Kojic acid scavenges free radicals while potentiating leukocyte functions including free radical generation

Inflammation ◽  
1991 ◽  
Vol 15 (4) ◽  
pp. 303-315 ◽  
Author(s):  
Yukie Niwa ◽  
Hirohiko Akamatsu
Keyword(s):  
Free Radicals ◽  
Free Radical ◽  
Kojic Acid ◽  
Free Radical Generation ◽  
Radical Generation

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.

scholarly journals Free Radicals and the Pathogenesis of Type 1 Diabetes:  -Cell Cytokine-Mediated Free Radical Generation Via Cyclooxygenase-2

Diabetes ◽  
2003 ◽  
Vol 52 (8) ◽  
pp. 1994-1999 ◽  
Author(s):  
T. Tabatabaie ◽  
A. Vasquez-Weldon ◽  
D. R. Moore ◽  
Y. Kotake
Keyword(s):  
Type 1 Diabetes ◽  
Free Radicals ◽  
Free Radical ◽  
Cyclooxygenase 2 ◽  
Free Radical Generation ◽  
Radical Generation

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.

Horseradish peroxidase. XL. The oxidation of native enzyme to Compound II

1980 ◽  
Vol 58 (23) ◽  
pp. 2504-2507 ◽  
Author(s):  
Alexander D. Nadezhdin ◽  
H. Brian Dunford
Keyword(s):  
Experimental Data ◽  
Free Radicals ◽  
Free Radical ◽  
Horseradish Peroxidase ◽  
Native Enzyme ◽  
Free Radical Generation ◽  
Radical Generation ◽  
Compound Ii ◽  
Native Horseradish Peroxidase

The oxidation of native horseradish peroxidase to Compound II by photochemically generated inorganic free radicals [Formula: see text], [Formula: see text], and [Formula: see text] was observed. The rates of Compound II accumulation for different rates of free radical generation and different reagent concentrations have been measured. The interpretation of the experimental data allowed us to estimate the rates of the reactions [Formula: see text], [Formula: see text], and [Formula: see text]: (3–6) × 106 M−1 s−1, (2.2–3.0) × 106 M−1, and [Formula: see text] respectively. Also obtained for all three oxidants were the ratios of the number of free radicals responsible for the heme oxidation to the total number of them attacking the enzyme.

scholarly journals Role of NAD+—Modulated Mitochondrial Free Radical Generation in Mechanisms of Acute Brain Injury

2020 ◽  
Vol 10 (7) ◽  
pp. 449
Author(s):  
Nina Klimova ◽  
Adam Fearnow ◽  
Tibor Kristian
Keyword(s):  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Free Radical ◽  
Brain Injury ◽  
Antioxidant System ◽  
Ros Generation ◽  
Ros Production ◽  
Oxygen Species ◽  
Free Radical Generation ◽  
Radical Generation

It is commonly accepted that mitochondria represent a major source of free radicals following acute brain injury or during the progression of neurodegenerative diseases. The levels of reactive oxygen species (ROS) in cells are determined by two opposing mechanisms—the one that produces free radicals and the cellular antioxidant system that eliminates ROS. Thus, the balance between the rate of ROS production and the efficiency of the cellular detoxification process determines the levels of harmful reactive oxygen species. Consequently, increase in free radical levels can be a result of higher rates of ROS production or due to the inhibition of the enzymes that participate in the antioxidant mechanisms. The enzymes’ activity can be modulated by post-translational modifications that are commonly altered under pathologic conditions. In this review we will discuss the mechanisms of mitochondrial free radical production following ischemic insult, mechanisms that protect mitochondria against free radical damage, and the impact of post-ischemic nicotinamide adenine mononucleotide (NAD+) catabolism on mitochondrial protein acetylation that affects ROS generation and mitochondrial dynamics. We propose a mechanism of mitochondrial free radical generation due to a compromised mitochondrial antioxidant system caused by intra-mitochondrial NAD+ depletion. Finally, the interplay between different mechanisms of mitochondrial ROS generation and potential therapeutic approaches are reviewed.

scholarly journals Anti-Inflammatory and Anti-Oxidative Activity of Indole-3-Acetic Acid Involves Induction of HO-1 and Neutralization of Free Radicals in RAW264.7 Cells

2020 ◽  
Vol 21 (5) ◽  
pp. 1579 ◽  
Author(s):  
Yun Ji ◽  
Wenzhen Yin ◽  
Yuan Liang ◽  
Lijun Sun ◽  
Yue Yin ◽  
...  
Keyword(s):  
Acetic Acid ◽  
Free Radicals ◽  
Free Radical ◽  
Inflammatory Response ◽  
Heme Oxygenase 1 ◽  
Free Radical Generation ◽  
Raw264.7 Macrophages ◽  
Radical Generation ◽  
Anti Inflammatory ◽  
Indole 3 Acetic Acid

The cellular and molecular mechanisms by which indole-3-acetic acid (IAA), a tryptophan-derived metabolite from gut microbiota, attenuates inflammation and oxidative stress has not been fully elucidated. The present study was to unearth the protective effect and underlying mechanism of IAA against lipopolysaccharide (LPS)-induced inflammatory response and free radical generation in RAW264.7 macrophages. IAA significantly ameliorated LPS-induced expression of interleukin-1β (IL-1β), interleukin-6 (IL-6), and monocyte chemoattractant protein-1 (MCP-1) as well as generation of reactive oxidative species (ROS) and nitric oxide (NO). LPS-triggered nuclear translocation of nuclear factor kappa B (NF-κB) p65 was mitigated by IAA treatment. Further, an up-regulation of heme oxygenase-1 (HO-1) was observed in IAA-treated cells in dose-dependent manner under both normal and LPS-stimulated condition. Interference of HO-1 activity by tin protoporphyrin IX (SnPP) impeded the alleviative effects of IAA on expression of IL-1β and IL-6 induced by LPS, whereas demonstrated no effect on its suppression of ROS and NO production. This result suggests a HO-1-dependent anti-inflammatory effect of IAA and its direct scavenging action on free radicals. Treatment with CH-223191, a specific antagonist of aryl hydrocarbon receptor (AhR), showed no significant effects on the beneficial role of IAA against inflammation and free radical generation. In summary, our findings indicate that IAA alleviates LPS-elicited inflammatory response and free radical generation in RAW264.7 macrophages by induction of HO-1 and direct neutralization of free radicals, a mechanism independent of AhR.

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