scholarly journals Quantitative Proteome Profiling of a S-Nitrosoglutathione Reductase (GSNOR) Null Mutant Reveals a New Class of Enzymes Involved in Nitric Oxide Homeostasis in Plants

2021 ◽  
Vol 12 ◽  
Author(s):  
Patrick Treffon ◽  
Jacopo Rossi ◽  
Giuseppe Gabellini ◽  
Paolo Trost ◽  
Mirko Zaffagnini ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Oxidation Products ◽  
Null Mutant ◽  
Chlorophyll Metabolism ◽  
New Class ◽  
Reduction Activity ◽  
Dependent Component ◽  
Dependent Activity ◽  
Major Route ◽  
Insight Into

Nitric oxide (NO) is a short-lived radical gas that acts as a signaling molecule in all higher organisms, and that is involved in multiple plant processes, including germination, root growth, and fertility. Regulation of NO-levels is predominantly achieved by reaction of oxidation products of NO with glutathione to form S-nitrosoglutathione (GSNO), the principal bioactive form of NO. The enzyme S-nitrosoglutathione reductase (GSNOR) is a major route of NADH-dependent GSNO catabolism and is critical to NO homeostasis. Here, we performed a proteomic analysis examining changes in the total leaf proteome of an Arabidopsis thaliana GSNOR null mutant (hot5-2/gsnor1-3). Significant increases or decreases in proteins associated with chlorophyll metabolism and with redox and stress metabolism provide insight into phenotypes observed in hot5-2/gsnor1-3 plants. Importantly, we identified a significant increase in proteins that belong to the aldo-keto reductase (AKR) protein superfamily, AKR4C8 and 9. Because specific AKRs have been linked to NO metabolism in mammals, we expressed and purified A. thaliana AKR4C8 and 9 and close homologs AKR4C10 and 11 and determined that they have NADPH-dependent activity in GSNO and S-nitroso-coenzyme A (SNO-CoA) reduction. Further, we found an increase of NADPH-dependent GSNO reduction activity in hot5-2/gsnor1-3 mutant plants. These data uncover a new, NADPH-dependent component of NO metabolism that may be integrated with NADH-dependent GSNOR activity to control NO homeostasis in plants.

scholarly journals New Insight into the Role of Nitric Oxide Pathways in Pancreas

2018 ◽  
Vol 51 (6) ◽  
pp. 167-172 ◽  
Author(s):  
Igor Buchwalow ◽  
Jürgen Schnekenburger ◽  
Vera Samoilova ◽  
Werner Boecker ◽  
Joachim Neumann ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Insight Into

scholarly journals Controlled nitric oxide production via O(<sup>1</sup>D)+N<sub>2</sub>O reactions for use in oxidation flow reactor studies

2017 ◽  
Author(s):  
Andrew Lambe ◽  
Paola Massoli ◽  
Xuan Zhang ◽  
Manjula Canagaratna ◽  
John Nowak ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Flow Reactor ◽  
Branching Ratio ◽  
Oxidation Products ◽  
Oh Radicals ◽  
Ionization Mass ◽  
Flow Reactors ◽  
Oxidative Aging ◽  
Gas Phase Oxidation

Abstract. Oxidation flow reactors that use low-pressure mercury lamps to produce hydroxyl (OH) radicals are an emerging technique for studying the oxidative aging of organic aerosols. Here, ozone (O3) is photolyzed at 254 nm to produce O(1D) radicals, which react with water vapor to produce OH. However, the need to use parts-per-million levels of O3 hinders the ability of oxidation flow reactors to simulate NOx-dependent SOA formation pathways. Simple addition of nitric oxide (NO) results in fast conversion of NOx (NO + NO2) to nitric acid (HNO3), making it impossible to sustain NO at levels that are sufficient to compete with hydroperoxy (HO2) radicals as a sink for organic peroxy (RO2) radicals. We developed a new method that is well suited to the characterization of NOx-dependent SOA formation pathways in oxidation flow reactors. NO and NO2 are produced via the reaction O(1D) + N2O→ 2NO, followed by the reaction NO + O3 → NO2+ O2. Laboratory measurements coupled with photochemical model simulations suggest that O(1D) + N2O reactions can be used to systematically vary the relative branching ratio of RO2 + NO reactions relative to RO2 + HO2 and/or RO2 + RO2 reactions over a range of conditions relevant to atmospheric SOA formation. We demonstrate proof of concept using high-resolution time-of-flight chemical ionization mass spectrometer (HR-ToF-CIMS) measurements with nitrate (NO3−) reagent ion to detect gas-phase oxidation products of isoprene and α-pinene previously observed in NOx-influenced environments and in laboratory chamber experiments.

Hypoxia inhibits nitric oxide synthesis in isolated rabbit lung

1997 ◽  
Vol 272 (6) ◽  
pp. L1167-L1173 ◽  
Author(s):  
S. P. Kantrow ◽  
Y. C. Huang ◽  
A. R. Whorton ◽  
E. N. Grayck ◽  
J. M. Knight ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Competitive Inhibitor ◽  
Oxidation Products ◽  
No Oxidation ◽  
Severe Hypoxia ◽  
No Production ◽  
Rabbit Lung ◽  
Vasoconstrictor Response ◽  
Hypoxic Vasoconstriction ◽  
Oxide Synthase

Nitric oxide (NO.) has been proposed to modulate hypoxic vasoconstriction in the lung. The activity of nitric oxide synthase (NOS) can be inhibited by hypoxia because molecular oxygen is a necessary substrate for the enzyme. On the basis of this mechanism, we hypothesized that NOS activity has a key role in regulation of pulmonary vascular tone during hypoxia. We measured oxidation products of NO. released into the vasculature of isolated buffer-perfused rabbit lung ventilated with normoxic (21% O2), moderately hypoxic (5% O2), or anoxic (0% O2) gas using two methods. Mean PO2 in perfusate exiting the lung was 25 Torr during anoxic ventilation and 47 Torr during moderately hypoxic ventilation. We found that the amount of the NO. oxidation product nitrite released into the perfusate was suppressed significantly during ventilation with anoxic but not moderately hypoxic gas. During normoxic ventilation, nitrite release was inhibited by pretreatment with NG-monomethyl-L-arginine, a competitive inhibitor of NOS. To confirm that changes in nitrite concentration reflected changes in NO. release into the perfusate, major oxidation products of NO. (NOx) were assayed using a method for reduction of these products to NO. by vanadium(III) Cl. Release of NOx into the perfusate was suppressed by severe hypoxia (anoxic ventilation), and this effect was reversed by normoxia. Pulmonary vasoconstriction was observed during severe but not moderate hypoxia and was related inversely to the rate of nitrite release. These observations provide evidence that decreased NO. production contributes to the pulmonary vasoconstrictor response during severe hypoxia.

scholarly journals Basal and stimulated nitric oxide in control of kidney function in the aging rat

1997 ◽  
Vol 272 (6) ◽  
pp. R1747-R1753 ◽  
Author(s):  
C. Hill ◽  
A. M. Lateef ◽  
K. Engels ◽  
L. Samsell ◽  
C. Baylis
Keyword(s):  
Nitric Oxide ◽  
Vascular Resistance ◽  
Pressor Response ◽  
Renal Vascular Resistance ◽  
Oxidation Products ◽  
No Oxidation ◽  
No Production ◽  
Sprague Dawley ◽  
Vasoconstrictor Response ◽  
Renal Vascular

To investigate the activity of nitric oxide (NO) in control of renal hemodynamics during aging, studies were conducted on conscious Sprague-Dawley rats aged 3-5 mo (young, Y) and 18-22 mo (old, O). Blood pressure (BP) and renal vascular resistance (RVR) were higher in O vs. Y in control, and acute systemic NO synthesis inhibition (NOSI) increased BP and RVR, with an enhanced renal vasoconstrictor response in O. Infusion of the NO substrate L-arginine produced similar, selective renal vasodilation in both groups. The endothelium-dependent vasodilator acetylcholine caused similar falls in BP and RVR, whereas sodium nitroprusside produced an exaggerated depressor response in O vs. Y without falls in RVR in either age group. Urinary excretion of the stable NO oxidation products (NOx) decreased with age, suggesting a decline in the overall somatic NO production. In conclusion, basal tonically produced NO has a more pronounced role in maintenance of renal perfusion in aging, whereas L-arginine- and agonist-stimulated renal vasodilation is not impaired with age. NO production from some source may be reduced with aging, as indicated by falls in 24-h NOX excretion, although the similarity in pressor response and enhanced renal vasoconstrictor response to NOSI suggests that the role of NO in control of total peripheral and renal vascular resistance is maintained.

scholarly journals Exogenous NO Therapy for the Treatment and Prevention of Atherosclerosis

2020 ◽  
Vol 21 (8) ◽  
pp. 2703 ◽  
Author(s):  
Tommaso Gori
Keyword(s):  
Nitric Oxide ◽  
Endothelial Dysfunction ◽  
Plaque Rupture ◽  
Nitric Oxide Donors ◽  
New Class ◽  
Amyl Nitrite ◽  
Treatment And Prevention ◽  
The Subject ◽  
Prevention Of Atherosclerosis ◽  
Nitric Oxide Pathway

Amyl nitrite was introduced in 1867 as the first molecule of a new class of agents for the treatment of angina pectoris. In the following 150 years, the nitric oxide pathway has been the subject of a number of pharmacological approaches, particularly since when this elusive mediator was identified as one of the most important modulators of vascular homeostasis beyond vasomotion, including platelet function, inflammation, and atherogenesis. While having potent antianginal and antiischemic properties, however, nitric oxide donors are also not devoid of side effects, including the induction of tolerance, and, as shown in the last decade, of oxidative stress and endothelial dysfunction. In turn, endothelial dysfunction is itself felt to be involved in all stages of atherogenesis, from the development of fatty streaks to plaque rupture and thrombosis. In the present review, we summarize the agents that act on the nitric oxide pathway, with a particular focus on their potentially beneficial antiatherosclerotic and unwanted pro-atherosclerotic effects.

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