Free radical-producing enzyme, xanthine oxidase, is undetectable in human hearts

1987 ◽  
Vol 253 (3) ◽  
pp. H709-H711 ◽  
Author(s):  
L. J. Eddy ◽  
J. R. Stewart ◽  
H. P. Jones ◽  
T. D. Engerson ◽  
J. M. McCord ◽  
...  
Keyword(s):  
Free Radicals ◽  
Free Radical ◽  
Xanthine Oxidase ◽  
Human Heart ◽  
Xanthine Dehydrogenase ◽  
Spectrophotometric Assay ◽  
Fluorometric Assay ◽  
Significant Source ◽  
Xanthine Oxidase Inhibitors ◽  
Therapeutic Value

Samples from four human hearts were analyzed for both their xanthine dehydrogenase and xanthine oxidase content. We used the conventional spectrophotometric assay and a more sensitive fluorometric assay to determine the content of enzyme in these samples. In no case could any activity be detected. We conclude that human hearts must contain less than 2.0 nU/g of activity. This makes it unlikely that xanthine oxidase is a significant source of O2 free radicals in the ischemic human heart or that xanthine oxidase inhibitors will be of therapeutic value in that setting.

Interaction of cytokinins with lipid-associated oxy free radicals during senescence: a prospective mode of cytokinin action

1984 ◽  
Vol 62 (12) ◽  
pp. 2943-2949 ◽  
Author(s):  
Ya'acov Y. Leshem
Keyword(s):  
Free Radicals ◽  
Free Radical ◽  
Xanthine Oxidase ◽  
Radical Scavenging ◽  
Free Radical Scavenger ◽  
Radical Formation ◽  
Radical Scavenger ◽  
Substrate Affinity ◽  
Xanthine Oxidase Inhibitors ◽  
Free Radical Formation

In senescence physiology, experimental data indicate causative relationships among cytokinin, lipoxygenation, anti-oxidation, and lipid-associated free radical scavenging. During both normal and induced senescence, there is a rise in lipoxygenase (LOX) which catalyzes the oxidation of polyunsaturated fatty acids containing the cis, cis-1,4-pentadiene configuration. These include linoleic and linolenic acids, which are of common occurrence in plants and inter alia may be situated in membranal phospholipids. Lipoxygenation causes the production of free radicals such as the superoxide, fatty acid, and peroxy species. Cytokinin (CK) lowers LOX and superoxide dismutase activities significantly in senescing foliage and is mimicked by the endogenous lipid antioxidant, α-tocopherol (vitamin E), in its chlorophyll-retaining and LOX-lowering effects. Further experimentation indicated that CK interaction with free radicals may occur in two ways, (i) CK may act as a direct free radical scavenger by virtue of the fact that the hydrogens of the α-carbon atom in the amine bond can be extracted, resulting in the formation of an amide: [Formula: see text][Formula: see text] (this mechanism may also, in part, explain polyamine effects), (ii) CK may serve as an incipient preventative of free radical formation by inhibiting oxidation of plant purine compounds, which at certain stages of breakdown release superoxide and hydroxyl free radicals. This effect is probably associated with a lowering of substrate affinity for xanthine oxidase. This assumption is further borne out by similar senescence-retarding effects of selective xanthine oxidase inhibitors such as allopurinol. These observations collectively indicate that prevention of free radical formation and (or) their direct scavenging should be included in the multifactorial antisencscence mode of action of cytokinin.

Role of xanthine dehydrogenase and oxidase in focal cerebral ischemic injury to rat

1991 ◽  
Vol 261 (6) ◽  
pp. H2051-H2057 ◽  
Author(s):  
S. Lindsay ◽  
T. H. Liu ◽  
J. A. Xu ◽  
P. A. Marshall ◽  
J. K. Thompson ◽  
...  
Keyword(s):  
Free Radical ◽  
Xanthine Oxidase ◽  
Focal Cerebral Ischemia ◽  
Infarct Volume ◽  
Primary Source ◽  
Ischemic Injury ◽  
Xanthine Dehydrogenase ◽  
Cerebral Ischemic Injury ◽  
Cerebral Ischemic

The role of xanthine dehydrogenase and oxidase as a source of free radicals contributing to focal cerebral ischemic injury was evaluated in Long-Evans rats after the middle cerebral artery was permanently occluded and both carotid arteries were clamped for 90 min. The fraction of xanthine dehydrogenase present as the free radical producing oxidase increased slightly from 22% in control cortex to 30% in the ischemic right cortex during the first 3 h of reperfusion and then remained relatively unchanged over the next 24 h. This increase may in part be due to entrapped plasma, which contained 4.5 +/- 0.8 nmol.min-1.ml-1 xanthine oxidase entirely in the free radical-producing form. Infarct volume was unaffected by pretreatment with 50 mg allopurinol/kg per day over 3 days before surgery but was decreased by 8% with 100 mg/kg and 24% with 150 mg/kg of allopurinol (P less than 0.05). However, inhibition of xanthine oxidase by dietary depletion of the essential molybdenum cofactor increased infarct volume by 19%, suggesting that protection by allopurinol at higher dosages was independent of xanthine oxidase inhibition. Neither xanthine oxidase present in rat brain nor circulating in plasma appears to be the primary source of oxygen radicals that contributes to infarction in focal cerebral ischemia.

2-Benzamido-4-methylthiazole-5-carboxylic Acid Derivatives as Potential Xanthine Oxidase Inhibitors and Free Radical Scavengers

2017 ◽  
Vol 350 (2) ◽  
pp. 1600313 ◽  
Author(s):  
Md. Rahmat Ali ◽  
Suresh Kumar ◽  
Obaid Afzal ◽  
Nishtha Shalmali ◽  
Wazid Ali ◽  
...  
Keyword(s):  
Free Radical ◽  
Carboxylic Acid ◽  
Xanthine Oxidase ◽  
Free Radical Scavengers ◽  
Radical Scavengers ◽  
Xanthine Oxidase Inhibitors

Improved DPPH determination for antioxidant activity spectrophotometric assay

2007 ◽  
Vol 61 (3) ◽  
Author(s):  
M. Szabo ◽  
C. Idiţoiu ◽  
D. Chambre ◽  
A. Lupea
Keyword(s):  
Antioxidant Activity ◽  
Free Radicals ◽  
Free Radical ◽  
Calibration Curve ◽  
Spectrophotometric Assay ◽  
Stable Form ◽  
Radical Concentration ◽  
Free Radical Concentration

AbstractAn improved procedure for determination of the residual DPPH (1,1-diphenyl-2-picrylhydrazyl) free radical concentration was proposed taking into account the absorbance of both DPPH free radicals and DPPH nonradical (1,1-diphenyl-2-picrylhydrazine) stable form. The calculated residual DPPH free radical concentrations were compared with those obtained from a calibration curve and variation coefficients below 10 % were found.

Myocardial Salvage by the Free Radical Scavenging Actions of Xanthine Oxidase Inhibitors

1988 ◽  
pp. 951-955
Author(s):  
Dipak K. Das ◽  
Richard M. Engelman ◽  
Ronald Clement ◽  
Hajime Otani ◽  
M. Renuka Prasad ◽  
...  
Keyword(s):  
Free Radical ◽  
Xanthine Oxidase ◽  
Radical Scavenging ◽  
Free Radical Scavenging ◽  
Myocardial Salvage ◽  
Xanthine Oxidase Inhibitors

Calcium and free radicals in hypoxia/reoxygenation injury of renal epithelial cells

1994 ◽  
Vol 266 (1) ◽  
pp. F13-F20 ◽  
Author(s):  
E. L. Greene ◽  
M. S. Paller
Keyword(s):  
Free Radicals ◽  
Xanthine Oxidase ◽  
Renal Cell ◽  
Superoxide Radical ◽  
Cell Injury ◽  
Oxygen Free Radicals ◽  
Xanthine Dehydrogenase ◽  
Oxygen Free Radical ◽  
Lactate Dehydrogenase Release ◽  
Radical Production

Hypoxia and reoxygenation (H/R) generate oxygen free radicals that result in renal cell injury. We tested the roles of calcium and calmodulin in mediating xanthine oxidase-derived oxygen free radical production during H/R. Lowering extracellular Ca2+ attenuated lethal cell injury. H/R increased superoxide radical production over basal levels, whereas removing extracellular Ca2+ before hypoxia decreased superoxide radical production to basal levels. Pretreatment with either 8-(N,N-diethylamino)octyl-3,4,5-trimethoxybenzoate hydrochloride or thapsigargin, to inhibit release or deplete stores of intracellular Ca2+, did not affect injury following H/R. Ionomycin increased lactate dehydrogenase release during H/R but did not increase superoxide radical to levels greater than that observed for H/R alone. The calmodulin inhibitors trifluoperazine, calmidazolium, or N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide decreased cell injury to varying degrees. Trifluoperazine also decreased superoxide radical production during H/R and was shown to inhibit the conversion of xanthine dehydrogenase to xanthine oxidase. Cell injury and superoxide radical production correlated with cytosolic free Ca2+ during H/R as determined with the Ca(2+)-sensitive fluoroprobe indo 1. Cytosolic free Ca2+ increased slightly during hypoxia and showed a dramatic increase as soon as cells were reoxygenated. Cells incubated in a Ca(2+)-free medium actually showed a small decrease in intracellular Ca2++ despite H/R. In summary, Ca2+ derived from extracellular sources promoted superoxide radical production and renal cell injury by a calmodulin-dependent conversion of xanthine dehydrogenase to xanthine oxidase, a major source of oxygen free radicals during H/R.

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