scholarly journals Cytokines promote lipolysis in 3T3-L1 adipocytes through induction of NADPH oxidase 3 expression and superoxide production

2018 ◽  
Vol 59 (12) ◽  
pp. 2321-2328 ◽  
Author(s):  
Nahla Issa ◽  
Gabriel Lachance ◽  
Kerstin Bellmann ◽  
Mathieu Laplante ◽  
Krisztian Stadler ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Superoxide Production

scholarly journals Chronic Ethanol Ingestion Increases Superoxide Production and NADPH Oxidase Expression in the Lung

2006 ◽  
Vol 34 (3) ◽  
pp. 314-319 ◽  
Author(s):  
John A. Polikandriotis ◽  
Heidi L. Rupnow ◽  
Shawn C. Elms ◽  
Roza E. Clempus ◽  
Duncan J. Campbell ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Chronic Ethanol ◽  
Superoxide Production ◽  
Ethanol Ingestion

Palmitate increases superoxide production through mitochondrial electron transport chain and NADPH oxidase activity in skeletal muscle cells

2008 ◽  
Vol 216 (3) ◽  
pp. 796-804 ◽  
Author(s):  
Rafael Herling Lambertucci ◽  
Sandro Massao Hirabara ◽  
Leonardo dos Reis Silveira ◽  
Adriana Cristina Levada‐Pires ◽  
Rui Curi ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Electron Transport ◽  
Nadph Oxidase ◽  
Oxidase Activity ◽  
Electron Transport Chain ◽  
Muscle Cells ◽  
Superoxide Production ◽  
Mitochondrial Electron Transport Chain ◽  
Nadph Oxidase Activity ◽  
Transport Chain

scholarly journals Olfactomedin 4 contributes to hydrogen peroxide-induced NADPH oxidase activation and apoptosis in mouse neutrophils

2018 ◽  
Vol 315 (4) ◽  
pp. C494-C501 ◽  
Author(s):  
Wenli Liu ◽  
Yueqin Liu ◽  
Hongzhen Li ◽  
Griffin P. Rodgers
Keyword(s):  
Hydrogen Peroxide ◽  
Nadph Oxidase ◽  
Molecular Mechanisms ◽  
Oxidase Inhibitor ◽  
Superoxide Production ◽  
Wild Type ◽  
Escherichia Coli Bacteria ◽  
Induced Apoptosis ◽  
Nadph Oxidase Activation ◽  
Deficient Mice

Neutrophils increase production of reactive oxygen species, including superoxide, hydrogen peroxide (H2O2), and hydroxyl radical, to destroy invading microorganisms under pathological conditions. Conversely, oxidative stress conditions, such as the presence of H2O2, induce neutrophil apoptosis, which helps to remove neutrophils after inflammation. However, the detailed molecular mechanisms that are involved in the latter process have not been elucidated. In this study, we investigated the potential role of olfactomedin 4 (Olfm4) in H2O2-induced superoxide production and apoptosis in mouse neutrophils. We have demonstrated that Olfm4 is not required for maximal-dosage PMA- and Escherichia coli bacteria-induced superoxide production, but Olfm4 contributes to suboptimal-dosage PMA- and H2O2-induced superoxide production. Using an NADPH oxidase inhibitor and gp91phox-deficient mouse neutrophils, we found that NAPDH oxidase was required for PMA-stimulated superoxide production and that Olfm4 mediated H2O2-induced superoxide production through NADPH oxidase, in mouse neutrophils. We have shown that neutrophils from Olfm4-deficient mice exhibited reduced H2O2-induced apoptosis compared with neutrophils from wild-type mice. We also demonstrated that neutrophils from Olfm4-deficient mice exhibited reduced H2O2-stimulated mitochondrial damage and membrane permeability, and as well as reduced caspase-3 and caspase-9 activity, compared with neutrophils from wild-type mice. Moreover, the cytoplasmic translocation of the proapoptotic mitochondrial proteins Omi/HtrA2 and Smac/DIABLO in response to H2O2was reduced in neutrophils from Olfm4-deficient mice compared with neutrophils from wild-type mice. Our study demonstrates that Olfm4 contributes to H2O2-induced NADPH oxidase activation and apoptosis in mouse neutrophils. Olfactomedin 4 might prove to be a potential target for future studies on inflammatory neutrophil biology and for inflammatory disease treatment.

Diabetes induces pulmonary artery endothelial dysfunction by NADPH oxidase induction

2008 ◽  
Vol 295 (5) ◽  
pp. L727-L732 ◽  
Author(s):  
Jose G. Lopez-Lopez ◽  
Javier Moral-Sanz ◽  
Giovanna Frazziano ◽  
Maria J. Gomez-Villalobos ◽  
Jorge Flores-Hernandez ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Nadph Oxidase ◽  
Pulmonary Arteries ◽  
Diabetic Rats ◽  
Oxidase Inhibitor ◽  
No Synthase ◽  
Superoxide Production ◽  
Regulatory Subunit ◽  
Sprague Dawley ◽  
Relaxant Response

Recent data suggest that diabetes is a risk factor for pulmonary hypertension. The aim of the present study was to analyze whether diabetes induces endothelial dysfunction in pulmonary arteries and the mechanisms involved. Male Sprague-Dawley rats were randomly divided into a control (saline) and a diabetic group (70 mg/kg−1 streptozotocin). After 6 wk, intrapulmonary arteries were mounted for isometric tension recording, and endothelial function was tested by the relaxant response to acetylcholine. Protein expression and localization were measured by Western blot and immunohistochemistry and superoxide production by dihydroethidium staining. Pulmonary arteries from diabetic rats showed impaired relaxant response to acetylcholine and reduced vasoconstrictor response to the nitric oxide (NO) synthase inhibitor l-NAME, whereas the response to nitroprusside and the expression of endothelial NO synthase remained unchanged. Endothelial dysfunction was reversed by addition of superoxide dismutase or the NADPH oxidase inhibitor apocynin. An increase in superoxide production and increased expression of the NADPH oxidase regulatory subunit p47phox were also found in pulmonary arteries from diabetic rats. In conclusion, the pulmonary circulation is a target for diabetes-induced endothelial dysfunction via enhanced NADPH oxidase-derived superoxide production.

195 THE RENIN ANGIOTENSIN SYSTEM MEDIATES CHRONIC ETHANOL-INDUCED INCREASES IN SUPEROXIDE PRODUCTION AND NADPH OXIDASE EXPRESSION IN THE LUNG

2005 ◽  
Vol 53 (1) ◽  
pp. S287.2-S287
Author(s):  
J. A. Polikandriots ◽  
H. L. Rupnow ◽  
R. L. Sutliff ◽  
L. S. Brown ◽  
D. M. Guidot ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Renin Angiotensin System ◽  
Chronic Ethanol ◽  
Superoxide Production ◽  
Angiotensin System ◽  
Renin Angiotensin

Tamoxifen promotes superoxide production in platelets by activation of PI3-Kinase and NADPH oxidase pathways

2012 ◽  
Vol 129 (1) ◽  
pp. 36-42 ◽  
Author(s):  
Vidhi P. Shah ◽  
Hesum A. Chegini ◽  
Susan R. Vishneski ◽  
Ross V. Weatherman ◽  
Peter F. Blackmore ◽  
...  
Keyword(s):  
Nadph Oxidase ◽  
Pi3 Kinase ◽  
Superoxide Production
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