FREE RADICAL GENERATION AND OXIDATIVE STRESS IN THE HEART ARE INTENSIFIED DURING AGING AND EXHAUSTIVE EXERCISE

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

Download Full-text

Abstract 444: Differential Contribution of Oxygenases in Glycerol-Induced Acute Renal Failure in the Rats

Arteriosclerosis Thrombosis and Vascular Biology ◽

10.1161/atvb.35.suppl_1.444 ◽

2015 ◽

Vol 35 (suppl_1) ◽

Author(s):

Mohammad Newaz

Keyword(s):

Oxidative Stress ◽

Renal Failure ◽

Acute Renal Failure ◽

Free Radical ◽

Disease Model ◽

Oxidase Inhibitor ◽

Sprague Dawley ◽

Free Radical Generation ◽

Sprague Dawley Rats ◽

Radical Generation

Oxidative stress has long been identified as one if the mechanism in glycerol-induced acute renal failure (ARF), a disease model of human rhabdomyolysis. Besides NAD(P)H Oxidase, cyclooxygenase (COX) and xanthine oxidase (XO) are important oxygenase system that contributes in free radical generation in the biological system. In this study we explore involvement of these oxygenase system as the source of free radical in ARF and investigate the relationship between NAD(P)H oxidase, COX and XO in this process. Renal failure was induced in male Sprague Dawley rats by injecting glycerol (8 ml / kg; 50% v/v; i.m) with or without pretreatment of apocynin (Apo: mg/kg in drinking water, 7 days) a NAD(P)H Oxidase inhibitor. Rats were sacrificed 24 hrs after inducing ARF and kidney tissues were analyzed for biochemical assays. Glycerol increased free radical production by 39% as evident by elevated 8-isoprostane. Inhibition of NAD(P)H oxidase by apocynin reduced free radicals by 46%. In ARF rats, NAD(P)H oxidase, COX and XO activities were elevated by 106%, 70%, and 208%, respectively. Apocynin prevented this attenuation of NAD(P)H oxidase (54%; p<0.05) and COX (62%; p<0.05) but did not alter XO activity. These data suggests that NAD(P)H oxidase, COX, and XO are involved in generating oxidative stress in ARF. We also propose that COX-mediated free radical generation requires a functional NAD(P)H oxidase.

Download Full-text

Mitochondrial free radical generation, oxidative stress, and aging11This article is dedicated to the memory of our dear friend, colleague, and mentor Lars Ernster (1920–1998), in gratitude for all he gave to us.

Free Radical Biology and Medicine ◽

10.1016/s0891-5849(00)00317-8 ◽

2000 ◽

Vol 29 (3-4) ◽

pp. 222-230 ◽

Cited By ~ 1775

Author(s):

Enrique Cadenas ◽

Kelvin J.A. Davies

Keyword(s):

Oxidative Stress ◽

Free Radical ◽

Free Radical Generation ◽

Radical Generation

Download Full-text

The effect of vitamin C and iron on dopamine-mediated free radical generation: implications to Parkinson's disease

Dalton Transactions ◽

10.1039/c7dt04373b ◽

2018 ◽

Vol 47 (12) ◽

pp. 4059-4069 ◽

Cited By ~ 8

Author(s):

Yingying Sun ◽

An Ninh Pham ◽

T. David Waite

Keyword(s):

Oxidative Stress ◽

Parkinson’S Disease ◽

Free Radical ◽

Combination Therapy ◽

Vitamin C ◽

Iron Chelation ◽

Iron Chelator ◽

Promising Direction ◽

Free Radical Generation ◽

Radical Generation

While the application of Asc alone may aggravate the progression of PD in view of the possible peroxidation of Asc bound Fe(ii), a combination therapy of Asc and strong clinically appropriate iron chelator would appear to be a promising direction for the treatment of PD as a result of the enhanced iron chelation and attenuation in oxidative stress and toxicity induced by DA derived quinones.

Download Full-text

Overexpression of Mitochondrial Hsp70/Hsp75 in Rat Brain Protects Mitochondria, Reduces Oxidative Stress, and Protects from Focal Ischemia

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.2008.125 ◽

2008 ◽

Vol 29 (2) ◽

pp. 365-374 ◽

Cited By ~ 97

Author(s):

Lijun Xu ◽

Ludmila A Voloboueva ◽

YiBing Ouyang ◽

Rona G Giffard

Keyword(s):

Oxidative Stress ◽

Free Radical ◽

Rat Brain ◽

Mitochondrial Function ◽

Infarct Volume ◽

Artery Occlusion ◽

Free Radical Generation ◽

Neurological Score ◽

Radical Generation ◽

Mitochondrial Hsp70

Mitochondria are known to be central to the cell's response to ischemia, because of their role in energy generation, in free radical generation, and in the regulation of apoptosis. Heat shock protein 75 (Hsp75/Grp75/mortalin/TRAP1) is a member of the HSP70 chaperone family, which is targeted to mitochondria. Overexpression of Hsp75 was achieved in rat brain by DNA transfection, and expression was observed in both astrocytes and neurons. Rats were subjected to 100 mins middle cerebral artery occlusion followed by assessment of infarct volume, neurological score, mitochondrial function, and levels of oxidative stress at 24 h reperfusion. Overexpression of Hsp75 reduced infarct area from 44.6%±21.1% to 25.7%±12.1% and improved neurological outcome significantly. This was associated with improved mitochondrial function as shown by protection of complex IV activity, marked reduction of free radical generation detected by hydroethidine fluorescence, reduction of lipid peroxidation detected by 4-hydroxy-2-nonenol immunoreactivity, and increased preservation of ATP levels. This suggests that targeting mitochondria for protection may be a useful strategy to reduce ischemic brain injury.

Download Full-text

Neutrophil-Free Radical Generation and Enzymatic Antioxidants in Migraine Patients

Cephalalgia ◽

10.1111/j.1468-2982.2004.00631.x ◽

2004 ◽

Vol 24 (1) ◽

pp. 37-43 ◽

Cited By ~ 14

Author(s):

R Shukla ◽

MK Barthwal ◽

N Srivastava ◽

P Sharma ◽

SAV Raghavan ◽

...

Keyword(s):

Oxidative Stress ◽

Free Radical ◽

Family History ◽

Univariate Analysis ◽

Positive Family History ◽

Polymorphonuclear Neutrophils ◽

Enzymatic Antioxidants ◽

Free Radical Generation ◽

Radical Generation ◽

Significant Change

The present study was undertaken to elucidate the role of circulating neutrophils if any in oxidative stress in migraine by evaluating free radical generation and activities of enzymatic antioxidants in the blood in 55 patients with migraine and 60 healthy controls. Free radical generation was assessed by flow cytometry, while activity of catalase, superoxide dismutase (SOD) and glutathione peroxidase (GPx) was estimated in blood polymorphonuclear neutrophils (PMNs) by standard procedures. Platelet SOD was also measured. No significant change was found in free radical generation and in the activity of catalase, SOD and GPx in migraine patients. Univariate analysis of PMN catalase level revealed that migraineurs with a positive family history had significantly lower catalase activity compared with those with a negative family history. No correlation was found in the activity of antioxidant enzymes with age, duration of disease, time since last attack and headache index. The platelet SOD also did not show any significant change in patients of migraine without aura. Platelet aggregation in the presence or absence of PMNs was also not altered significantly. Thus the findings of the present study suggest that neutrophils are not the cause of oxidative stress observed in migraine patients.

Download Full-text