scholarly journals The  -galactoside binding immunomodulatory lectin galectin-3 reverses the desensitized state induced in neutrophils by the chemotactic peptide f-Met-Leu-Phe: role of reactive oxygen species generated by the NADPH-oxidase and inactivation of the agonist

Glycobiology ◽  
2008 ◽  
Vol 18 (11) ◽  
pp. 905-912 ◽  
Author(s):  
H. Forsman ◽  
E. Salomonsson ◽  
K. Onnheim ◽  
J. Karlsson ◽  
A. Bjorstad ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Chemotactic Peptide ◽  
Galectin 3

scholarly journals NADPH Oxidase as a Therapeutic Target for Oxalate Induced Injury in Kidneys

2013 ◽  
Vol 2013 ◽  
pp. 1-18 ◽  
Author(s):  
Sunil Joshi ◽  
Ammon B. Peck ◽  
Saeed R. Khan
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Tissue Injury ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Renal Tissue ◽  
Oxygen Species ◽  
Gene Expressions

A major role of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase family of enzymes is to catalyze the production of superoxides and other reactive oxygen species (ROS). These ROS, in turn, play a key role as messengers in cell signal transduction and cell cycling, but when they are produced in excess they can lead to oxidative stress (OS). Oxidative stress in the kidneys is now considered a major cause of renal injury and inflammation, giving rise to a variety of pathological disorders. In this review, we discuss the putative role of oxalate in producing oxidative stress via the production of reactive oxygen species by isoforms of NADPH oxidases expressed in different cellular locations of the kidneys. Most renal cells produce ROS, and recent data indicate a direct correlation between upregulated gene expressions of NADPH oxidase, ROS, and inflammation. Renal tissue expression of multiple NADPH oxidase isoforms most likely will impact the future use of different antioxidants and NADPH oxidase inhibitors to minimize OS and renal tissue injury in hyperoxaluria-induced kidney stone disease.

scholarly journals Role of reactive oxygen species produced by NADPH oxidase in gibberellin biosynthesis during barley seed germination

2016 ◽  
Vol 11 (5) ◽  
pp. e1180492 ◽  
Author(s):  
Kyohei Kai ◽  
Shinsuke Kasa ◽  
Masatsugu Sakamoto ◽  
Nozomi Aoki ◽  
Gaku Watabe ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Seed Germination ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Barley Seed ◽  
Gibberellin Biosynthesis ◽  
Oxygen Species

Role of reactive oxygen species and NADPH-oxidase in the development of rat cerebellum

2013 ◽  
Vol 62 (7) ◽  
pp. 998-1011 ◽  
Author(s):  
Angélica Coyoy ◽  
Mauricio Olguín-Albuerne ◽  
Patricio Martínez-Briseño ◽  
Julio Morán
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Rat Cerebellum

Mo2060 Pathogenic Role of NADPH Oxidase 1 (NOX1)-Derived Reactive Oxygen Species in 5-Fluorouracil-Induced Intestinal Mucositis in Mice

2012 ◽  
Vol 142 (5) ◽  
pp. S-731
Author(s):  
Masashi Yasuda ◽  
Shinichi Kato ◽  
Naoki Yamanaka ◽  
Maho Iimori ◽  
Kazumi Iwata ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Pathogenic Role ◽  
Nadph Oxidase 1 ◽  
Intestinal Mucositis

scholarly journals The Role of NADPH Oxidase 1–Derived Reactive Oxygen Species in Paraquat-Mediated Dopaminergic Cell Death

2009 ◽  
Vol 11 (9) ◽  
pp. 2105-2118 ◽  
Author(s):  
Ana Clara Cristóvão ◽  
Dong-Hee Choi ◽  
Graça Baltazar ◽  
M. Flint Beal ◽  
Yoon-Seong Kim
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Dopaminergic Cell ◽  
Nadph Oxidase 1

scholarly journals Hypoxia-inducible Factor-1 Activation in Nonhypoxic Conditions: The Essential Role of Mitochondrial-derived Reactive Oxygen Species

2010 ◽  
Vol 21 (18) ◽  
pp. 3247-3257 ◽  
Author(s):  
David A. Patten ◽  
Véronique N. Lafleur ◽  
Geneviève A. Robitaille ◽  
Denise A. Chan ◽  
Amato J. Giaccia ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Hypoxia Inducible Factor ◽  
Reactive Oxygen ◽  
Protein Stabilization ◽  
Complex Iii ◽  
Oxygen Species ◽  
Ang Ii ◽  
Hypoxia Inducible Factor 1

Hypoxia-inducible factor-1 (HIF-1) is a key transcription factor for responses to low oxygen. Different nonhypoxic stimuli, including hormones and growth factors, are also important HIF-1 activators in the vasculature. Angiotensin II (Ang II), the main effecter hormone in the renin-angiotensin system, is a potent HIF-1 activator in vascular smooth muscle cells (VSMCs). HIF-1 activation by Ang II involves intricate mechanisms of HIF-1α transcription, translation, and protein stabilization. Additionally, the generation of reactive oxygen species (ROS) is essential for HIF-1 activation during Ang II treatment. However, the role of the different VSMC ROS generators in HIF-1 activation by Ang II remains unclear. This work aims at elucidating this question. Surprisingly, repression of NADPH oxidase-generated ROS, using Vas2870, a specific inhibitor or a p22phox siRNA had no significant effect on HIF-1 accumulation by Ang II. In contrast, repression of mitochondrial-generated ROS, by complex III inhibition, by Rieske Fe-S protein siRNA, or by the mitochondrial-targeted antioxidant SkQ1, strikingly blocked HIF-1 accumulation. Furthermore, inhibition of mitochondrial-generated ROS abolished HIF-1α protein stability, HIF-1–dependent transcription and VSMC migration by Ang II. A large number of studies implicate NADPH oxidase–generated ROS in Ang II–mediated signaling pathways in VSMCs. However, our work points to mitochondrial-generated ROS as essential intermediates for HIF-1 activation in nonhypoxic conditions.

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