The homeostatic role of hydrogen peroxide, superoxide anion and nitric oxide in the vasculature

2020 ◽  
Author(s):  
Tiago J. Costa ◽  
Paula Rodrigues Barros ◽  
Cristina Arce ◽  
Jeimison Duarte Santos ◽  
Júlio da Silva-Neto ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Peroxide ◽  
Superoxide Anion

scholarly journals Resistance to the Nitric Oxide/Cyclic Guanosine 5′-Monophosphate/Protein Kinase G Pathway in Vascular Smooth Muscle Cells from the Obese Zucker Rat, a Classical Animal Model of Insulin Resistance: Role of Oxidative Stress

Endocrinology ◽  
2007 ◽  
Vol 149 (4) ◽  
pp. 1480-1489 ◽  
Author(s):  
I. Russo ◽  
P. Del Mese ◽  
G. Doronzo ◽  
L. Mattiello ◽  
M. Viretto ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Hydrogen Peroxide ◽  
Smooth Muscle ◽  
Superoxide Anion ◽  
Zucker Rats ◽  
No Donor ◽  
Vasp Phosphorylation ◽  
Donor Ability

Some in vivo and ex vivo studies demonstrated a resistance to the vasodilating effects of nitric oxide (NO) in insulin-resistant states and, in particular, obese Zucker rats (OZR). To evaluate the biochemical basis of this phenomenon, we aimed to identify defects of the NO/cGMP/cGMP-dependent protein kinase (PKG) pathway in cultured vascular smooth muscle cells (VSMCs) from OZR and lean Zucker rats (LZR) by measuring: 1) NO donor ability to increase cGMP in the absence and presence of inhibitors of soluble guanylate cyclase (sGC) and phosphodiesterases (PDEs); 2) NO and cGMP ability to induce, via PKG, vasodilator-stimulated phosphoprotein (VASP) phosphorylation at serine 239 and PDE5 activity; 3) protein expression of sGC, PKG, total VASP, and PDE5; 4) superoxide anion concentrations and ability of antioxidants (superoxide dismutase+catalase and amifostine) to influence the NO/cGMP/PKG pathway activation; and 5) hydrogen peroxide influence on PDE5 activity and VASP phosphorylation. VSMCs from OZR vs. LZR showed: 1) baseline cGMP concentrations higher, at least in part owing to reduced catabolism by PDEs; 2) impairment of NO donor ability to increase cGMP, even in the presence of PDE inhibitors, suggesting a defect in the NO-induced sGC activation; 3) reduction of NO and cGMP ability to activate PKG, indicated by the impaired ability to phosphorylate VASP at serine 239 and to increase PDE5 activity via PKG; 4) similar baseline protein expression of sGC, PKG, total VASP, and PDE5; and 5) higher levels of superoxide anion. Antioxidants partially prevented the defects of the NO/cGMP/PKG pathway observed in VSMCs from OZR, which were reproduced by hydrogen peroxide in VSMCs from LZR, suggesting the pivotal role of oxidative stress.

Research of corrosion fracture of D16t and AMg6 aluminum alloys exposed to microscopic fungi

2021 ◽  
pp. 163-183
Author(s):  
D. V. Belov ◽  
S. N. Belyaev ◽  
M. V. Maksimov ◽  
G. A. Gevorgyan
Keyword(s):  
Hydrogen Peroxide ◽  
Aluminum Alloys ◽  
Superoxide Anion ◽  
Anion Radical ◽  
Corrosion Damage ◽  
Oxygen Species ◽  
Microscopic Fungi ◽  
Reductive Activation ◽  
Activation Of Oxygen

This paper presents an experimental study of biocorrosion of D16T and AMg6 aluminum alloys. The determining role of reactive oxygen species in aluminum biocorrosion by a consortium of molds has been shown. A model is proposed, according to which the initiators of corrosion damage to the metal surface are superoxide anion radical and hydrogen peroxide released during the life of micromycetes. It is assumed that the initiation and development of biocorrosion occurs, among other things, as a result of the process of reductive activation of oxygen and the Fenton decomposition of hydrogen peroxide. A conclusion is made about the mechanism of the occurrence of intergranular and pitting corrosion of aluminum alloys interacting with microscopic fungi.

The role of nitric oxide in the cardiac effects of hydrogen peroxide

1996 ◽  
Vol 159 (1) ◽  
Author(s):  
Guro Wen ◽  
Tove Skjelbakken ◽  
Jarle Wage
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Peroxide ◽  
Cardiac Effects

Nitrogen(II) Oxide (Nitric Oxide, NO): Its Origin, Fate and Physiological Significance. A Review

1997 ◽  
Vol 62 (9) ◽  
pp. 1355-1383 ◽  
Author(s):  
Petr Vetrovsky ◽  
Gustav Entlicher
Keyword(s):  
Nitric Oxide ◽  
Superoxide Anion ◽  
De Novo ◽  
Soluble Guanylate Cyclase ◽  
No Synthase ◽  
Transcriptional Level ◽  
Immune Systems ◽  
Important Target ◽  
Target Molecules

The nitrogen oxide (NO), a free radical molecule, plays a key role in the regulation of mammalian physiology and pathophysiology, e.g., in cardiovascular, nervous or immune systems. This molecule is produced from guanidino moiety of amino acid L-arginine with NG-hydroxy-L-arginine as intermediate and L-citrulline as a co-product of this reaction. This conversion is catalyzed by an ezyme called NO-synthase. The NO-synthase belongs to the cytochrome P450 superfamily and four its isoenzymes are known so far. Two (denoted NOS-I and III) are constitutive, generate lower amounts (pmol) of NO and are regulated by Ca++/calmodulin system. The others (NOS-II and IV) are inducible, produce a larger quantity of NO (nmol) and are regulated at a transcriptional level. The constitutive form is present, for example, in endothelial and neuronal cells whereas the inducible form is de novo synthesized as a consequence of certain stimuli (including cytokines) in macrophages, vascular smooth muscle cells and other cells. There are several target molecules for NO depending on cells. The most frequent target is supposed to be the soluble guanylate cyclase. However, superoxide anion is a very important target for NO, too. The reaction between these two molecules leads to the production of peroxynitrite, the fate of which depends on environmental conditions. Therefore, the importance of this reaction is still debated. This review deals with the nature of NO, the mechanisms of its production, the role of intermediate NG-hydroxy-L-arginine and summarizes the biology of superoxide anion with respect to its reaction with NO. A review with 218 references.

Abstract 3629: Crucial Role of Nitric Oxide Synthases System in Endothelium-Dependent Hyperpolarization in Mice

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Aya Takaki ◽  
Keiko Morikawa ◽  
Yoshinori Murayama ◽  
Ender Tekes ◽  
Hiroto Yamagishi ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Peroxide ◽  
Antihypertensive Treatment ◽  
Direct Evidence ◽  
No Synthase ◽  
Mesenteric Arteries ◽  
Superoxide Anions ◽  
Nos Isoforms ◽  
Nos Gene

We have previously demonstrated that endothelium-derived hydrogen peroxide (H 2 O 2 ) is an endothelium-derived hyperpolarizing factor (EDHF) in mouse and human mesenteric arteries and porcine coronary microvessels. We also have demonstrated that endothelial NO synthase (eNOS) is a major source of EDHF/H 2 O 2 , where Cu,Zn-superoxide dismutase (SOD) plays an important role to dismutate eNOS-derived superoxide anions to EDHF/H 2 O 2 in animals and humans. However, the mechanism for the endothelial production of H 2 O 2 as an endogenous EDHF remains to be elucidated. Indeed, some EDHF-mediated responses still remain in singly eNOS −/− mice and the remaining responses are also sensitive to catalase that dismutates H 2 O 2 to form water and oxygen. It is widely known that 3 NOS isoforms (neuronal, inducible, and endothelial) compensate each other. In this study, we examined the effects of genetic disruption of all NOS isoforms (n/i/eNOS −/− ) on EDHF responses in mice. We examined the contribution of the whole NOS system to EDHF-mediated responses in eNOS −/− , n/eNOS −/− and n/i/eNOS −/− mice that we have recently generated. Isometric tensions and membrane potentials were recorded by organ chamber experiments and microelectrode technique, respectively. EDHF-mediated relaxations and hyperporalizations in response to acetylcholine of mesenteric arteries were progressively reduced as the number of disrupted NOS genes increased (n=6 each), whereas vascular smooth muscle functions were preserved (n=6 each). Expressions of endothelial NOS isoforms in the NOSs −/− mice were compensated by NOS gene that had not been disrupted (n=5 each). Laser confocal microscopic examination demonstrated that endothelial H 2 O 2 and superoxide production was absent in n/i/eNOS −/− mice (n=3–5), whereas antihypertensive treatment with hydralazine failed to improve the EDHF-mediated responses (n= 4). Involvement of NOS uncoupling was ruled out as modulation of BH 4 synthesis had no effects (n=6–7) and BH 4 /BH 2 ratio (an index of BH 4 bioavailability) was preserved (n=4). These results provide the first direct evidence that EDHF-mediated responses are totally dependent on endothelial NOSs system in mouse mesenteric arteries.

Role of nitric oxide in hydrogen peroxide-dependent induction of abiotic stress tolerance by brassinosteroids in cucumber

2010 ◽  
Vol 34 (2) ◽  
pp. 347-358 ◽  
Author(s):  
JIN-XIA CUI ◽  
YAN-HONG ZHOU ◽  
JIAN-GANG DING ◽  
XIAO-JIAN XIA ◽  
KAI SHI ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Peroxide ◽  
Abiotic Stress ◽  
Stress Tolerance ◽  
Abiotic Stress Tolerance

Role of nitric oxide and superoxide anion in leukotoxin-, 9,10-epoxy-12-octadecenoate-induced mitochondrial dysfunction

1996 ◽  
Vol 20 (4) ◽  
pp. 607-612 ◽  
Author(s):  
Tetsuo Sakai ◽  
Takeshi Ishizaki ◽  
Tsuguhiko Nakai ◽  
Susumu Miyabo ◽  
Shigeru Matsukawa ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Mitochondrial Dysfunction ◽  
Superoxide Anion

scholarly journals Crucial role of nitric oxide synthases system in endothelium-dependent hyperpolarization in mice

2008 ◽  
Vol 205 (9) ◽  
pp. 2053-2063 ◽  
Author(s):  
Aya Takaki ◽  
Keiko Morikawa ◽  
Masato Tsutsui ◽  
Yoshinori Murayama ◽  
Ender Tekes ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Hydrogen Peroxide ◽  
Muscle Function ◽  
Antihypertensive Treatment ◽  
No Synthase ◽  
Mesenteric Arteries ◽  
Enos Expression ◽  
Smooth Muscle Function ◽  
Nos Isoforms

The endothelium plays an important role in maintaining vascular homeostasis by synthesizing and releasing several relaxing factors, such as prostacyclin, nitric oxide (NO), and endothelium-derived hyperpolarizing factor (EDHF). We have previously demonstrated in animals and humans that endothelium-derived hydrogen peroxide (H2O2) is an EDHF that is produced in part by endothelial NO synthase (eNOS). In this study, we show that genetic disruption of all three NOS isoforms (neuronal [nNOS], inducible [iNOS], and endothelial [eNOS]) abolishes EDHF responses in mice. The contribution of the NOS system to EDHF-mediated responses was examined in eNOS−/−, n/eNOS−/−, and n/i/eNOS−/− mice. EDHF-mediated relaxation and hyperpolarization in response to acetylcholine of mesenteric arteries were progressively reduced as the number of disrupted NOS genes increased, whereas vascular smooth muscle function was preserved. Loss of eNOS expression alone was compensated for by other NOS genes, and endothelial cell production of H2O2 and EDHF-mediated responses were completely absent in n/i/eNOS−/− mice, even after antihypertensive treatment with hydralazine. NOS uncoupling was not involved, as modulation of tetrahydrobiopterin (BH4) synthesis had no effect on EDHF-mediated relaxation, and the BH4/dihydrobiopterin (BH2) ratio was comparable in mesenteric arteries and the aorta. These results provide the first evidence that EDHF-mediated responses are dependent on the NOSs system in mouse mesenteric arteries.

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