Effect of acetyl-l-carnitine on lipid peroxidation and xanthine oxidase activity in rat skeletal muscle

1993 ◽  
Vol 18 (11) ◽  
pp. 1157-1162 ◽  
Author(s):  
C. Di Giacomo ◽  
F. Latteri ◽  
C. Fichera ◽  
V. Sorrenti ◽  
A. Campisi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Lipid Peroxidation ◽  
Xanthine Oxidase ◽  
Oxidase Activity ◽  
Rat Skeletal Muscle ◽  
Xanthine Oxidase Activity

Xanthine oxidase and activated neutrophils cause oxidative damage to skeletal muscle after contractile claudication

2004 ◽  
Vol 286 (1) ◽  
pp. H252-H256 ◽  
Author(s):  
A. R. Judge ◽  
S. L. Dodd
Keyword(s):  
Skeletal Muscle ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Xanthine Oxidase ◽  
Muscle Damage ◽  
Protein Oxidation ◽  
Oxidase Activity ◽  
Neutrophil Infiltration ◽  
Xanthine Oxidase Activity ◽  
Infiltration Control

We previously showed oxidative damage and edema within skeletal muscle after contractile claudication. To investigate the sources of this oxidative damage in the gastrocnemius muscle, we administered allopurinol (Allo, to inhibit xanthine oxidase) and cyclophosphamide (Cyclo, to deplete neutrophils) before inducing contractile claudication in male Sprague Dawley rats. Contractile claudication (ligated stimulated, LS) caused a significant increase in xanthine oxidase activity [sham ligated stimulated (SS) = 2.57 ± 0.07; LS = 3.22 ± 0.07] and neutrophil infiltration (SS = 0.47 ± 0.03; LS = 0.91 ± 0.10) compared with controls (SS), and this was associated with increased lipid peroxidation, protein oxidation, muscle damage, and edema. Pretreatment with Allo attenuated the increase in xanthine oxidase activity and attenuated lipid hydroperoxides (control LS = 12.85 ± 0.50; Allo LS = 9.96 ± 0.71), muscle damage, and neutrophil infiltration (control LS = 0.91 ± 0.10; Allo LS = 0.61 ± 0.07). This latter finding suggests that xanthine oxidase-derived oxidants are chemotactic to neutrophils. Pretreatment with Cyclo reduced neutrophil infiltration (control LS = 0.91 ± 0.10; Cyclo LS = 0.55 ± 0.02) and attenuated lipid peroxidation (control LS = 12.85 ± 0.50; Cyclo LS = 6.462 ± 0.62), protein oxidation (control LS = 2.59 ± 0.47; Cyclo LS = 1.77 ± 0.60), muscle damage, and edema. Together, these data indicate that contractile claudication causes an increase in xanthine oxidase activity and neutrophils in muscle and that inhibition of these oxidant sources protects against oxidative stress, muscle damage, and edema.

Role of xanthine oxidase in postischemic microvascular injury in skeletal muscle

1989 ◽  
Vol 257 (6) ◽  
pp. H1782-H1789 ◽  
Author(s):  
J. K. Smith ◽  
D. L. Carden ◽  
R. J. Korthuis
Keyword(s):  
Skeletal Muscle ◽  
Xanthine Oxidase ◽  
Vascular Permeability ◽  
Oxidase Activity ◽  
Ischemia Reperfusion ◽  
Oxidase Inhibitor ◽  
Xanthine Oxidase Inhibitor ◽  
Microvascular Injury ◽  
Xanthine Oxidase Activity

Previous reports indicate that allopurinol, a xanthine oxidase inhibitor, attenuates the microvascular injury produced by reperfusion of ischemic skeletal muscle. To further assess the role of xanthine oxidase in ischemia/reperfusion (I/R) injury, we examined the effect of xanthine oxidase depletion or inhibition on the increase in microvascular permeability produced by I/R. Changes in vascular permeability were assessed by measurement of the solvent drag reflection coefficient for total plasma proteins (sigma) in rat hindquarters subjected to 2 h of ischemia and 30 min of reperfusion in xanthine oxidase-replete and -depleted animals and in animals pretreated with the xanthine oxidase inhibitor oxypurinol. Xanthine oxidase depletion was accomplished by administration of a tungsten-supplemented (0.7 g/kg diet), molybdenum-deficient diet. In animals fed the tungsten diet, muscle total xanthine dehydrogenase plus xanthine oxidase activity was decreased to less than 10% of control values. Estimates of sigma averaged 0.85 +/- 0.04 in nonischemic (continuous perfusion for 2.5 h) hindquarters, whereas muscle xanthine oxidase activity averaged 3.3 +/- 0.4 mU/g wet wt. I/R was associated with a marked decrease in sigma (0.54 +/- 0.02), whereas xanthine oxidase activity was increased to 5.8 +/- 0.5 mU/g wet wt. These results indicate that I/R produced a dramatic increase in vascular permeability coincident with an increase in muscle xanthine oxidase activity. Xanthine oxidase depletion with the tungsten diet or pretreatment with oxypurinol attenuated this permeability increase (sigma = 0.72 +/- 0.03 and 0.77 +/- 0.7, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Author response for "A pilot assessment of xanthine oxidase activity in plasma from patients with hematological malignancies using a highly‐sensitive assay"

2019 ◽  
Author(s):  
Noboru Hokama ◽  
Takashi Shirakura ◽  
Sumito Sunagawa ◽  
Satoko Morishima ◽  
Sawako Nakachi ◽  
...  
Keyword(s):  
Xanthine Oxidase ◽  
Oxidase Activity ◽  
Hematological Malignancies ◽  
Author Response ◽  
Sensitive Assay ◽  
Xanthine Oxidase Activity ◽  
Highly Sensitive

scholarly journals HYDROXYLAMINE INHIBITION OF XANTHINE OXIDASE ACTIVITY

1956 ◽  
Vol 219 (1) ◽  
pp. 375-382 ◽  
Author(s):  
L.S. Dietrich ◽  
Eleanor Borries
Keyword(s):  
Xanthine Oxidase ◽  
Oxidase Activity ◽  
Xanthine Oxidase Activity

Xanthine oxidase activity in the brain

1968 ◽  
Vol 24 (11) ◽  
pp. 1101-1102 ◽  
Author(s):  
G. G. Villela
Keyword(s):  
Xanthine Oxidase ◽  
Oxidase Activity ◽  
Xanthine Oxidase Activity ◽  
The Brain

Stabilization of Xanthine Oxidase Activity by Salicylate

Nature ◽  
1956 ◽  
Vol 178 (4524) ◽  
pp. 88-89 ◽  
Author(s):  
F. BERGEL ◽  
R. C. BRAY
Keyword(s):  
Xanthine Oxidase ◽  
Oxidase Activity ◽  
Xanthine Oxidase Activity
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