scholarly journals Intracellular free radical production by peripheral blood T lymphocytes from patients with systemic sclerosis: role of NADPH oxidase and ERK1/2

2015 ◽  
Vol 17 (1) ◽  
Author(s):  
Donatella Amico ◽  
Tatiana Spadoni ◽  
Marina Rovinelli ◽  
Marta Serafini ◽  
Giovanna D’Amico ◽  
...  
Keyword(s):  
Systemic Sclerosis ◽  
Free Radical ◽  
T Lymphocytes ◽  
Nadph Oxidase ◽  
Peripheral Blood ◽  
Free Radical Production ◽  
Radical Production

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.

scholarly journals Role of Carvedilol in Prevention of Adrenaline Induced Myocardial Infraction in Experimental Animal

2016 ◽  
Vol 12 (2) ◽  
pp. 127-134
Author(s):  
Wahida Rahman ◽  
Nargis Akhter ◽  
Md Abrar Hossain ◽  
Sayeda Nazrina
Keyword(s):  
Free Radical ◽  
Reduced Glutathione ◽  
Myocardial Necrosis ◽  
Myocardial Damage ◽  
Antioxidant Property ◽  
Free Radical Production ◽  
Group Iii ◽  
Radical Production ◽  
Group I

Introduction: Acute myocardial infarction (AMI) is the most important form of ischemic heart disease (IHD). Coronary artery disease (CAD) is an increasingly important medical and public health problem and is the leading cause of mortality in Bangladesh. AMI is the rapid development of myocardial necrosis caused by a critical imbalance between the oxygen supply and demand of the myocardium. Total occlusion of the coronary arteries for more than 4-6 hrs results in irreversible myocardial necrosis, but reperfusion within this period can salvage the myocardium and reduce morbidity and mortality. Objectives: To assess the role of carvedilol in prevention of adrenaline induced cardiac damage in experimental animal. Materials and Methods: This experimental study was carried out in the department of pharmacology, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka for a period of One year spanning from July 2004 to June 2005. Fifty two healthy rats of Long Evan Norwegian strains, 3-4 months of ages of both sexes, weight between 180-220g were used. The experiment was divided into two parts: Part-I and Part-II. Thirty two rats were selected for Part-I experiment and subdivided into Group-I and Group-II. In Part-II experiment, 20 rats were selected and placed as Group-III. Group-I (12 rats) of control group was treated with 02 doses of inj distilled water (D/W) subcutaneously (S.C.) 24 hrs apart and serum creatine kinase-MB (CK-MB) level and hepatic and cardiac reduced glutathione (GSH) contents were estimated from 06 (Group-Ia) rats after 12 hrs and serum aspartate aminotransferase (AST) level and hepatic and cardiac reduced GSH contents were estimated from 06 (Group-Ib) rats after 24 hrs of 2nd inj of D/W. Group-II (20 rats) was treated with 02 doses of inj adrenaline (2mg/kg) S.C. in 24 hrs interval and in above mentioned way serum CK-MB level, GSH (hepatic and cardiac) contents and serum AST and GSH (hepatic and cardiac) contents were estimated 12 hrs and 24 hrs after the 2nd inj of adrenaline respectively. In experimental group (Group-III) all the rats (20) were treated with carvedilol (1 mg/kg) orally for 14 consecutive days and then were given 02 doses of inj adrenaline with the interval of 24 hrs and again serum CK-MB level and GSH (hepatic and cardiac) contents were estimated from half of the rats (10) after 12 hrs of injection and serum AST level and GSH (hepatic and cardiac) contents were measured from half of the rats (10) after 24 hrs of 2nd injection of adrenaline. Results: Adrenaline (2mg/kg) induced myocardial damage was evaluated biochemically by significant (P˂0.001) increase in CK-MB and AST levels. Free radical production following adrenaline induced myocardial damage was reflected by significant (P˂0.001) depletion in hepatic and cardiac reduced glutathione (GSH) contents. Cardioprotection provided by carvedilol pretreatment in adrenaline induced myocardial infarction was assessed by significant prevention of increase in serum CK-MB and AST levels. Antioxidant property of carvedilol was evaluated by significant (P<0.001) prevention of depletion in hepatic and cardiac GSH contents. The results of the study indicated that carvedilol pretreatment provided effective prevention in adrenaline induced myocardial damage and also provided effective antioxidative action. Conclusion: This study indicated that adrenaline administration induced myocardial damage as evidenced by increase in serum CK-MB and AST levels which was associated with free radical production as reflected by depletion in hepatic and cardiac GSH contents. It was observed that carvedilol through their antioxidant property in addition to their β-blocking effect prevents free radical mediated injury of catecholamine assault following MI. Journal of Armed Forces Medical College Bangladesh Vol.12(2) 2016: 127-134

Intracellular free radical production in synovial T lymphocytes from patients with rheumatoid arthritis

2005 ◽  
Vol 52 (7) ◽  
pp. 2003-2009 ◽  
Author(s):  
P. H. J. Remans ◽  
M. van Oosterhout ◽  
T. J. M. Smeets ◽  
M. Sanders ◽  
W. M. Frederiks ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Free Radical ◽  
T Lymphocytes ◽  
Free Radical Production ◽  
Radical Production

scholarly journals Role of Nitric Oxide Synthase Inhibition in Leukocyte-Endothelium Interaction in the Rat Pial Microvasculature

1996 ◽  
Vol 16 (6) ◽  
pp. 1143-1152 ◽  
Author(s):  
Ute Lindauer ◽  
Jens Dreier ◽  
Klemens Angstwurm ◽  
Inger Rubin ◽  
Arno Villringer ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Free Radical ◽  
Oxygen Free Radical ◽  
Sodium Fluorescein ◽  
Free Radical Production ◽  
Physiological Conditions ◽  
Cranial Window ◽  
Radical Production ◽  
Bbb Permeability

We investigated the role of nitric oxide (NO) in leukocyte-endothelium interaction, blood-brain barrier (BBB) function and oxygen free-radical production in the rat pial microcirculation. In a closed cranial window preparation (dura removed) over the parietal cortex of pentobarbital-anesthetized Wistar rats, NO synthase (NOS) was inhibited by systemic and/or topical application of Nω-nitro-l-arginine (l-NNA) under physiological conditions and during leukotriene B4 (LTB4) activation. Circulating leukocytes were labeled by intravenous injection of rhodamine 6G. We used a confocal laser scanning microscope (CLSM) and studied leukocyte rolling and sticking in pial veins and arteries before and after NOS inhibition. At the end of the experiments, sodium-fluorescein was injected intravenously to test BBB integrity. Brain cortex oxygen free-radical production was investigated in the cranial window preparation using lucigenin-enhanced chemiluminescence (CL). l-NNA application did not lead to significant changes in leukocyte-endothelium interaction, BBB function, and oxygen free-radical production under physiological conditions [leukocyte-endothelium interaction: control (n = 5), l-NNA systemically (n = 5), l-NNA topically (n = 5): at baseline rollers/100 μm: 0.76 ± 0.55, 0.64 ± 0.94, 0.44 ± 0.55 and stickers/100 μm: 0.90 ± 0.28, 0.76 ± 0.24, 0.84 ± 0.42; at 60 min rollers/100 μm: 1.49 ± 0.66, 1.21 ± 0.99, 0.67 ± 0.66 and stickers/100 μm: 1.04 ± 0.20, 1.19 ± 0.23, 1.21 ± 0.54; oxygen free-radical production (n = 4): CL count before l-NNA application 35 ± 17 cps, after 1 h of topical superfusion of l-NNA 38 ± 14 cps; p < 0.05]. In contrast to the results achieved under physiological conditions, a significant further increase of rolling leukocytes and BBB permeability occurred due to NOS inhibition under LTB4-activated conditions [76 ± 47% significant ( p ≤ 0.01, n = 7) further increase of rollers/100 μm due to 60 min l-NNA application following the activation period of 120 min LTB4 superfusion]. Our results support a modulatory role for NO in leukocyte-endothelium interaction and BBB permeability in the pial microcirculation when this interaction is increased.

Increased free radical production in hypertension due to increased expression of the NADPH oxidase subunit p22phox in lymphoblast cell lines

2002 ◽  
Vol 20 (4) ◽  
pp. 677-683 ◽  
Author(s):  
Andrew I. Pettit ◽  
Richard K. M. Wong ◽  
Virginia Lee ◽  
Sonja Jennings ◽  
Pauline A. Quinn ◽  
...  
Keyword(s):  
Free Radical ◽  
Nadph Oxidase ◽  
Cell Lines ◽  
Free Radical Production ◽  
Oxidase Subunit ◽  
Radical Production

Effect of Aluminium on Superoxide Dismutase

1989 ◽  
Vol 77 (5) ◽  
pp. 463-466 ◽  
Author(s):  
Ruth Shainkin-Kestenbaum ◽  
Andrew J. Adler ◽  
Geoffrey M. Berlyne ◽  
C. Caruso
Keyword(s):  
Superoxide Dismutase ◽  
Free Radical ◽  
Elevated Serum ◽  
Oxygen Free Radical ◽  
Protective Role ◽  
Free Radical Production ◽  
Radical Production ◽  
Excessive Oxygen

1. The effect of Al3+ on superoxide dismutase in vitro was studied, since in uraemia there is excessive superoxide production and frequently an elevated serum Al3+ level. Thus, the protective role of superoxide dismutase is particularly important. 2. Al3+ in concentrations similar to those found in the serum of uraemic patients inhibits superoxide dismutase activity. The degree of inhibition is directly proportional to the Al3+ level. 3. The combination of excessive oxygen free radical production with an increased Al3+ level may contribute to a variety of complications, including aluminium dementia or initiation and promotion of carcinogenic processes, which are known to be more common in uraemic patients.

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