depletion of glutathione with concentrations of glutathione during ischemia correlating (r = 0.85) with the observed concentration of reversible XO. While a large increase in the extent of liver damage occurs concurrently with conversion in an in vivo liver model of liver ischemia, an ischemia-reperfusion regimen (1 h of ischemia plus 0.5 h of reperfusion) that resulted in no conversion caused significant elevations in serum glutamic pyruvic transaminase and serum glutamic-oxaloacetic transaminase. Rats depleted of XO by tungsten dieting release 65% less enzyme after the same insult, suggesting that endogenous XO may also participate in the damage process independent of any conversion.


Life Sciences ◽  
2005 ◽  
Vol 76 (16) ◽  
pp. 1835-1847 ◽  
Author(s):  
Yasuhiro Takano ◽  
Kumiko Hase-Aoki ◽  
Hideki Horiuchi ◽  
Lin Zhao ◽  
Yoshinori Kasahara ◽  
...  

2008 ◽  
Vol 36 (01) ◽  
pp. 149-157 ◽  
Author(s):  
Cai Guo Huang ◽  
Yan Jun Shang ◽  
Jun Zhang ◽  
Jian Rong Zhang ◽  
Wen Jie Li ◽  
...  

Phenylpropanoid glycoside acteoside was extracted from the traditional Chinese medicine Scrophularia ningpoenis Hemsl. In the present study, we investigated the effects of acteoside administration on serum uric acid levels in mice rendered hyperuricemic with the uricase inhibitor potassium oxonate. When administered orally for 3 days at doses of 50, 100 and 150 mg/kg, acteoside reduced serum uric acid levels by 15.2, 23.8 and 33.1%, respectively, relative to vehicle-treated hyperuricemic mice. Importantly, in non-hyperuricemic mice, the serum uric acid levels were not affected by acetoside treatment. Acteoside also inhibited mouse liver xanthine dehydrogenase XDH and xanthine oxidase XO activity at all three doses. These results suggest that the hypouricemic action of acteoside may be attributable to its inhibition of XDH/XO activity.


1988 ◽  
Vol 65 (5) ◽  
pp. 2349-2353 ◽  
Author(s):  
L. S. Terada ◽  
C. J. Beehler ◽  
A. Banerjee ◽  
J. M. Brown ◽  
M. A. Grosso ◽  
...  

Xanthine oxidase (XO) and xanthine dehydrogenase (XD) activities decreased in lungs isolated from rats and cultured lung endothelial cells that had been exposed to hyperoxia. Purified XO activity also decreased after addition of a variety of chemically generated O2 metabolite species (superoxide anion, hydrogen peroxide, hydroxyl radical, or hypochlorous acid), hypoxanthine, or stimulated neutrophils in vitro. XO inactivation by chemically, self-, or neutrophil-generated O2 metabolites was decreased by simultaneous addition of various O2 metabolite scavengers but not their inactive analogues. Since XO appears to contribute to a variety of biological processes and diseases, hyperoxia- or O2 metabolite-mediated decreases in XO activity may be an important cellular control mechanism.


2008 ◽  
Vol 11 (14) ◽  
pp. 1779-1784 ◽  
Author(s):  
Fatemeh Haidari ◽  
Mohammad Reza Rashidi ◽  
Seid Ali Keshavarz ◽  
Soltan Ali Mahboob ◽  
Mohammad Reza Eshraghian ◽  
...  

1990 ◽  
Vol 258 (2) ◽  
pp. F232-F236 ◽  
Author(s):  
M. Joannidis ◽  
G. Gstraunthaler ◽  
W. Pfaller

The conversion rates of xanthine dehydrogenase (XDH) to xanthine oxidase (XO) were compared with the time course of in vivo lipid peroxidation (LPO) in an ischemia-reperfusion model of acute renal failure in the rat. LPO, measured as the renal release of malondialdehyde (MDA), was found to be markedly elevated only during the first 5 min of blood reflow following a 45-min interval of ischemia (arteriovenous MDA difference -277.3 +/- 53.5 vs. 3.7 +/- 5.7 nmol/l in controls, n = 14). After 30 min of reperfusion, arteriovenous MDA differences nearly reached control values (9.7 +/- 31.8 nmol/l, n = 7). In contrast to enhanced LPO, no significant conversion of XDH to XO was found (XO activity in controls: 23 +/- 1% of XO plus XDH activity vs. 26 +/- 3% after 45 min of ischemia, n = 7). Therefore XO-derived superoxide anion radicals cannot be considered causative for LPO in the reperfusion interval of experimental ischemic acute renal failure.


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