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

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

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

Free Radical Biology and Medicine ◽

10.1016/0891-5849(92)90070-w ◽

1992 ◽

Vol 13 (2) ◽

pp. 101-106 ◽

Cited By ~ 73

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

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Effect of aminoguanidine on vascular reactivity and oxygen free radical generation in thoracic aorta from streptozotocin-induced diabetic rats

The Japanese Journal of Pharmacology ◽

10.1016/s0021-5198(19)47086-8 ◽

1995 ◽

Vol 67 ◽

pp. 280

Author(s):

Hiroyuki Miura ◽

Masako Morikawa ◽

Michiko Inoue ◽

Hiroshi Kogo

Keyword(s):

Free Radical ◽

Thoracic Aorta ◽

Vascular Reactivity ◽

Oxygen Free Radical ◽

Diabetic Rats ◽

Free Radical Generation ◽

Radical Generation

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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.

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