Free radical production during phenylhydrazine-induced hemolysis

1982 ◽  
Vol 60 (12) ◽  
pp. 1528-1531 ◽  
Author(s):  
H. A. O. Hill ◽  
P. J. Thornalley
Keyword(s):  
Spin Trap ◽  
Spin Adduct ◽  
Phenyl Radical ◽  
Erythrocyte Suspension ◽  
Phenyl Radicals ◽  
Spin Traps ◽  
Free Radical Production ◽  
Radical Trapping ◽  
Radical Production ◽  
Moderate Yield

The production of phenyl radicals during phenylhydrazine-induced hemolysis has been demonstrated by the use of the spin traps, DMPO, M4PO, and LINPyBN. The phenyl spin adducts of DMPO and M4PO were produced in moderate yield by an oxygenated 1% erythrocyte suspension. With the lipid soluble spin trap LINPyBN, a dramatic increase (400%) in the yield of phenyl spin adduct was observed despite little increase in the rate of phenyl radical trapping. The production of phenyl spin adducts was decreased when phenylhydrazine-4-sulphonic acid or carbonmonoxyhemoglobin-containing erythrocytes were used. These results suggest that the reaction of phenylhydrazine with oxyhemoglobin leads to the formation of phenyl radicals that are preferentially trapped in the erythrocyte membrane.

scholarly journals The oxidation of oxyhaemoglobin by glyceraldehyde and other simple monosaccharides

1984 ◽  
Vol 217 (3) ◽  
pp. 615-622 ◽  
Author(s):  
P J Thornalley ◽  
S P Wolff ◽  
M J C Crabbe ◽  
A Stern
Keyword(s):  
Free Radicals ◽  
Free Radical ◽  
Phosphate Buffer ◽  
Spin Trap ◽  
Spin Trapping ◽  
Free Radical Production ◽  
Radical Production ◽  
Hydroxyalkyl Radical ◽  
Aldehyde Derivative

Glyceraldehyde and other simple monosaccharides oxidize oxyhaemoglobin to methaemoglobin in phosphate buffer at pH 7.4 and 37 degrees C, with the concomitant production of H2O2 and an alpha-oxo aldehyde derivative of the monosaccharide. Simple monosaccharides also reduce methaemoglobin to ferrohaemichromes (non-intact haemoglobin) at pH 7.4 and 37 degrees C. Carbonmonoxyhaemoglobin is unreactive towards oxidation by autoxidizing glyceraldehyde. Free-radical production from autoxidizing monosaccharides with haemoglobins was observed by the e.s.r. technique of spin trapping with the spin trap 5,5-dimethyl-l-pyrroline N-oxide. Hydroxyl and l-hydroxyalkyl radical production observed from monosaccharide autoxidation was quenched in the presence of oxyhaemoglobin and methaemoglobin. The haemoglobins appear to quench the free radicals by reaction with the free radicals and/or the ene-diol precursor of the free radical.

scholarly journals Mononuclear phagocytes have the potential for sustained hydroxyl radical production. Use of spin-trapping techniques to investigate mononuclear phagocyte free radical production.

1988 ◽  
Vol 168 (6) ◽  
pp. 2367-2372 ◽  
Author(s):  
B E Britigan ◽  
T J Coffman ◽  
D R Adelberg ◽  
M S Cohen
Keyword(s):  
Spin Trap ◽  
Spin Trapping ◽  
Mononuclear Phagocyte ◽  
Mononuclear Phagocytes ◽  
Tartrate Resistant Acid Phosphatase ◽  
Ifn Gamma ◽  
Free Radical Production ◽  
Radical Production ◽  
Inflammatory Tissue

Monocytes lack lactoferrin and have much less myeloperoxidase than neutrophils. They also acquire a potential catalyst for .OH production (tartrate-resistant acid phosphatase) as they differentiate into macrophages. Consequently, the nature of free radicals produced by these cells was examined using the previously developed spin-trapping system. When stimulated with either PMA or OZ neither monocytes nor monocyte-derived macrophages (MDM) exhibited spin trap evidence of .OH formation. Pretreatment with IFN-gamma failed to induce MDM .OH production. When provided with an exogenous Fe+3 catalyst, both stimulated monocytes and MDM, but not PMN, exhibited sustained .OH production, presumably due to the absence of lactoferrin in mononuclear phagocytes. Sustained production of .OH could contribute to the microbicidal activity of mononuclear phagocytes as well as inflammatory tissue damage under in vivo conditions where catalytic Fe+3 may be present.

Chemiluminescence as an index of drug-induced free radical production in pancreatic islets

Diabetes ◽  
1984 ◽  
Vol 33 (2) ◽  
pp. 160-163 ◽  
Author(s):  
K. Asayama ◽  
D. English ◽  
A. E. Slonim ◽  
I. M. Burr
Keyword(s):  
Free Radical ◽  
Pancreatic Islets ◽  
Drug Induced ◽  
Free Radical Production ◽  
Radical Production

Features of the oxidative status in patients with lupus nephritis

2020 ◽  
Vol 24 (1) ◽  
pp. 39-44
Author(s):  
E. V. Smirnova ◽  
E. V. Proskurnina ◽  
T. N. Krasnova
Keyword(s):  
Oxidative Stress ◽  
Free Radical ◽  
Lupus Nephritis ◽  
Blood Plasma ◽  
Respiratory Burst ◽  
Oxidative Status ◽  
Free Radical Production ◽  
Radical Production ◽  
Neutrophil Activity ◽  
Kidney Involvement

BACKGROUND. Oxidative status impairment plays a significant role in the pathogenesis of SLE and lupus nephritis (LN). The data about oxidative status in this disease are incomplete, that’s why it’s necessary to use a new approach to study it. THE AIM: To study oxidative status in SLE patients with kidney involvement. PATIENTS AND METHODS:53 patients with SLE were included in this prospective study, among them 40 patients with different severity of kidney involvement, control group were 87 healthy donors. Oxidative stress parameters were measured: antioxidant activity (AOA) of blood plasma and parameters, characterizing the state of the main source of reactive oxygen species (ROS) – neutrophils, more specifically: specific spontaneous neutrophil activity, specific stimulated activity (peak and integral), coefficient of respiratory burst attenuation, representing the rate of free radical production decrease after stimulation, the higher the value of this parameter, the slower is free radical production decrease. RESULTS. It was shown elevation of neutrophil free radical-producing activity parameters and elevation of blood plasma AOA in patients with LN, comparing to healthy controls. Immunosuppressive therapy with glucocorticosteroids (GCS) and cytostatics (CS) increased blood plasma AOA comparing to monotherapy with GCS. A correlation between oxidative status impairment and intensity of inflammatory reactions was found: correlation of respiratory burst attenuation coefficient with blood sedimentation rate was shown. Reduction of spontaneous free radical-producing neutrophil activity was found in LN patients with NS, which might be the result of neutrophil functional activity attenuation in high disease activity. CONCLUSION. The increased free radical-producing neutrophil activity was shown, which might be the cause of oxidative stress in SLE with LN. It seems warranted investigation of these parameters in samples of larger volume to search targets aimed at neutrophils. The necessity of antioxidant therapy in patients with SLE seems doubtful, as they show significant increase of blood plasma AOA, which might result from compensatory reaction of human organism to oxidative stress and therapy with GCS and CS.

scholarly journals Estimation of the Postmortem Duration of Mouse Tissue by Electron Spin Resonance Spectroscopy

2011 ◽  
Vol 2011 ◽  
pp. 1-11
Author(s):  
Shinobu Ito ◽  
Tomohisa Mori ◽  
Hideko Kanazawa ◽  
Toshiko Sawaguchi
Keyword(s):  
Free Radicals ◽  
Electron Spin Resonance ◽  
Electron Spin ◽  
Spin Trap ◽  
Detection Sensitivity ◽  
Mouse Tissue ◽  
Spin Adduct ◽  
Simple Method ◽  
Oxidation Stress ◽  
Spin Resonance

Electron spin resonance (ESR) method is a simple method for detecting various free radicals simultaneously and directly. However, ESR spin trap method is unsuited to analyze weak ESR signals in organs because of water-induced dielectric loss (WIDL). To minimize WIDL occurring in biotissues and to improve detection sensitivity to free radicals in tissues, ESR cuvette was modified and used with 5,5-dimethtyl-1-pyrroline N-oxide (DMPO). The tissue samples were mouse brain, hart, lung, liver, kidney, pancreas, muscle, skin, and whole blood, where various ESR spin adduct signals including DMPO-ascorbyl radical (AsA∗), DMPO-superoxide anion radical (OOH), and DMPO-hydrogen radical (H) signal were detected. Postmortem changes in DMPO-AsA∗and DMPO-OOH were observed in various tissues of mouse. The signal peak of spin adduct was monitored until the 205th day postmortem. DMPO-AsA∗in liver (y=113.8–40.7 log (day),R1=-0.779,R2=0.6,P<.001) was found to linearly decrease with the logarithm of postmortem duration days. Therefore, DMPO-AsA∗signal may be suitable for detecting an oxidation stress tracer from tissue in comparison with other spin adduct signal on ESR spin trap method.

Free radical production in the rat retina

1992 ◽  
Vol 55 ◽  
pp. 248
Author(s):  
H. Zhang ◽  
E. Agardh ◽  
C-D. Agardh
Keyword(s):  
Free Radical ◽  
Rat Retina ◽  
Free Radical Production ◽  
Radical Production

Glutamine-induced free radical production in cultured astrocytes

Glia ◽  
2004 ◽  
Vol 46 (3) ◽  
pp. 296-301 ◽  
Author(s):  
Arumugam R. Jayakumar ◽  
K.V. Rama Rao ◽  
Arne Schousboe ◽  
Michael D. Norenberg
Keyword(s):  
Free Radical ◽  
Free Radical Production ◽  
Radical Production ◽  
Cultured Astrocytes

scholarly journals Direct evidence of iNOS-mediated in vivo free radical production and protein oxidation in acetone-induced ketosis

2008 ◽  
Vol 295 (2) ◽  
pp. E456-E462 ◽  
Author(s):  
Krisztian Stadler ◽  
Marcelo G. Bonini ◽  
Shannon Dallas ◽  
Danielle Duma ◽  
Ronald P. Mason ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Free Radical ◽  
Nadph Oxidase ◽  
Knockout Mice ◽  
Protein Oxidation ◽  
Ketone Bodies ◽  
Free Radical Production ◽  
Radical Production ◽  
Inos Knockout Mice

Diabetic patients frequently encounter ketosis that is characterized by the breakdown of lipids with the consequent accumulation of ketone bodies. Several studies have demonstrated that reactive species are likely to induce tissue damage in diabetes, but the role of the ketone bodies in the process has not been fully investigated. In this study, electron paramagnetic resonance (EPR) spectroscopy combined with novel spin-trapping and immunological techniques has been used to investigate in vivo free radical formation in a murine model of acetone-induced ketosis. A six-line EPR spectrum consistent with the α-(4-pyridyl-1-oxide)- N-t-butylnitrone radical adduct of a carbon-centered lipid-derived radical was detected in the liver extracts. To investigate the possible enzymatic source of these radicals, inducible nitric oxide synthase (iNOS) and NADPH oxidase knockout mice were used. Free radical production was unchanged in the NADPH oxidase knockout but much decreased in the iNOS knockout mice, suggesting a role for iNOS in free radical production. Longer-term exposure to acetone revealed iNOS overexpression in the liver together with protein radical formation, which was detected by confocal microscopy and a novel immunospin-trapping method. Immunohistochemical analysis revealed enhanced lipid peroxidation and protein oxidation as a consequence of persistent free radical generation after 21 days of acetone treatment in control and NADPH oxidase knockout but not in iNOS knockout mice. Taken together, our data demonstrate that acetone administration, a model of ketosis, can lead to protein oxidation and lipid peroxidation through a free radical-dependent mechanism driven mainly by iNOS overexpression.

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