Nitric Oxide: A Simple Free Radical with Complex Chemistry and Biology

2003 ◽  
pp. 1-19
Author(s):  
Jason P. Eiserich
Keyword(s):  
Nitric Oxide ◽  
Free Radical ◽  
Complex Chemistry

scholarly journals Nitric Oxide Is a Factor in the Stabilization of Hypoxia-Inducible Factor-1α in Cancer: Role of Free Radical Formation

2006 ◽  
Vol 66 (2) ◽  
pp. 770-774 ◽  
Author(s):  
Marisol Quintero ◽  
Peter A. Brennan ◽  
Gareth J. Thomas ◽  
Salvador Moncada
Keyword(s):  
Nitric Oxide ◽  
Free Radical ◽  
Hypoxia Inducible Factor ◽  
Radical Formation ◽  
Hypoxia Inducible Factor 1Α ◽  
Free Radical Formation

scholarly journals The detection and inhibition of free radical chain reactions

1942 ◽  
Vol 180 (982) ◽  
pp. 237-256 ◽  
Keyword(s):  
Nitric Oxide ◽  
Free Radical ◽  
Chemical Analysis ◽  
Diethyl Ether ◽  
Pressure Increase ◽  
Stationary States ◽  
Decomposition Rates ◽  
Radical Chain ◽  
Chain Reactions ◽  
Limiting Values

Part I. Comparison of nitric oxide and propylene as inhibitors The reduction by propylene of the rate of pressure increase in the decomposition of propaldehyde at 550° has been shown by chemical analysis to represent a true inhibition of the reaction, and not to be due n an important degree to an induced polymerization of the propylene. With propaldehyde and with diethyl ether the limiting values to which the decomposition rates are reduced by nitric oxide and by propylene respectively are the same, although much more propylene is required to produce a given degree of inhibition. From this it is concluded that the limiting rates are more probably those of independent non-chain processes, than those characteristic of stationary states where the inhibitor starts and stops chains with equal efficiency.

A radiometric analysis of nitric oxide synthase activity in Hymenolepis diminuta

Parasitology ◽  
2000 ◽  
Vol 120 (1) ◽  
pp. 91-95 ◽  
Author(s):  
N. B. TERENINA ◽  
M. V. ONUFRIEV ◽  
N. V. GULYAEVA ◽  
A. M. LINDHOLM ◽  
M. K. S. GUSTAFSSON
Keyword(s):  
Nitric Oxide ◽  
Free Radical ◽  
Nitric Oxide Synthase ◽  
Nadph Diaphorase ◽  
Hymenolepis Diminuta ◽  
Complete Reduction ◽  
Radiometric Analysis ◽  
Nos Inhibitors ◽  
Oxide Synthase ◽  
Nitric Oxide Synthase Activity

The free radical nitric oxide (NO) is a neuronal messenger which is synthesized from L-arginine and O2 by nitric oxide synthase (NOS). In the synthesis NO and L-citrulline are produced in a stoichiometric 1[ratio ]1 relation. The activity of NOS was analysed in homogenates of the rat tapeworm Hymenolepis diminuta by measuring the formation of L-[3H]citrulline after incubation with L-[3H]arginine. The nature of NOS in H. diminuta was determined by studying the effect of 3 types of NOS inhibitors: (1) L-NAME, (2) EGTA, (3) 7-nitro-indazole. All inhibitors caused a significant but not complete reduction in the formation of L-[3H]citrulline. The results are discussed against the background of nerve cells and fibres positive for NADPH-diaphorase staining in H. diminuta.

scholarly journals NITRIC OXIDE AND ALLYL ALCOHOL INDUCED HEPATOTOXICITY

2014 ◽  
Vol 1 (1) ◽  
Author(s):  
M. M. Korda
Keyword(s):  
Nitric Oxide ◽  
Free Radical ◽  
Blood Serum ◽  
Allyl Alcohol ◽  
Calcium Ionophore ◽  
Free Radical Oxidation ◽  
No Synthase ◽  
Nitrate Content ◽  
Radical Oxidation ◽  
Nos Inhibitors

<p><strong>Background.</strong> Nitric oxide (NO) is an important mediator of hepatotoxicity. NO in liver can be derived from two sources: (1) constitutive NO synthase (eNOS) in endothelial cells, and (2) inducible NO synthase (iNOS) in hepatocytes and Kupffer cells.<br /><strong>Objectives.</strong> The present study was aimed to examine the effect of nonselective NOS inhibitor (L-NAME) and selective iNOS inhibitor (1400W) on the development of allyl alcohol (AA) induced hepatitis in rats.<br /><strong>Methods.</strong> Male Wistar rats were treated with intraperitoneal injection of saline or AA and L-NAME or 1400W. NO in liver was measured by electrochemical method after eNOS stimulation by calcium ionophore. Total NOS activity and nitrite/nitrate content were measured in liver and blood serum. The activity of free radical oxidation in liver was measured by chemiluminescent method. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activities were assayed in blood serum<br /><strong>Results.</strong> AA increased the activity of free radical processes in liver and markers of cytolysis in serum, as well as decreased eNOS and increased iNOS activities. L-NAME considerably inhibited eNOS and augmented the necrosogenic properties of AA, whereas 1400W partially prevented liver damage.<br /><strong>Conclusion.</strong> It has been concluded that in AA intoxication NO produced from eNOS is beneficial to the liver, but NO derived from the upregulated iNOS has deleterious effect.</p><p><strong>KEY WORDS:</strong> nitric oxide, toxic hepatitis, NOS inhibitors.<br /><br /></p>

scholarly journals Oxygen radicals, nitric oxide, and peroxynitrite: Redox pathways in molecular medicine

2018 ◽  
Vol 115 (23) ◽  
pp. 5839-5848 ◽  
Author(s):  
Rafael Radi
Keyword(s):  
Nitric Oxide ◽  
Free Radical ◽  
Mammalian Cells ◽  
Oxygen Radicals ◽  
Biochemical Characterization ◽  
Cell Function ◽  
Molecular Medicine ◽  
Antioxidant Systems ◽  
Cellular Functions ◽  
Cell Degeneration

Oxygen-derived free radicals and related oxidants are ubiquitous and short-lived intermediates formed in aerobic organisms throughout life. These reactive species participate in redox reactions leading to oxidative modifications in biomolecules, among which proteins and lipids are preferential targets. Despite a broad array of enzymatic and nonenzymatic antioxidant systems in mammalian cells and microbes, excess oxidant formation causes accumulation of new products that may compromise cell function and structure leading to cell degeneration and death. Oxidative events are associated with pathological conditions and the process of normal aging. Notably, physiological levels of oxidants also modulate cellular functions via homeostatic redox-sensitive cell signaling cascades. On the other hand, nitric oxide (•NO), a free radical and weak oxidant, represents a master physiological regulator via reversible interactions with heme proteins. The bioavailability and actions of •NO are modulated by its fast reaction with superoxide radical (O2•−), which yields an unusual and reactive peroxide, peroxynitrite, representing the merging of the oxygen radicals and •NO pathways. In this Inaugural Article, I summarize early and remarkable developments in free radical biochemistry and the later evolution of the field toward molecular medicine; this transition includes our contributions disclosing the relationship of •NO with redox intermediates and metabolism. The biochemical characterization, identification, and quantitation of peroxynitrite and its role in disease processes have concentrated much of our attention. Being a mediator of protein oxidation and nitration, lipid peroxidation, mitochondrial dysfunction, and cell death, peroxynitrite represents both a pathophysiologically relevant endogenous cytotoxin and a cytotoxic effector against invading pathogens.

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