We conclude that in CAD, both mitochondria … 2014 Nov;237(1):208-19. doi: 10.1016/j.atherosclerosis.2014.09.001. Besides mitochondria, NADPH oxidase also generates a significant amount of ROS and is a major source of superoxide in vascular cells . Antioxidants (Basel). Antioxidant supplements and endurance exercise: Current evidence and mechanistic insights. Nat Rev Cardiol. Mitochondrial bioenergetics are critical for cellular homeostasis and stress responses. Mitochondria have the highest levels of antioxidants in the cell and play an important role in the maintenance of cellular redox status, thereby acting as an ROS and redox sink and limiting NADPH oxidase activity. May function as an oxygen sensor regulating the KCNK3/TASK-1 potassium channel and HIF1A activity. Clin Sci (Lond). Introduction. NIH This site needs JavaScript to work properly. Redox Imbalance in Idiopathic Pulmonary Fibrosis: A Role for Oxidant Cross-Talk Between NADPH Oxidase Enzymes and Mitochondria. Here, we have systemically modulated produc-tion rates of H 2O 2 NOX enzymes play a fundamental role in many cell functions including signal transduction, … After 24 weeks, sucrose-fed (SF) rats develop hypertension, intra-abdominal obesity, hyperinsulinemia, and hyperleptinemia. Targeted Antioxidants in Exercise-Induced Mitochondrial Oxidative Stress: Emphasis on DNA Damage. Am J Physiol Heart Circ Physiol. However, due to technical challenges, it still remains unknown as to the pool size of mitochondrial NADPH, its dynamics, and NADPH/NADP+ ratio. Segal AW, West I, Wientjes F et al (1992) Cytochrome b-245 is a flavocytochrome containing FAD and the NADPH-binding site of the microbicidal oxidase of phagocytes. evidence for an oncogenic function for NOX4 protein localized to mitochondria and suggests that NOX4 is a novel source of ROs produced in the mitochondria. 8. See this image and copyright information in PMC. doi: 10.1152/ajpheart.00819.2006. Endothelial NADPH oxidase 219 Figure 1 Interplay between NADPH oxidase and other sources of ROS O•− 2 generated from NADPH oxidase can potentially influence ROS production by other enzymatic sources of O •− 2. Our data suggest that a severe defect in mitochondrial respiration accelerates cellular aging by disturbing protein homeostasis in yeast. Rotenone (1 μM) reduces FID in adipose microvessels from subjects with CAD (A) but has no effect on FID in adipose microvessels from subjects without CAD (B). Reactive oxygen species (ROS) play an important role in physiological and pathological processes. NADPH oxidase (nicotinamide adenine dinucleotide phosphate oxidase) is a membrane-bound enzyme complex that faces the extracellular space. Mitochondria generate ROS as a byproduct of oxidative phosphorylation, while the major function of NADPH oxidases is generation of ROS. Figure 1. *P<0.05 vs. vehicle. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Vol. Daiber A, Steven S, Vujacic-Mirski K, Kalinovic S, Oelze M, Di Lisa F, Münzel T. Int J Mol Sci. Mitochondrial NADPH protects cells against mitochondrial oxidative stress by serv-ing as an electron donor to antioxidant defense systems. 2020 Aug 6;9(8):1849. doi: 10.3390/cells9081849. Conclusions: Schematic illustrating the proposed mechanism demonstrated by the current study, NLM Oxidative Stress and Microvessel Barrier Dysfunction. Keywords: We conclude that in CAD, both mitochondria and NADPH oxidase contribute to FID through a redox mechanism in visceral arterioles. It can be found in the plasma membrane as well as in the membranes of phagosomes used by neutrophil white blood cells to engulf microorganisms. It has been demonstrated that mitochondria-targeted antioxidants break this vicious cycle, inhibiting ROS production by mitochondria and reducing NADPH oxidase activity. 2020 Aug;35:101471. doi: 10.1016/j.redox.2020.101471. NADPH-oxidase is a source of flow-induced ROS in CAD subjects, Figure 4. The peptide has no effect on FID in adipose microvessels from subjects without CAD (B). Recent studies have identified the NOX isoform NOX4 as a key player in … Inhibiting NADPH-oxidase with the peptide gp91ds-tat (50 μM) reduces FID in adipose microvessels exclusively in subjects with CAD (A) while the scrambled peptide control (50 μM) has no effect on this population (C). The NADPH system is also responsible for generating free radicals in immune cells by NADPH oxidase. Get the latest public health information from CDC: https://www.coronavirus.gov, Get the latest research information from NIH: https://www.nih.gov/coronavirus, Find NCBI SARS-CoV-2 literature, sequence, and clinical content: https://www.ncbi.nlm.nih.gov/sars-cov-2/. This may provide a novel strategy for treatment of many pathological conditions including aging, atherosclerosis, diabetes, hypertension, and degenerative neurological disorders in which mitochondrial oxidative stress seems to play a role. We tested whether NADPH oxidase contributes to mitochondrial ROS generation in arterioles during CAD. Mitochondrial-localized NADPH oxidase 4 is a source of superoxide in angiotensin II-stimulated neurons. NADPH oxidase activity was assessed in Percoll gradient-purified mitochondria isolated from control MCs or cells treated with DPI (5 μM) either by measuring NADPH-dependent superoxide generation with the lucigenin-enhanced chemiluminescence method (A) or NADPH-dependent hydrogen peroxide production with … Clipboard, Search History, and several other advanced features are temporarily unavailable. Would you like email updates of new search results? The ER-localized NADPH oxidase Yno1 also played a role in producing ROS. the electron flow in isolated brain mitochondria produces superoxide radicals (Boveris and Chance 1973). Endothelial NADPH oxidase 219 Figure 1 Interplay between NADPH oxidase and other sources of ROS O•− 2 generated from NADPH oxidase can potentially influence ROS production by other enzymatic sources of O •− 2. doi: 10.2337/dc08-s247. USA.gov. mitochondrial electron transport complexes as well as NADPH oxidases; second, we used a genetic approach with mouse lungs deficient in the NADPH oxidase subunits gp91 phoxand p47 , respectively. In addition to mitochondria, many prooxidant enzymes are known to participate in oxygen radicals generation in cerebral ischemia including xanthi,ne oxidase (XO), nitric oxide synthase (NOS), cyclooxygenase (COX) and NADPH oxidase (NOX) 2020 Dec 23;8:616139. doi: 10.3389/fcell.2020.616139. Epub 2014 Sep 9. Pathophysiology of sepsis-induced cardiomyopathy. 2013 Oct 4;288(40):28668-86. doi: 10.1074/jbc.M113.470971. Antibodies directed against NADPH oxidase subunits and their sources were as follows. Biochim Biophys Acta. National Center for Biotechnology Information, Unable to load your collection due to an error, Unable to load your delegates due to an error. In addition to mitochondria, many prooxidant enzymes are known to participate in oxygen radicals generation in cerebral ischemia including xanthi,ne oxidase (XO), nitric oxide synthase (NOS), cyclooxygenase (COX) and NADPH oxidase (NOX) NADPH oxidase 4 is an oncoprotein localized to mitochondria Kelly Graham,a. Inhibition of mitochondrial complex I prevents the flow-induced increase in H 2 O…, Figure 3. 16 Importantly, mitochondria act in concert with other sources of ROS, such as NADPH oxidases. NADPH oxidase is activated by many agonists including angiotensin II, PDGF, TNF, alpha 1 agonists and multiple others depending on the NADPH oxidase isozyme and the cell type. 1866, No. 2014 Aug 15;115(5):525-32. doi: 10.1161/CIRCRESAHA.115.303881. Regulation of Vascular Function and Inflammation via Cross Talk of Reactive Oxygen and Nitrogen Species from Mitochondria or NADPH Oxidase-Implications for Diabetes Progression. 1 There are seven identified family members in the NADPH family: five NADPH Oxidases (NOX), NOX1–5, and two NOX homologues, DUOX1 and DUOX2. 33–37 For the establishment of our control groups, a subset of rats was randomly assigned to receive a daily injection (i.p.) 2010 Jun-Jul;1797(6-7):897-906. doi: 10.1016/j.bbabio.2010.01.032. Dilator responses and ROS production during flow were determined in the presence and absence of the NADPH oxidase inhibitor gp91ds-tat and the mitochondrial electron transport inhibitor rotenone. Oxidative Stress … Under physiological conditions, ROS levels are found in a Biochem J 284:781–788 PubMed PubMedCentral Google Scholar Cell Death Discov. In our study, the NOX2 and NOX4 expression was significantly increased by cyclic stretch. COVID-19 is an emerging, rapidly evolving situation. doi: 10.1016/j.freeradbiomed.2011.06.033. 8. Proposed crosstalk between mitochondria and…. Mitochondria, however, are not only a target for ROS produced by NADPH oxidase but also a significant source of ROS, which under certain conditions may stimulate NADPH oxidases. NADPH oxidase (nicotinamide adenine dinucleotide phosphate oxidase) is a membrane-bound enzyme complex that faces the extracellular space. Redox signaling (cross-talk) from and to mitochondria involves mitochondrial pores and reactive oxygen species. Inhibition of mitochondrial complex I…, Figure 2. 2021 Jan 20. doi: 10.1038/s41569-020-00492-2. Visceral adipose arterioles obtained from patients with or without CAD were cannulated and pressurized for videomicroscopic measurement of arteriolar diameters. Finally, NADPH oxidase (NOX) and mitochondria were identified as the main sources of superoxide anion in our model. In endothelial cells (EC), intracellular reactive oxygen species (ROS) are generated from several different sources including NADPH oxidases, mitochondria, cytochrome P450 and xanthine oxidase. 3, pp. Angiogenesis, a new vessel formation from the pre-existing ones, is essential for embryonic development, wound repair and treatment of ischemic heart and limb diseases. Mitochondrial superoxide production during flow was attenuated by gp91ds-tat in arterioles from CAD patients. @article{Daiber2017CrosstalkOM, title={Crosstalk of mitochondria with NADPH oxidase via reactive oxygen and nitrogen species signalling and its role for vascular function}, author={A. Daiber and F. Di Lisa and M. Oelze and S. Kr{\"o}ller-Sch{\"o}n and … eCollection 2020. These radicals are used to destroy pathogens in a process termed the respiratory burst .  |  Ceramide changes the mediator of flow-induced vasodilation from nitric oxide to hydrogen peroxide in the human microcirculation. mitochondrial electron transport complexes as well as NADPH oxidases; second, we used a genetic approach with mouse lungs deficient in the NADPH oxidase subunits gp91 phoxand p47 , respectively. NADPH oxidase via reactive oxygen and nitrogen species signalling and its role for vascular function Andreas Daiber1,FabioDiLisa2, Matthias Oelze1, Swenja Kröller-Schön1, ... mitochondria represent key players and amplifiers of the burden of oxidative stress. 2020 Nov 17;9(11):1142. doi: 10.3390/antiox9111142. NADPH oxidase-2 derived superoxide drives mitochondrial transfer from bone marrow stromal cells to leukemic blasts Proposed crosstalk between mitochondria and NADPH oxidases. 2013;305:H19–28. Cancer Biology & Therapy: Vol. Here, we have systemically modulated produc-tion rates of H 2O Among these, NAPDH oxidase is the only system which generate ROS as the primary and maybe the unique function. Essentially, we found that the mitochondrial respi-ratory chain complex I … [9] It is the source of reducing equivalents for cytochrome P450 hydroxylation of aromatic compounds , steroids , alcohols , and drugs . Tomas A. Schiffer, Jon O. Lundberg, Eddie Weitzberg, Mattias Carlström, Modulation of mitochondria and NADPH oxidase function by the nitrate-nitrite-NO pathway in metabolic disease with focus on type 2 diabetes, Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 10.1016/j.bbadis.2020.165811, (165811), (2020). of 0.9% saline (n = 14 Sed and 12 Ex). This study also identifies a possible treatment of NOX4-induced breast cancer by antioxidant treatment. However, the subcellular localization and function of … 2018 Nov;175(22):4266-4280. doi: 10.1111/bph.14492. Callera GE, Tostes RC, Yogi A, Montezano AC, Touyz RM. Shear stress implemented on the vascular wall activates endothelial NADPH-oxidase in subjects afflicted with CAD leading to a RIRR cascade. Reactive oxygen species (ROS) derived from NADPH oxidase (NOX) as well as mitochondria play an important role in promoting the angiogenic switch from quiescent endothelial cells (ECs). Emerging evidence shows that mitochondria and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase are dominant mechanisms of ROS production in the diabetic heart.  |  CAS PubMed PubMed Central Article Google Scholar 89. Freed JK, Beyer AM, LoGiudice JA, Hockenberry JC, Gutterman DD. LINKED ARTICLES Cunha-Oliveira T, Montezinho L, Mendes C, Firuzi O, Saso L, Oliveira PJ, Silva FSG. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Vol. This site needs JavaScript to work properly. In our study, the NOX2 and NOX4 expression was significantly increased by cyclic stretch. between mitochondria and NADPH oxidase that sug-gests mitochondria may be a key player and trigger in amplifying the burden of oxidative stress [31–33]. These radicals are used to destroy pathogens in a process termed the respiratory burst . Constitutive NADPH oxidase which generates superoxide intracellularly upon formation of a complex with CYBA/p22phox. Epub 2014 Jun 11. Epub 2010 Feb 1.  |  Given that the NADPH oxidase is considered a strong source of ROS, 4 the observations of this study are unexpected. A major source for vascular and renal … Br J Pharmacol. *P<0.05 vs. vehicle.  |  N=5–6. The NADPH system is also responsible for generating free radicals in immune cells by NADPH oxidase. H2 O2 contributes to FID of human arterioles. 223-231. These findings indicate that ROS produced by NADPH oxidase are an upstream component of the mitochondria-dependent pathway contributing to flow-dependent H2 O2 generation and dilation in peripheral microvessels from patients with CAD. Diabetes Care. the electron flow in isolated brain mitochondria produces superoxide radicals (Boveris and Chance 1973). Mitochondrial dysfunction, oxidative phosphorylation and superoxide radical degradation pathway were among the most altered in non-surviving patients. For non-phagocytic cells, one major source of cellular oxidants is the mitochondrial electron transport chain (12). NADPH oxidases, reactive oxygen species, and hypertension: clinical implications and therapeutic possibilities. Nox activity in mitochondria. Circ Res. Methods: An anti-p22 phox monoclonal antibody (mAb449) was a kind gift from Dr. A. Verhoeven (Central Laboratory of Blood Transfusion, Amsterdam, The Netherlands) ().Rabbit polyclonal antibodies against recombinant p40 phox, p47 phox, p67 phox, and Rac1 … 2020 May 12;21(10):3405. doi: 10.3390/ijms21103405. Introduction. Online ahead of print. Essentially, we found that the mitochondrial respi-ratory chain complex I and, particularly, complex IV, have a Mitochondria and NADPH oxidase are considered as the main sources of ROS in cardiovascular tissue and are involved in different physiological and pathological pro-cesses depending on the intensity of ROS generation [6–9]. Mitochondria have the highest levels of antioxidants in the cell and play an important role in the maintenance of cellular redox status, thereby acting as an ROS and redox sink and limiting NADPH oxidase activity. However, how highly diffusible ROS produced from different sources and location can communicate with each other to regulate angiogenesis remains unclear. An emerging hypothesis is that Nox4, a member of the NADPH oxidase family, is localized in mitochondria and actively produces ROS under pathological conditions and during aging [12, 13]. evidence for an oncogenic function for NOX4 protein localized to mitochondria and suggests that NOX4 is a novel source of ROs produced in the mitochondria. Curr Hypertens Rep. 2020 Feb 29;22(3):23. doi: 10.1007/s11906-020-1022-z. While the NADPH-oxidase is the primary source of oxidants in phagocytes, oxidants are also produced by other oxidases and peroxidases in subcellular compartments (2, 11). 2020 Nov 22;22(1):3. doi: 10.1208/s12249-020-01873-z. The interactions between the main cellular sources of ROS, such as mitochondria and NADPH oxidases, however, remain obscure. Carmen Veith, Agnes W. Boots, Musa Idris, Frederik-Jan van Schooten, and ; Albert van der Vliet Structural homology of the vascular NADPH oxidases. Herein, we demonstrate that phagocytes lacking a functional NADPH-oxidase, namely primary CGD phagocytes and a gp91 phox-deficient cell line, display elevated levels of ROS derived from mitochondria. 2003 Nov;30(11):855-9. doi: 10.1046/j.1440-1681.2003.03920.x. It can be found in the plasma membrane as well as in the membranes of phagosomes used by neutrophil white blood cells to engulf microorganisms. Objectives: In recent years, a feed-forward regulation of the ROS sources has been reported. Chang X, Zhang W, Zhao Z, Ma C, Zhang T, Meng Q, Yan P, Zhang L, Zhao Y. 2006 Feb;110(2):243-53. doi: 10.1042/CS20050307. Please enable it to take advantage of the complete set of features! Please enable it to take advantage of the complete set of features! NLM Results: Mitochondria are the most important sources of ROS and accumulating evidence suggest of crosstalk between mitochondria and NADPH oxidase in vascular oxidative stress injury , , . 1–4 Since mitochondrial oxidative phosphorylation contributes very little to EC’s ATP synthesis, Rac1-dependent NADPH oxidase (NOX) acts as a major source of endothelial ROS. Among these, NAPDH oxidase is the only system which generate ROS as the primary and maybe the unique function. Oxid Med Cell Longev. Schematic illustrating the proposed mechanism…, Figure 5. NADPH can be produced in both cytosol and mitochondria. The reactive oxygen species-generating enzyme, NADPH oxidase 4 (Nox4), regulates a number of physiological and pathological processes, including cellular differentiation, host defense, and tissue fibrosis. 10, No. 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. Both dilation and H2 O2 generation during flow were reduced in the presence of rotenone (13.5±8% vs 97±% without rotenone) or gp91ds-tat in patients with CAD, while patients without CAD exhibited H2 O2 -independent dilations. However, a recent research reported that the increase in free radical generation is attributed not to the mitochondrial electron transport chain (ETC) but to the endoplasmic reticulum (ER)-localized NADPH oxidase Yno1 , indicating that the issue of ROS accumulation in living cells remains complex and multifactorial. The two major reactive oxygen species (ROS) generating sources within cells are mitochondria and nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (NOXs) [ 2, 3 ]. The production of ROS from any one source can lead to activation of the NADPH oxidases, conversion of xanthine dehydrogenase to xanthine oxidase, can stimulate the production of mitochondrial ROS or result in uncoupling of the endothelial nitric oxide synthase (eNOS).  |  Cerebral vascular effects of reactive oxygen species: recent evidence for a role of NADPH-oxidase. Mason SA, Trewin AJ, Parker L, Wadley GD. As NADPH oxidase, mitochondria are considered as the main source of ROS such as superoxide anion (O 2⋅−) generated by leak of electrons from the redox centers of respiratory complexes I … Antibodies and Immunoblotting. Modulation of mitochondria and NADPH oxidase function by the nitrate-nitrite-NO pathway in metabolic disease with focus on type 2 diabetes. NIH R01 HL094469/HL/NHLBI NIH HHS/United States, R01 HL094469-02/HL/NHLBI NIH HHS/United States. In the sections below, we will focus upon evidence con-cerning the biology, distribution and role of the various NADPH oxidase family members in brain injury and neurodegenerative disorders. eCollection 2020. K23 HL085614/HL/NHLBI NIH HHS/United States, R01 HL095701/HL/NHLBI NIH HHS/United States, R01 HL113612/HL/NHLBI NIH HHS/United States, R01 HL130513/HL/NHLBI NIH HHS/United States. Deragon MA, McCaig WD, Patel PS, Haluska RJ, Hodges AL, Sosunov SA, Murphy MP, Ten VS, LaRocca TJ. NADPH oxidase 4 is an oncoprotein localized to mitochondria. Here 27–29 To block mitochondria-dependent ROS signalling, we used mitoTEMPO 30–32 or Bendavia. Would you like email updates of new search results? Endothelin-1-induced oxidative stress in DOCA-salt hypertension involves NADPH-oxidase-independent mechanisms. Madni A, Rehman S, Sultan H, Khan MM, Ahmad F, Raza MR, Rai N, Parveen F. AAPS PharmSciTech. Inhibition of mitochondrial complex I…, Figure 1. 15 The NADH pool in mitochondria communicates with the NADPH pool through multiple mitochondrial enzymes such as the isocitrate dehydrogenase reaction coupled to the nicotinamide nucleotide transhydrogenase reaction. Mitochondrial ROS prime the hyperglycemic shift from apoptosis to necroptosis. In the present study, we used apocynin, an inhibitor of NADPH oxidase [ 10 ] and MitoQ, a mitochondria-targeted antioxidant [ 11 , 12 ], to explore the importance of mitochondria versus NADPH oxidase derived ROS in glucose-induced apoptosis of cultured retinal capillary pericytes. Hyperpolarization of the mitochondrial inner membrane potentials and impaired mitochondrial function promote ROS production in the mitochondria of the dia- Increased ROS production (termed “oxidative stress”) has been implicated in various pathologies, including hypertension, atherosclerosis, diabetes, and chronic kidney disease. The different members of the NADPH oxidase family produce superoxide anions or hydrogen peroxide. Vascular oxidative stress, nitric oxide and atherosclerosis. (2010). Epub 2010 Feb 1. Mitochondrial ROS formation, among others, depends on the shape of the mitochondrial network, controlled by fission and fusion of the organells. It is conceivable that the use of mitochondria-targeted treatments would be effective in these conditions. [9] It is the source of reducing equivalents for cytochrome P450 hydroxylation of aromatic compounds , steroids , alcohols , and drugs . The production of ROS…, Schematic presentation of the mitochondrial…, Schematic presentation of the mitochondrial electron transport chain and production of mitochondrial O…. The mechanism of flow-induced dilation in human adipose arterioles involves hydrogen peroxide during CAD. NADPH oxidases are multi-subunit enzymes that primary catalytic function is the generation of reactive oxygen species. 2008 Feb;31 Suppl 2:S170-80. particular, the NADPH oxidase family proteins are unique enzymes which purposefully produce O2-[1, 10, 11]. Reactive oxygen species (ROS) derived from NADPH oxidase (NOX) as well as mitochondria … HHS They function as electron transporters, using reduced NADPH as electron donor and molecular oxygen as electron acceptor to … Get the latest public health information from CDC: https://www.coronavirus.gov, Get the latest research information from NIH: https://www.nih.gov/coronavirus, Find NCBI SARS-CoV-2 literature, sequence, and clinical content: https://www.ncbi.nlm.nih.gov/sars-cov-2/. Segal AW, West I, Wientjes F et al (1992) Cytochrome b-245 is a flavocytochrome containing FAD and the NADPH-binding site of the microbicidal oxidase of phagocytes. This study is designed to examine the roles of mitochondria and NADPH oxidase in modulating the release of ROS and in mediating FID. Clin Exp Pharmacol Physiol. However, dysregulated angiogenesis contributes to various pathologies such as diabetic retinopathy, atherosclerosis and cancer. Choi DH, Cristovao … cardiac hypertrophy; NAD(P)H oxidase; superoxide; mitochondria; Oxidative stress plays an important role in regulating a wide variety of cellular functions, including gene expression, cell growth, and death ().Reactive oxygen species (ROS) posttranslationally modulate signaling molecules and transcription factors (2, 3).A number of molecules in the heart are … NADPH-oxidase is upstream of mitochondria-derived…, Figure 4. 2010 Jun-Jul;1797(6-7):897-906. doi: 10.1016/j.bbabio.2010.01.032. Redox signaling (cross-talk) from and to mitochondria involves mitochondrial pores and reactive oxygen species. Oxidative Stress in Amyotrophic Lateral Sclerosis: Pathophysiology and Opportunities for Pharmacological Intervention. This study also identifies a possible treatment of NOX4-induced breast cancer by antioxidant treatment. 2007 Jan;292(1):H93-100. Ó 2005 Elsevier Inc. 2020 Nov 26;6(1):132. doi: 10.1038/s41420-020-00370-3. : 10.1208/s12249-020-01873-z other sources of reactive oxygen species, and Cytotoxicity of Nanoparticles Targeting... During flow was attenuated by gp91ds-tat in arterioles from CAD patients S Eid! The roles of mitochondria and reducing NADPH oxidase which generates superoxide intracellularly upon formation of a complex CYBA/p22phox. 12 Ex ) sources has been reported 6-7 ):897-906. doi: 10.1046/j.1440-1681.2003.03920.x: 10.1074/jbc.M113.470971 mitochondrial superoxide production during was. 2010 Jun-Jul ; 1797 ( 6-7 ):897-906. doi: 10.1016/j.bbabio.2010.01.032 2014 ;. Recent evidence for a role of nadph-oxidase and angiogenesis by the family NADPH! 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