Cerebrovascular disease and oxidative stress

1999 ◽  
Vol 9 (3) ◽  
pp. 197-206
Author(s):  
SE Gariballa ◽  
AJ Sinclair
Keyword(s):  
Free Radicals ◽  
Free Radical ◽  
Brain Damage ◽  
Indirect Evidence ◽  
Essential Nutrients ◽  
Ischaemia And Reperfusion ◽  
Radical Generation ◽  
The Brain ◽  
And Oxidative Stress ◽  
Ischaemic Episode

There is strong indirect evidence that free radical production appears to be an important mechanism of brain injury after exposure to ischaemia and reperfusion. Although significant brain damage occurs during an ischaemic episode, new cerebral damage can occur after reperfusion. One proposed mechanism for the brain damage that occurs during reperfusion involves generation of free radicals. Body defences against free radicals depends on the balance between free radical generation and the antioxidant protective defence system. Many of these protective antioxidants are essential nutrients or have essential nutrients as part of their molecule that has to be obtained from diet.

scholarly journals Cyclosporine Treatment Reduces Oxygen Free Radical Generation and Oxidative Stress in the Brain of Hypoxia-Reoxygenated Newborn Piglets

PLoS ONE ◽  
2012 ◽  
Vol 7 (7) ◽  
pp. e40471 ◽  
Author(s):  
Richdeep S. Gill ◽  
Tze-Fun Lee ◽  
Jiang-Qin Liu ◽  
Hetal Chaudhary ◽  
Dion R. Brocks ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Oxygen Free Radical ◽  
Free Radical Generation ◽  
Newborn Piglets ◽  
Radical Generation ◽  
The Brain ◽  
And Oxidative Stress

scholarly journals Acidosis-Induced Ischemic Brain Damage: Are Free Radicals Involved?

1991 ◽  
Vol 11 (4) ◽  
pp. 587-596 ◽  
Author(s):  
Johan Lundgren ◽  
Hui Zhang ◽  
Carl-David Agardh ◽  
Maj-Lis Smith ◽  
Patrica J. Evans ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Free Radical ◽  
Substantia Nigra ◽  
Brain Damage ◽  
Oxygen Species ◽  
Total Glutathione ◽  
Free Radical Damage ◽  
Free Iron ◽  
Radical Damage

Substantial evidence exists that reactive oxygen species participate in the pathogenesis of brain damage following both sustained and transient cerebral ischemia, adversely affecting the vascular endothelium and contributing to the formation of edema. One likely triggering event for free radical damage is derealization of protein-bound iron. The binding capacity for some iron-binding proteins is highly pH sensitive and, consequently, the release of iron is enhanced by acidosis. In this study, we explored whether enhanced acidosis during ischemia triggers the production of reactive oxygen species. To that end, enhanced acidosis was produced by inducing ischemia in hyperglycemic rats, with normoglycemic ones serving as controls. Production of H2O2, estimated from the decrease in catalase activity after 3-amino-1,2,4-triazole (AT) administration, was measured in the cerebral cortex, caudoputamen, hippocampus, and substantia nigra (SN) after 15 min of ischemia followed by 5, 15, and 45 min of recovery, respectively (in substantia nigra after 45 min of recovery only). Free iron in cerebrospinal fluid (CSF) was measured after ischemia and 45 min of recovery. Levels of total glutathione (GSH + GSSH) in cortex and hippocampus, and levels of α-tocopherol in cortex, were also measured after 15 min of ischemia followed by 5, 15, and 45 min of recovery. The results confirm previous findings that brief ischemia in normoglycemic animals does not measurably increase H2O2 production in AT-injected animals. Ischemia under hyperglycemic conditions likewise failed to induce increased H2O2 production. No difference in free iron in CSF was observed between animals subjected to ischemia under hyper- and normoglycemic conditions. The moderate decrease in total glutathione or α-tocopherol levels did not differ between normo- and hyperglycemic animals in any brain region or at any recovery time. Thus, the results failed to give positive evidence for free radical damage following brief periods of ischemia complicated by excessive acidosis. However, it is possible that free radical production is localized to a small subcellular compartment within the tissue, thereby escaping detection. Also, the results do not exclude the possibility that free radicals are pathogenetically important after ischemia of longer duration.

scholarly journals Has Oxidative Stress any Role on Mechanisms of Aminophylline – Induced Seizures? An Animal Study

2015 ◽  
Vol 12 (4) ◽  
pp. 269-274 ◽  
Author(s):  
UK Roy ◽  
M Pal ◽  
S Datta ◽  
S Harlalka
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Free Radical ◽  
Molecular Mechanisms ◽  
Clinical History ◽  
Antioxidant Vitamin ◽  
Dependent Manner ◽  
Free Radical Generation ◽  
Radical Generation ◽  
Pre Treatment

Background Aminophylline can trigger seizures in patients without known underlying epilepsy or added risk factor for seizure exacerbation in epilepsy. Most of these seizures are difficult to control and are underappreciated compared to other drug toxicities. Despite a long clinical history of aminophylline-induced seizures, relatively little is known about the underlying molecular mechanisms that contribute to methylxanthine-induced seizure generation.Objective The present study evaluated the possible involvement of free radicals in aminophylline induced seizures in rat.Method The rats were divided into two groups. The first group graded single doses of aminophylline from 100 to 300 mg/kg were administered intraperitoneally. On the basis of the results Aminophylline, a dose (300 mg/kg) producing tonic-clonic seizures and mortality in 100% animals was selected as control in the study. The second group were subjected to single antioxidant (Vitamin E or Vitamin C) or in combination for 45 days then single doses of aminophylline 300 mg/kg administered intraperitoneally to rats.Result Aminophylline induced convulsions in rats in a dose-dependent manner, and both incidence of seizure and mortality were maximum at 300 mg/kg and there was significant increase of free radical generation. But though pre-treatment with antioxidants showed differential attenuating effects on aminophylline induced free radical generation as we all known but they were very much ineffective in antagonizing aminophylline induced seizures and post-seizure mortality by any appreciable extent.Conclusion Though Aminophylline induces oxidative stress the results are suggestive that at least free radicals is not only cause of convulsiogenic effects and post-seizure mortality of aminophylline.Kathmandu University Medical Journal Vol.12(4) 2014; 269-274

Diaphragmatic free radical generation increases in an animal model of heart failure

2005 ◽  
Vol 99 (3) ◽  
pp. 1078-1084 ◽  
Author(s):  
Gerald S. Supinski ◽  
Leigh A. Callahan
Keyword(s):  
Heart Failure ◽  
Free Radicals ◽  
Free Radical ◽  
Protein Carbonyl ◽  
Protein Carbonyls ◽  
Force Frequency ◽  
Free Radical Generation ◽  
Coronary Ligation ◽  
Radical Generation ◽  
Frequency Relationship

Heart failure evokes diaphragm weakness, but the mechanism(s) by which this occurs are not known. We postulated that heart failure increases diaphragm free radical generation and that free radicals trigger diaphragm dysfunction in this condition. The purpose of the present study was to test this hypothesis. Experiments were performed using halothane-anesthetized sham-operated control rats and rats in which myocardial infarction was induced by ligation of the left anterior descending coronary artery. Animals were killed 6 wk after surgery, the diaphragms were removed, and the following were assessed: 1) mitochondrial hydrogen peroxide (H2O2) generation, 2) free radical generation in resting and contracting intact diaphragm using a fluorescent-indicator technique, 3) 8-isoprostane and protein carbonyls (indexes of free radical-induced lipid and protein oxidation), and 4) the diaphragm force-frequency relationship. In additional experiments, a group of coronary ligation animals were treated with polyethylene glycol-superoxide dismutase (PEG-SOD, 2,000 units·kg−1·day−1) for 4 wk. We found that coronary ligation evoked an increase in free radical formation by the intact diaphragm, increased diaphragm mitochondrial H2O2 generation, increased diaphragm protein carbonyl levels, and increased diaphragm 8-isoprostane levels compared with controls ( P < 0.001 for the first 3 comparisons, P < 0.05 for 8-isoprostane levels). Force generated in response to 20-Hz stimulation was reduced by coronary ligation ( P < 0.05); PEG-SOD administration restored force to control levels ( P < 0.03). These findings indicate that cardiac dysfunction due to coronary ligation increases diaphragm free radical generation and that free radicals evoke reductions in diaphragm force generation.

Free radical generation in the brain precedes hyperbaric oxygen-induced convulsions

1992 ◽  
Vol 13 (2) ◽  
pp. 101-106 ◽  
Author(s):  
Dan Torbati ◽  
Daniel F. Church ◽  
Joell M. Keller ◽  
William A. Pryor
Keyword(s):  
Free Radical ◽  
Hyperbaric Oxygen ◽  
Free Radical Generation ◽  
Radical Generation ◽  
The Brain

Free radicals as potential mediators of metal-allergy: Ni2+- and Co2+-mediated free radical generation

1998 ◽  
Vol 6 (4) ◽  
pp. 279-286 ◽  
Author(s):  
Leon T Van den Broeke ◽  
Astrid Gräslund ◽  
J.Lars G Nilsson ◽  
Jan E. Wahlberg ◽  
Annika Scheynius ◽  
...  
Keyword(s):  
Free Radicals ◽  
Free Radical ◽  
Metal Allergy ◽  
Free Radical Generation ◽  
Radical Generation

Discovery of New N-hydrazinecarbothioamide Indazole Hybrids: As Potential Radical (ABTS and DPPH) Scavengers

2020 ◽  
Vol 17 (9) ◽  
pp. 1177-1185
Author(s):  
Rafaila Rafique ◽  
Arshia ◽  
Kanwal ◽  
Khalid Mohammed Khan ◽  
Sridevi Chigurupati ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
Ascorbic Acid ◽  
Free Radicals ◽  
Free Radical ◽  
Radical Scavenging ◽  
Free Radical Scavengers ◽  
Radical Scavengers ◽  
Synthetic Compounds ◽  
Free Radical Generation ◽  
Radical Generation

Background: Free radicals are the main cause of numerous diseases. Their overproduction needs to be controlled in order to combat several ailments. The current study deals with the discovery of new free radical scavengers. Methods: Substituted N-hydrazinecarbothioamide indazoles 1-18 were evaluated for DPPH and ABTS radical scavenging activities. Results: All synthetic compounds possess good radical DPPH and ABTS scavenging potential in the ranges of IC50 = 2.11 ± 0.17 - 5.3 ± 0.11 μM and IC50 = 2.31 ± 0.06 - 5.5 ± 0.07 μM, respectively, as compared to standard ascorbic acid having IC50 = 2.02 ± 0.11 μM for DPPH and IC50 = 2.1 ± 0.07 μM for ABTS. Conclusion: These compounds could serve as leads for antioxidant activity that have the ability to control free radical generation and ward off free radical-induced disorders.

Myocardial vitamin E is consumed during cardiopulmonary bypass: indirect evidence of free radical generation in human ischemic heart

1992 ◽  
Vol 37 (3) ◽  
pp. 339-343 ◽  
Author(s):  
Renata Barsacchi ◽  
Gualtiero Pelosi ◽  
Stefano Maffei ◽  
Monica Baroni ◽  
Leonardo Salvatore ◽  
...  
Keyword(s):  
Cardiopulmonary Bypass ◽  
Free Radical ◽  
Vitamin E ◽  
Indirect Evidence ◽  
Ischemic Heart ◽  
Free Radical Generation ◽  
Radical Generation
Sign in / Sign up

Export Citation Format

Share Document