In vivo topical EPR spectroscopy and imaging of nitroxide free radicals and polynitroxyl-albumin

1998 ◽  
Vol 40 (6) ◽  
pp. 806-811 ◽  
Author(s):  
Periannan Kuppusamy ◽  
Penghai Wang ◽  
Ravi A. Shankar ◽  
Li Ma ◽  
Charles E. Trimble ◽  
...  
Keyword(s):  
Free Radicals ◽  
Epr Spectroscopy

Exercise-induced brachial artery vasodilation: role of free radicals

2007 ◽  
Vol 292 (3) ◽  
pp. H1516-H1522 ◽  
Author(s):  
Russell S. Richardson ◽  
Anthony J. Donato ◽  
Abhimanyu Uberoi ◽  
D. Walter Wray ◽  
Lesley Lawrenson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Brachial Artery ◽  
Epr Spectroscopy ◽  
Vascular Function ◽  
Paramagnetic Resonance ◽  
Healthy State ◽  
Total Antioxidant ◽  
Exercise Induced

Originally thought of as simply damaging or toxic “accidents” of in vivo chemistry, free radicals are becoming increasingly recognized as redox signaling molecules implicit in cellular homeostasis. Indeed, at the vascular level, it is plausible that oxidative stress plays a regulatory role in normal vascular function. Using electron paramagnetic resonance (EPR) spectroscopy, we sought to document the ability of an oral antioxidant cocktail (vitamins C, E, and α-lipoic acid) to reduce circulating free radicals, and we employed Doppler ultrasound to examine the consequence of an antioxidant-mediated reduction in oxidative stress on exercise-induced vasodilation. A total of 25 young (18–31 yr) healthy male subjects partook in these studies. EPR spectroscopy revealed a reduction in circulating free radicals following antioxidant administration at rest (∼98%) and as a consequence of exercise (∼85%). Plasma total antioxidant capacity and vitamin C both increased following the ingestion of the antioxidant cocktail, whereas vitamin E levels were not influenced by the ingestion of the antioxidants. Brachial artery vasodilation during submaximal forearm handgrip exercise was greater with the placebo (7.4 ± 1.8%) than with the antioxidant cocktail (2.3 ± 0.7%). These data document the efficacy of an oral antioxidant cocktail in reducing free radicals and suggest that, in a healthy state, the aggressive disruption of the delicate balance between pro- and antioxidant forces can negatively impact vascular function. These findings implicate an exercise-induced reliance upon pro-oxidant-stimulated vasodilation, thereby revealing an important and positive vascular role for free radicals.

In vivo generation of free radicals in the skin of live mice under ultraviolet light, measured by L-band EPR spectroscopy

2006 ◽  
Vol 40 (5) ◽  
pp. 876-885 ◽  
Author(s):  
Keizo Takeshita ◽  
Cuiping Chi ◽  
Hiroshi Hirata ◽  
Mitsuhiro Ono ◽  
Toshihiko Ozawa
Keyword(s):  
Free Radicals ◽  
Ultraviolet Light ◽  
Epr Spectroscopy ◽  
L Band

scholarly journals In Vivo EPR Spectroscopy of Free Radicals in the Heart

1994 ◽  
Vol 102 ◽  
pp. 45 ◽  
Author(s):  
Jay L. Zweier ◽  
Periannan Kuppusamy
Keyword(s):  
Free Radicals ◽  
Epr Spectroscopy ◽  
In Vivo Epr

scholarly journals In vivo EPR spectroscopy of free radicals in the heart.

1994 ◽  
Vol 102 (suppl 10) ◽  
pp. 45-51 ◽  
Author(s):  
J L Zweier ◽  
P Kuppusamy
Keyword(s):  
Free Radicals ◽  
Epr Spectroscopy ◽  
In Vivo Epr

scholarly journals Oxidized LDLs as Signaling Molecules

Antioxidants ◽  
2021 ◽  
Vol 10 (8) ◽  
pp. 1184
Author(s):  
Jean-Marc Zingg ◽  
Adelina Vlad ◽  
Roberta Ricciarelli
Keyword(s):  
Free Radicals ◽  
Cellular Response ◽  
Vascular System ◽  
Signaling Molecules ◽  
Scavenger Receptors ◽  
Physiological Relevance ◽  
Reactive Radicals ◽  
Accumulation Of Lipids

Levels of oxidized low-density lipoproteins (oxLDLs) are usually low in vivo but can increase whenever the balance between formation and scavenging of free radicals is impaired. Under normal conditions, uptake and degradation represent the physiological cellular response to oxLDL exposure. The uptake of oxLDLs is mediated by cell surface scavenger receptors that may also act as signaling molecules. Under conditions of atherosclerosis, monocytes/macrophages and vascular smooth muscle cells highly exposed to oxLDLs tend to convert to foam cells due to the intracellular accumulation of lipids. Moreover, the atherogenic process is accelerated by the increased expression of the scavenger receptors CD36, SR-BI, LOX-1, and SRA in response to high levels of oxLDL and oxidized lipids. In some respects, the effects of oxLDLs, involving cell proliferation, inflammation, apoptosis, adhesion, migration, senescence, and gene expression, can be seen as an adaptive response to the rise of free radicals in the vascular system. Unlike highly reactive radicals, circulating oxLDLs may signal to cells at more distant sites and possibly trigger a systemic antioxidant defense, thus elevating the role of oxLDLs to that of signaling molecules with physiological relevance.

Ethane production as a measure of lipid peroxidation after renal ischemia

1986 ◽  
Vol 251 (5) ◽  
pp. F839-F843 ◽  
Author(s):  
M. S. Paller ◽  
R. P. Hebbel
Keyword(s):  
Lipid Peroxidation ◽  
Free Radicals ◽  
Superoxide Radical ◽  
Oxygen Free Radicals ◽  
Tissue Injury ◽  
Renal Ischemia ◽  
Radical Scavenger ◽  
Base Line ◽  
Ethane Production

After renal ischemia, oxygen free radicals are formed and produce tissue injury, in large part, through peroxidation of polyunsaturated fatty acids. We used an in vivo method to monitor lipid peroxidation after renal ischemia, the measurement of ethane in expired gas, to determine the time course of lipid peroxidation and the effect of several agents to limit lipid peroxidation after renal ischemia. In anesthetized rats there was no significant increase in ethane production during 60 min of renal ischemia. During the first 10 min of renal reperfusion, there was a prompt increase in ethane production from 2.9 +/- 1.3 to 6.3 +/- 1.9 pmol/min (P less than 0.05). Ethane production was significantly increased during the first 50 min of reperfusion and then rapidly tapered to base-line levels. Preischemic administration of allopurinol to prevent superoxide radical generation or the superoxide radical scavenger superoxide dismutase prevented the increase in ethane production during postischemic reperfusion. These studies confirm that there is increase lipid peroxidation following renal ischemia that can be prevented by agents which limit the formation or accumulation of oxygen free radicals. This in vivo method for measuring lipid peroxidation could also be employed to study the effects of ischemia on lipid peroxidation in other organs, as well as to monitor lipid peroxidation in other forms of injury.

In vivo measurement of oxygen-derived free radicals during reperfusion injury

Microsurgery ◽  
2002 ◽  
Vol 22 (3) ◽  
pp. 108-113 ◽  
Author(s):  
Rolf Büttemeyer ◽  
Andreas W. Philipp ◽  
Julian W. Mall ◽  
Bixia Ge ◽  
Frieder W. Scheller ◽  
...  
Keyword(s):  
Free Radicals ◽  
Reperfusion Injury ◽  
In Vivo Measurement ◽  
Oxygen Derived Free Radicals

Pharmacological Blocker of NF-κb and Mitochondrial Ros Restrict NLRP3 Inflammasome Activation and Rescue Dopaminergic Neurons in Vitro and in Vivo Parkinson’s Disease

2021 ◽  
Author(s):  
Sahabuddin Ahmed ◽  
Samir Ranjan Panda ◽  
Mohit Kwatra ◽  
Bidya Dhar Sahu ◽  
VGM Naidu
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Free Radicals ◽  
Nlrp3 Inflammasome ◽  
Nuclear Translocation ◽  
Inflammasome Activation ◽  
Mitochondrial Ros ◽  
Nlrp3 Inflammasome Activation

Abstract Several activators of NLRP3 inflammasome have been described; however, the central mechanisms of NLRP3 inflammasome activation in brain microglia, especially at the activating step through free radical generation, still require further clarification. Hence the present study aimed to investigate the role of free radicals in activating NLRP3 inflammasome driven neurodegeneration and elucidated the neuroprotective role of perillyl alcohol (PA) in vitro and in vivo models of Parkinson’s disease. Initial priming of microglial cells with lipopolysaccharide (LPS) following treatment with hydrogen peroxide (H2O2) induces NF-κB translocation to nucleus with robust generation of free radicals that act as Signal 2 in augmenting NLRP3 inflammasome assembly and its downstream targets. PA treatment suppresses nuclear translocation of NF-κB and maintains cellular redox homeostasis in microglia that limits NLRP3 inflammasome activation along with processing active caspase-1, IL-1β and IL-18. To further correlates the in vitro study with in vivo MPTP model, treatment with PA also inhibits the nuclear translocation of NF-κB and downregulates the NLRP3 inflammasome activation. PA administration upregulates various antioxidant enzymes levels and restored the level of dopamine and other neurotransmitters in the striatum of the mice brain with improved behavioural activities. Additionally, treatment with Mito-TEMPO (a mitochondrial ROS inhibitor) was also seen to inhibit NLRP3 inflammasome and rescue dopaminergic neuron loss in the mice brain. Therefore, we conclude that NLRP3 inflammasome activation requires a signal from damaged mitochondria for its activation. Further pharmacological scavenging of free radicals restricts microglia activation and simultaneously supports neuronal survival via targeting NLRP3 inflammasome pathway in Parkinson’s disease.

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