Hypoxanthine, Uric Acid and Allantoin as Indicators of in Vivo Free Radical Reactions. Description of a HPLC Method and Human Brain Microdialysis Data

2000 ◽  
Vol 142 (10) ◽  
pp. 1135-1142 ◽  
Author(s):  
N. Marklund ◽  
B. Östman ◽  
L. Nalmo ◽  
L. Persson ◽  
L. Hillered
Keyword(s):  
Uric Acid ◽  
Free Radical ◽  
Human Brain ◽  
Hplc Method ◽  
Radical Reactions ◽  
Brain Microdialysis ◽  
Free Radical Reactions

scholarly journals Measurement of allantoin and uric acid in human body fluids. A potential index of free-radical reactions in vivo?

1987 ◽  
Vol 243 (3) ◽  
pp. 803-808 ◽  
Author(s):  
M Grootveld ◽  
B Halliwell
Keyword(s):  
Uric Acid ◽  
Free Radical ◽  
Human Body ◽  
Body Fluids ◽  
Radical Reactions ◽  
Free Radical Reactions ◽  
Potential Index ◽  
Free Radical Attack ◽  
Radical Attack

Free-radical attack upon uric acid generates allantoin [Ames, Cathcart, Schwiers & Hochstein (1981) Proc. Natl. Acad. Sci. U.S.A. 78, 6858-6862]. Methods are described for the accurate measurement of uric acid and allantoin in human body fluids. The concentrations of uric acid and allantoin in human serum and synovial fluid are reported. It is suggested that measurement of changes in allantoin concentration may be a useful index of free-radical reactions taking place in vivo.

Further studies on free-radical pathology in the major central nervous system disorders: effect of very high doses of methylprednisolone on the functional outcome, morphology, and chemistry of experimental spinal cord impact injury

1982 ◽  
Vol 60 (11) ◽  
pp. 1415-1424 ◽  
Author(s):  
H. B. Demopoulos ◽  
E. S. Flamm ◽  
M. L. Seligman ◽  
D. D. Pietronigro ◽  
J. Tomasula ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Nervous System ◽  
Free Radical ◽  
Tissue Injury ◽  
Functional Restoration ◽  
Radical Reactions ◽  
Free Radical Reactions ◽  
Cord Injury

The hypothesis that pathologic free-radical reactions are initiated and catalyzed in the major central nervous system (CNS) disorders has been further supported by the current acute spinal cord injury work that has demonstrated the appearance of specific, cholesterol free-radical oxidation products. The significance of these products is suggested by the fact that: (i) they increase with time after injury; (ii) their production is curtailed with a steroidal antioxidant; (iii) high antioxidant doses of the steroidal antioxidant which curtail the development of free-radical product prevent tissue degeneration and permit functional restoration. The role of pathologic free-radical reactions is also inferred from the loss of ascorbic acid, a principal CNS antioxidant, and of extractable cholesterol. These losses are also prevented by the steroidal antioxidant. This model system is among others in the CNS which offer distinctive opportunities to study, in vivo, the onset and progression of membrane damaging free-radical reactions within well-defined parameters of time, extent of tissue injury, correlation with changes in membrane enzymes, and correlation with readily measurable in vivo functions.

Measuring free radical reactions in vivo

1993 ◽  
Vol 49 (3) ◽  
pp. 494-505 ◽  
Author(s):  
A E Holley ◽  
K H Cheeseman
Keyword(s):  
Free Radical ◽  
Radical Reactions ◽  
Free Radical Reactions

In Vivo ESR Measurement of Free Radical Reactions in Living Mice

1998 ◽  
pp. 13-22
Author(s):  
Hideo Utsumi ◽  
Keizo Takeshita ◽  
Kazuhiro Ichikawa ◽  
Hiroaki Sano ◽  
Toshiki Masumizu ◽  
...  
Keyword(s):  
Free Radical ◽  
Radical Reactions ◽  
Free Radical Reactions

Iron-mediated radical reactions upon reperfusion contribute to myocardial "stunning"

1990 ◽  
Vol 259 (6) ◽  
pp. H1901-H1911 ◽  
Author(s):  
R. Bolli ◽  
B. S. Patel ◽  
M. O. Jeroudi ◽  
X. Y. Li ◽  
J. F. Triana ◽  
...  
Keyword(s):  
Free Radical ◽  
Myocardial Stunning ◽  
Time Window ◽  
Contractile Function ◽  
Myocardial Dysfunction ◽  
Venous Blood ◽  
Radical Reactions ◽  
Free Radical Reactions ◽  
Group I

Recent evidence suggests that postischemic myocardial dysfunction ("stunning") is mediated by iron-catalyzed free radical reactions, but the exact time window during which the critical iron-mediated damage develops remains unknown. Furthermore, the evidence that iron promotes free radical reactions in vivo is indirect. Thus open-chest dogs undergoing a 15-min coronary occlusion and 4 h of reperfusion were given one of the following intracoronary infusions: desferrioxamine (DF) beginning 2 min before reperfusion (group I), DF beginning 1 min after reperfusion (group II), iron-loaded DF in dosage identical to group I (group III), or vehicle (controls, group IV). Recovery of contractile function was substantially greater in group I than in controls, whereas in groups II and III it was indistinguishable from controls. To determine whether the protection afforded by DF was due to inhibition of free radical reactions, myocardial production of free radicals was directly assessed by intracoronary infusion of the spin trap alpha-phenyl N-tert-butyl nitrone (PBN). In controls (group VI), radical adducts of PBN were released in the coronary venous blood after reperfusion. DF given as in group I (group V) markedly suppressed myocardial production of PBN adducts. These results strongly suggest that a substantial portion of the damage responsible for myocardial stunning is caused by iron-catalyzed free radical reactions that develop in the initial seconds of reperfusion and can be prevented by administration of iron chelators started just before reflow. Furthermore, the results demonstrate that attenuation of postischemic dysfunction by DF is associated with attenuation of free radical reactions in vivo, thereby providing direct evidence for a pathogenetic role of iron-catalyzed free radical reactions in myocardial stunning in the intact animal.

A new hypothesis about the relationship between free radical reactions and hemorheological properties in vivo

1993 ◽  
Vol 41 (6) ◽  
pp. 516-520 ◽  
Author(s):  
Mo Jian ◽  
Fan Jiajung ◽  
Guo Zhengren ◽  
Hunag Chen ◽  
Yan Bo ◽  
...  
Keyword(s):  
Free Radical ◽  
Radical Reactions ◽  
Free Radical Reactions ◽  
The Relationship ◽  
New Hypothesis

scholarly journals THE STUDY OF NITRIC OXIDE ACTION IN VIVO ON NA+ , K+ -ÀÒPASE IN RAT AORTA

2009 ◽  
Vol 55 (1) ◽  
pp. 27-35
Author(s):  
O.V. Akopova ◽  
◽  
O.N. Kharlamova ◽  
A.V. Kotsiuruba ◽  
Yu.P. Korkach ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Free Radical ◽  
Atpase Activity ◽  
Rat Aorta ◽  
Radical Reactions ◽  
Hypotensive Action ◽  
No Donor ◽  
Free Radical Reactions ◽  
Stimulation Of

The influence of nitric oxide on Na+,K+-ATPase activity in rat aorta was studied by means of stimulation of endogenous NO synthesis after injections of bacterial lipopolysaccharide (LPS) and pharmacological NO donor nitroglycerine (NG). It was shown that NO action on Na+,K+-ATPase in vivo is dose-de­pendent. Stimulation of the endogenous NO synthesis by LPS as well as the administration of low doses of NG lead to the activation of Na+,K+-ATPase and favor the conclusion that NO-dependent Na+,K+-ATPase stimulation mediates vasodilatory and hypotensive action of nitric oxide. The Na+,K+-ATPase activity in rat aorta depends on the balance between the level of reactive oxygen and nitrogen species (ROS and RNS), forma­tion of NO depots in the tissue of aorta as high- and low mo­lecular weight nitrosothiols, and also on the intensity of free-radical reactions resulting in the generation of hydroperoxide radicals. The results obtained suggest that NOS- and cGMP-dependent pathway takes part in Na+,K+-ATPase activation by LPS and NG, but the enzyme inhibition by nitric oxide in vivo is not cGMP-dependent and is determined by the activation of free-radical reactions and dramatic enhancement of nitrosylation level in rat aorta tissue.

In vivo ESR measurements of free radical reactions in living mice

1995 ◽  
Vol 82-83 ◽  
pp. 561-565 ◽  
Author(s):  
Hideo Utsumi ◽  
Kazuhiro Ichikawa ◽  
Keizo Takeshita
Keyword(s):  
Free Radical ◽  
Radical Reactions ◽  
Free Radical Reactions
Sign in / Sign up

Export Citation Format

Share Document