scholarly journals Enhanced nitric oxide and reactive oxygen species production and damage after inhalation of silica

2002 ◽  
Vol 283 (2) ◽  
pp. L485-L493 ◽  
Author(s):  
Dale W. Porter ◽  
Lyndell Millecchia ◽  
Victor A. Robinson ◽  
Ann Hubbs ◽  
Patsy Willard ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Bronchoalveolar Lavage ◽  
Reactive Oxygen ◽  
Lavage Fluid ◽  
Nuclear Factor Κb ◽  
No Synthase ◽  
Ros Production ◽  
Oxygen Species ◽  
Inducible No Synthase

In previous reports from this study, measurements of pulmonary inflammation, bronchoalveolar lavage cell cytokine production and nuclear factor-κB activation, cytotoxic damage, and fibrosis were detailed. In this study, we investigated the temporal relationship between silica inhalation, nitric oxide (NO), and reactive oxygen species (ROS) production, and damage mediated by these radicals in the rat. Rats were exposed to a silica aerosol (15 mg/m3silica, 6 h/day, 5 days/wk) for 116 days. We report time-dependent changes in 1) activation of alveolar macrophages and concomitant production of NO and ROS, 2) immunohistochemical localization of inducible NO synthase and the NO-induced damage product nitrotyrosine, 3) bronchoalveolar lavage fluid NOxand superoxide dismutase concentrations, and 4) lung lipid peroxidation levels. The major observations made in this study are as follows: 1) NO and ROS production and resultant damage increased during silica exposure, and 2) the sites of inducible NO synthase activation and NO-mediated damage are associated anatomically with pathological lesions in the lungs.

Induction of inducible nitric oxide synthase increases the production of reactive oxygen species in RAW264.7 macrophages

2010 ◽  
Vol 30 (4) ◽  
pp. 233-241 ◽  
Author(s):  
Kai Zhao ◽  
Zhen Huang ◽  
Hongling Lu ◽  
Juefei Zhou ◽  
Taotao Wei
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Nitric Oxide Synthase ◽  
Reactive Oxygen ◽  
Inos Expression ◽  
Raw264.7 Cells ◽  
Ros Production ◽  
Oxygen Species ◽  
Raw264.7 Macrophages ◽  
Oxide Synthase

Macrophages produce a large volume of ROS (reactive oxygen species) through respiratory burst. However, the influence of iNOS [inducible NOS (nitric oxide synthase)] activation on ROS production remains unclear. In the present study, the kinetic generation of ROS in RAW264.7 murine macrophages was monitored by chemiluminescence. PMA induces a robust chemiluminescence in RAW264.7 cells, suggesting PKC (protein kinase C)-related assembly and activation of NOX (NADPH oxidase). The effects of iNOS induction on ROS production were examined. Induction of iNOS expression in RAW264.7 cells with LPS (lipopolysaccharide; 1 μg/ml) causes a significant increase in PMA-induced chemiluminescence, which could be enhanced by the NOS substrate, L-arginine, and could be abolished by the NOS inhibitor, L-NNA (NG-nitro-L-arginine). Further experiments reveal that induction of iNOS expression enhances the PMA-stimulated phosphorylation of the p47phox subunit of NOX, and promotes the relocalization of cytosolic p47phox and p67phox subunits to the membrane. Inhibition of PKCζ by its myristoylated pseudosubstrate significantly decreased the PMA-stimulated phosphorylation of the p47phox in LPS-pretreated cells, suggesting that PKCζ is involved in the iNOS-dependent assembly and activation of NOX. Taken together, the present study suggests that the induction of iNOS upregulates the PMA-induced assembly of NOX and leads to the enhanced production of ROS via a PKCζ-dependent mechanism.

Mechanisms of homocysteine-induced oxidative stress

2005 ◽  
Vol 289 (6) ◽  
pp. H2649-H2656 ◽  
Author(s):  
Neetu Tyagi ◽  
Kara C. Sedoris ◽  
Mesia Steed ◽  
Alexander V. Ovechkin ◽  
Karni S. Moshal ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
No Synthase ◽  
Oxygen Species ◽  
Neuronal No Synthase ◽  
Endothelial No Synthase ◽  
Inducible No Synthase ◽  
Cardiovascular Morbidity And Mortality

Hyperhomocysteinemia decreases vascular reactivity and is associated with cardiovascular morbidity and mortality. However, pathogenic mechanisms that increase oxidative stress by homocysteine (Hcy) are unsubstantiated. The aim of this study was to examine the molecular mechanism by which Hcy triggers oxidative stress and reduces bioavailability of nitric oxide (NO) in cardiac microvascular endothelial cells (MVEC). MVEC were cultured for 0–24 h with 0–100 μM Hcy. Differential expression of protease-activated receptors (PARs), thioredoxin, NADPH oxidase, endothelial NO synthase, inducible NO synthase, neuronal NO synthase, and dimethylarginine-dimethylaminohydrolase (DDAH) were measured by real-time quantitative RT-PCR. Reactive oxygen species were measured by using a fluorescent probe, 2′,7′-dichlorofluorescein diacetate. Levels of asymmetric dimethylarginine (ADMA) were measured by ELISA and NO levels by the Griess method in the cultured MVEC. There were no alterations in the basal NO levels with 0–100 μM Hcy and 0–24 h of treatment. However, Hcy significantly induced inducible NO synthase and decreased endothelial NO synthase without altering neuronal NO synthase levels. There was significant accumulation of ADMA, in part because of reduced DDAH expression by Hcy in MVEC. Nitrotyrosine expression was increased significantly by Hcy. The results suggest that Hcy activates PAR-4, which induces production of reactive oxygen species by increasing NADPH oxidase and decreasing thioredoxin expression and reduces NO bioavailability in cultured MVEC by 1) increasing NO2-tyrosine formation and 2) accumulating ADMA by decreasing DDAH expression.

scholarly journals GPR120 Inhibits RANKL-Induced Osteoclast Formation and Resorption by Attenuating Reactive Oxygen Species Production in RAW264.7 Murine Macrophages

2021 ◽  
Vol 22 (19) ◽  
pp. 10544
Author(s):  
Cynthia Sithole ◽  
Carla Pieterse ◽  
Kayla Howard ◽  
Abe Kasonga
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Nuclear Factor Κb ◽  
Osteoclast Formation ◽  
Ros Production ◽  
Oxygen Species ◽  
Murine Macrophages ◽  
Multinucleated Cells ◽  
Raw264.7 Macrophages ◽  
Inhibit Osteoclast Formation

Osteoclasts are large, multinucleated cells that are responsible for the resorption of bone. Bone degenerative diseases, such as osteoporosis, are characterized by overactive osteoclasts. Receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL) binding to its receptor on osteoclast precursors will trigger osteoclast formation and resorption. The production of reactive oxygen species (ROS) is known to play a crucial role in RANKL-induced osteoclast formation and resorption. G-protein coupled receptor 120 (GPR120) signalling has been shown to affect osteoclast formation, but the exact mechanisms of action require further investigation. RAW264.7 murine macrophages were seeded into culture plates and exposed to the GPR120 agonist, TUG-891, at varying concentrations (20–100 µM) and RANKL to induce osteoclast formation. TUG-891 was shown to inhibit osteoclast formation and resorption without affecting cell viability in RAW264.7 macrophages. TUG-891 further decreased ROS production when compared to RANKL only cells. Antioxidant proteins, Nrf2, HO-1 and NQO1 were shown to be upregulated while the ROS inducing protein, Nox1, was downregulated by TUG-891. Gene silencing revealed that TUG-891 exerted its effects specifically through GPR120. This study reveals that GPR120 signalling may inhibit osteoclast formation and resorption through inhibition on ROS production.

scholarly journals Nitro-Oleic Acid Induced Reactive Oxygen Species Formation and Plant Defense Signaling in Tomato Cell Suspensions

2018 ◽  
Author(s):  
Andrés Arruebarrena Di Palma ◽  
Luciano M. Di Fino ◽  
Sonia R. Salvatore ◽  
Juan Martín D’Ambrosio ◽  
Gustavo Esteban Gergoff Grozeff ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Fatty Acids ◽  
Oleic Acid ◽  
Nitrogen Dioxide ◽  
Plant Defense ◽  
Reduced Glutathione ◽  
Reactive Oxygen ◽  
Ros Production ◽  
Oxygen Species

ABSTRACTNitrated fatty acids (NO2-FAs) are formed by the addition reaction of nitric oxide- and nitrite-derived nitrogen dioxide with unsaturated fatty acids. Nitrated fatty acids act as signaling molecules in mammals through the formation of covalent adducts with cellular thiols. The study of NO2-FAs in plant systems constitutes an interesting and emerging area. The presence of NO2-FA has been reported in olives, peas, rice and in Arabidopsis. To gain a better understanding of the role of NO2-FA on plant physiology, we analyzed the effects of exogenous application of nitro-oleic acid (NO2-OA) to tomato cell cultures. We found that NO2-OA induced reactive oxygen species (ROS) production in a dose-dependent manner via activation of NADPH oxidases, which requires calcium entry from the extracellular compartment and protein kinase activation, a mechanism that resembles the plant defense responses. NO2-OA-induced ROS production, expression of plant defense genes and led to cell death. The mechanism of action of NO2-OA involves a reduction in the glutathione cellular pool and covalently addition reactions with protein thiols and reduced glutathione. Altogether, these results indicate that NO2-OA triggers responses associated with plant defense, revealing its possible role as a signal molecule in biotic stress.Abbreviations•NO2nitrogen dioxide•NOnitric oxideFAfatty acidGSHreduced glutathioneH2O2hydrogen peroxydeNO2-FAnitro fatty acidsNO2-Lnnitro-linolenic acidNO2-OAnitro-oleic acidOAoleic acidROSreactive oxygen species

scholarly journals Effect of an inhaled glucocorticoid on reactive oxygen species production by bronchoalveolar lavage cells from smoking COPD patients

2000 ◽  
Vol 9 (2) ◽  
pp. 109-113 ◽  
Author(s):  
Gert T. Verhoeven ◽  
Annemarie J.M. Wijkhuijs ◽  
Herbert Hooijkaas ◽  
Henk C. Hoogsteden ◽  
Wim Sluiter
Keyword(s):  
Reactive Oxygen Species ◽  
Bronchoalveolar Lavage ◽  
Reactive Oxygen ◽  
Published Data ◽  
Inverse Association ◽  
Ros Production ◽  
Oxygen Species ◽  
Heavy Smoking ◽  
Correlation Analyses ◽  
Copd Patients

Oxidative stress in the lung is important in the pathogenesis of COPD. Published data indicate that glucocorticoids inhibit blood cells in their capacity to produce reactive oxygen species (ROS). We investigated the effect of Fluticasone propionate (FP) on the ROS production capabilities of pulmonary cells. Bronchoalveolar lavage (BAL) was performed in smoking COPD patients, before and after a six month, placebo-controlled treatment with FP. BAL cells were stimulated with phorbol myristrate acetate (PMA) alone, and together with superoxide dismutase (SOD). From kinetic plots of ferricytochrome-c conversion we calculated the maximal rate of superoxide production:Vmax. We also examined BAL cell subsets and performed correlation analyses on ROS production and relevant clinical determinants. Paired results were obtained from 6 FP- and 9 placebo-treated patients. No significant change ofVmaxwas found in both patient groups. Also BAL cellularity was unchanged. Correlation analyses showed a significant (inverse) association ofVmaxwith the number of cigarettes smoked per day. We concluded that a potent inhaled glucocorticoid had no effect on the ROS production capability of BAL cells from smoking COPD patients. Apparently, heavy smoking impaired the ability of alveolar macrophages to produce ROS, which was not further decreased by FP.

The production of reactive oxygen species in peripheral blood neutrophils is modulated by airway mucous

Open Medicine ◽  
2009 ◽  
Vol 4 (2) ◽  
pp. 245-252 ◽  
Author(s):  
Agne Babusyte ◽  
Jolanta Jeroch ◽  
Rimantas Stakauskas ◽  
Raimundas Sakalauskas
Keyword(s):  
Reactive Oxygen Species ◽  
Peripheral Blood ◽  
Reactive Oxygen ◽  
Lavage Fluid ◽  
Chronic Obstructive ◽  
Ros Generation ◽  
Ros Production ◽  
Oxygen Species ◽  
Copd Patients ◽  
Blood Neutrophils

AbstractNeutrophils are a major source of reactive oxygen species (ROS). The role of airway mucous on ROS production is unknown. The aim of our study was to investigate the direct influence of bronchoalveolar lavage fluid (BALF) and induced sputum (IS) alone or in combination with chemical/biological stimulus on ROS production in peripheral blood neutrophils during chronic obstructive pulmonary disease (COPD). Neutrophils were isolated from peripheral blood of 47 patients with moderate COPD and 14 healthy individuals (HI). BALF/RPMI (1:1) or IS/RPMI (1:1) from COPD patients were used to stimulate neutrophils alone or in combination with phorbolmyristate- acetate (PMA) (0.1–30 nM) or Staphylococcus aureus bacteria (0.7–500 bact/neutrophil). Relative generation of ROS was measured flow cytometrically. BALF/RPMI and in combination with relatively low PMA or all bacteria concentrations stimulated ROS; while, combination with relatively high PMA concentrations suppressed ROS in of COPD patients and HI. IS/RPMI and its combination with PMA inhibited ROS generation in both groups; whereas, IS stimulated or had a tendency to stimulate ROS production with relatively high bacteria concentrations. In conclusion, BALF and IS directly or in combination with chemical/biological factors modulated ROS production. This effect was stronger in neutrophils from COPD patients and depended on chemical/biological stimulus intensity.

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