scholarly journals APOCYNIN, AN INHIBITOR OF THE NADPH OXIDASE COMPLEX

2020 ◽  
Vol 17 (34) ◽  
pp. 478-501
Author(s):  
Camila Nascimento GIONGO ◽  
Vanessa Falchetti LOPES ◽  
Diana Fortkamp GRIGOLETTO ◽  
Eduardo Hösel MIRANDA
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Superoxide Anion ◽  
Therapeutic Potential ◽  
Inflammatory Diseases ◽  
Reactive Oxygen ◽  
Enzyme Complex ◽  
Oxygen Species ◽  
Phagocytic Cells ◽  
Oxidative Species

Apocynin is a phenolic compound isolated from the plant Picrorhiza kurroa Royle ex Benth. Such a compound has been extensively investigated for its therapeutic potential in diseases involving inflammatory processes or oxidative stress due to its ability to inhibit the NADPH oxidase multienzyme complex. This complex consists of two transmembrane proteins (Nox2 and p22phox) and four cytosolic regulatory proteins (p67phox, p47phox, p40phox, and GTPase-Rac) and their activation occurs after the stimulation of phagocytic cells by the mediation of the enzyme myeloperoxidase (MPO). NADPH oxidase is the only enzyme complex that is intended for the production of superoxide anion that is precursor of highly oxidizing substances classified as reactive oxygen species (ROS). NADPH oxidase is an enzyme complex that produces superoxide anion from molecular oxygen. Ta the same time, the superoxide anion is a precursor to reactive oxygen species (ROS) catalyzed by enzymes.These oxidative species, when in excess, can induce burst, causing irreparable tissue damage. They can act by modifying the redox state of DNA, protein or lipid molecules, playing a central role in the development of chronic pathologies and various health complications. One can cite vascular problems, hyperglycemia, diabetes, hypertension, Alzheimer's disease, and cancer, among others. Apocynin, previously activated by MPO, blocks the enzyme complex and prevents the formation of these oxidative species. Therefore, the central biological function of compound is to modulate the action of NADPH oxidase, promoting a positive effect in the prevention/remediation of inflammatory diseases.

The function of the NADPH oxidase of phagocytes, and its relationship to other NOXs

2007 ◽  
Vol 35 (5) ◽  
pp. 1100-1103 ◽  
Author(s):  
P. Behe ◽  
A.W. Segal
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Ion Fluxes ◽  
Oxygen Species ◽  
Phagocytic Cells ◽  
Alternative Scenario ◽  
Ph Changes ◽  
Primary Function ◽  
A Charge

The NADPH oxidase of ‘professional’ phagocytic cells transfers electrons across the wall of the phagocytic vacuole, forming superoxide in the lumen. It is generally accepted that this system promotes microbial killing through the generation of reactive oxygen species and through the activity of myeloperoxidase. An alternative scenario exists in which the passage of electrons across the membrane alters the pH and generates a charge that drives ions into, and out of, the vacuole. It is proposed that the primary function of the oxidase is to produce these pH changes and ion fluxes, and the issues surrounding these processes are considered in this review. The neutrophil oxidase is the prototype of a whole family of NOXs (NAPDH oxidases) that exist throughout biology, from plants to humans, which might function, at least in part, in a similar fashion.

scholarly journals Reactive Oxygen Species from NADPH Oxidase and Mitochondria Participate in the Proliferation of Aortic Smooth Muscle Cells from a Model of Metabolic Syndrome

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Ocarol López-Acosta ◽  
María de los Angeles Fortis-Barrera ◽  
Miguel Angel Barrios-Maya ◽  
Angélica Ruiz Ramírez ◽  
Francisco Javier Alarcón Aguilar ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Metabolic Syndrome ◽  
Smooth Muscle ◽  
Cell Growth ◽  
Nadph Oxidase ◽  
Superoxide Anion ◽  
Metabolic Diseases ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
And Control

In metabolic diseases, the increased reactive oxygen species (ROS) represents one of the pathogenic mechanisms for vascular disease probably by promoting vascular smooth muscle cell (SMC) proliferation that contributes to the development of arterial remodeling and stenosis, hypertension, and atherosclerosis. Therefore, this work was undertaken to evaluate the participation of ROS from NADPH oxidase and mitochondria in the proliferation of SMCs from the aorta in a model of metabolic syndrome induced by sucrose feeding in rats. After 24 weeks, sucrose-fed (SF) rats develop hypertension, intra-abdominal obesity, hyperinsulinemia, and hyperleptinemia. In addition SMCs from SF rats had a higher growth rate and produce more ROS than control cells. The treatment of SMCs with DPI and apocynin to inhibit NADPH oxidase and with tempol to scavenge superoxide anion significantly blocked the proliferation of both SF and control cells suggesting the participation of NADPH oxidase as a source of superoxide anion. MitoTEMPO, which targets mitochondria within the cell, also significantly inhibited the proliferation of SMCs having a greater effect on cells from SF than from the control aorta. The higher rate of cell growth from the SF aorta is supported by the increased content of cyclophilin A and CD147, proteins involved in the mechanism of cell proliferation. In addition, caldesmon, α-actin, and phosphorylated myosin light chain, contractile phenotype proteins, were found significantly lower in SF cells in no confluent state and increased in confluent state but without difference between both cell types. Our results suggest that ROS from NADPH oxidase and mitochondria significantly participate in the difference found in the rate of cell growth between SF and control cells.

scholarly journals Glycosylation with O-linked β-N-acetylglucosamine induces vascular dysfunction via production of superoxide anion/reactive oxygen species

2018 ◽  
Vol 96 (3) ◽  
pp. 232-240
Author(s):  
Leonardo Souza-Silva ◽  
Rheure Alves-Lopes ◽  
Jéssica Silva Miguez ◽  
Vanessa Dela Justina ◽  
Karla Bianca Neves ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Dysfunction ◽  
Nadph Oxidase ◽  
Protein Expression ◽  
Vascular Function ◽  
Superoxide Anion ◽  
Vascular System ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Endothelium Dependent Relaxation

Overproduction of superoxide anion (•O2−) and O-linked β-N-acetylglucosamine (O-GlcNAc) modification in the vascular system are contributors to endothelial dysfunction. This study tested the hypothesis that increased levels of O-GlcNAc-modified proteins contribute to •O2− production via activation of NADPH oxidase, resulting in impaired vasodilation. Rat aortic segments and vascular smooth muscle cells (VSMCs) were incubated with vehicle (methanol) or O-(2-acetamido-2-deoxy-d-glucopyranosylidenamino) N-phenylcarbamate (PUGNAc) (100 μM). PUGNAc produced a time-dependent increase in O-GlcNAc levels in VSMC and decreased endothelium-dependent relaxation, which was prevented by apocynin and tiron, suggesting that •O2− contributes to endothelial dysfunction under augmented O-GlcNAc levels. Aortic segments incubated with PUGNAc also exhibited increased levels of reactive oxygen species, assessed by dihydroethidium fluorescence, and augmented •O2− production, determined by lucigenin-enhanced chemiluminescence. Additionally, PUGNAc treatment increased Nox-1 and Nox-4 protein expression in aortas and VSMCs. Translocation of the p47phox subunit from the cytosol to the membrane was greater in aortas incubated with PUGNAc. VSMCs displayed increased p22phox protein expression after PUGNAc incubation, suggesting that NADPH oxidase is activated in conditions where O-GlcNAc protein levels are increased. In conclusion, O-GlcNAc levels reduce endothelium-dependent relaxation by overproduction of •O2− via activation of NADPH oxidase. This may represent an additional mechanism by which augmented O-GlcNAc levels impair vascular function.

scholarly journals A Novel Tetrapeptide Derivative Exhibits In Vitro Inhibition of Neutrophil-Derived Reactive Oxygen Species and Lysosomal Enzymes Release

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Sumitra Miriyala ◽  
Manikandan Panchatcharam ◽  
Meera Ramanujam ◽  
Rengarajulu Puvanakrishnan
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Anion ◽  
Lysosomal Enzymes ◽  
Reactive Oxygen ◽  
Peptide Sequence ◽  
Ros Generation ◽  
Oxygen Species ◽  
Complement Factors

Neutrophil infiltration plays a major role in the pathogenesis of myocardial injury. Oxidative injury is suggested to be a central mechanism of the cellular damage after acute myocardial infarction. This study is pertained to the prognostic role of a tetrapeptide derivative PEP1261 (BOC-Lys(BOC)-Arg-Asp-Ser(tBu)-OtBU), a peptide sequence (39–42) of lactoferrin, studied in the modulation of neutrophil functions in vitro by measuring the reactive oxygen species (ROS) generation, lysosomal enzymes release, and enhanced expression of C proteins. The groundwork experimentation was concerned with the isolation of neutrophils from the normal and acute myocardial infarct rats to find out the efficacy of PEP1261 in the presence of a powerful neutrophil stimulant, phorbol 12-myristate 13 acetate (PMA). Stimulation of neutrophils with PMA resulted in an oxidative burst of superoxide anion and enhanced release of lysosomal enzymes and expression of complement proteins. The present study further demonstrated that the free radicals increase the complement factors in the neutrophils confirming the role of ROS. PEP1261 treatment significantly reduced the levels of superoxide anion and inhibited the release of lysosomal enzymes in the stimulated control and infarct rat neutrophils. This study demonstrated that PEP1261 significantly inhibited the effect on the ROS generation as well as the mRNA synthesis and expression of the complement factors in neutrophils isolated from infarct heart.

scholarly journals Role of NADPH Oxidase-Mediated Reactive Oxygen Species in Podocyte Injury

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Shan Chen ◽  
Xian-Fang Meng ◽  
Chun Zhang
Keyword(s):  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Epithelial To Mesenchymal Transition ◽  
Kidney Diseases ◽  
Treatment Strategies ◽  
Reactive Oxygen ◽  
Glomerular Sclerosis ◽  
Oxygen Species ◽  
Podocyte Injury ◽  
Mesenchymal Transition

Proteinuria is an independent risk factor for end-stage renal disease (ESRD) (Shankland, 2006). Recent studies highlighted the mechanisms of podocyte injury and implications for potential treatment strategies in proteinuric kidney diseases (Zhang et al., 2012). Reactive oxygen species (ROS) are cellular signals which are closely associated with the development and progression of glomerular sclerosis. NADPH oxidase is a district enzymatic source of cellular ROS production and prominently expressed in podocytes (Zhang et al., 2010). In the last decade, it has become evident that NADPH oxidase-derived ROS overproduction is a key trigger of podocyte injury, such as renin-angiotensin-aldosterone system activation (Whaley-Connell et al., 2006), epithelial-to-mesenchymal transition (Zhang et al., 2011), and inflammatory priming (Abais et al., 2013). This review focuses on the mechanism of NADPH oxidase-mediated ROS in podocyte injury under different pathophysiological conditions. In addition, we also reviewed the therapeutic perspectives of NADPH oxidase in kidney diseases related to podocyte injury.

Reactive oxygen species produced via plasma membrane NADPH oxidase regulate anthocyanin synthesis in apple peel

Planta ◽  
2014 ◽  
Vol 240 (5) ◽  
pp. 1023-1035 ◽  
Author(s):  
Jiangli Zhang ◽  
Changsheng Chen ◽  
Di Zhang ◽  
Houhua Li ◽  
Pengmin Li ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Plasma Membrane ◽  
Nadph Oxidase ◽  
Reactive Oxygen ◽  
Anthocyanin Synthesis ◽  
Oxygen Species ◽  
Apple Peel
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