Kinetics of the Reaction of Nitric Oxide with Oxygen in Aqueous Solutions

Lewis, Randy S.; Deen, William M.

doi:10.1021/tx00040a013

Cited by 277 publications

(230 citation statements)

References 15 publications

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“…6A) suggest that shear at 21% O 2 may increase eNOS activity to a greater extent than shear at lower PO 2 levels, leading to enhanced ONOO Ϫ formation and suppression of respiration. Since NO 3 Ϫ is the degradation product of ONOO Ϫ and its nitrating intermediates (43) and ONOO Ϫ formation is enhanced under shear at 21% O 2 ( Fig. 3 and Ref.…”

Section: Discussionmentioning

confidence: 95%

Endothelial cell respiration is affected by the oxygen tension during shear exposure: role of mitochondrial peroxynitrite

Jones¹,

Han²,

Presley³

et al. 2008

American Journal of Physiology-Cell Physiology

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Cultured vascular endothelial cell (EC) exposure to steady laminar shear stress results in peroxynitrite (ONOO Ϫ ) formation intramitochondrially and inactivation of the electron transport chain. We examined whether the "hyperoxic state" of 21% O2, compared with more physiological O2 tensions (PO2), increases the shear-induced nitric oxide (NO) synthesis and mitochondrial superoxide (O2 ⅐ Ϫ ) generation leading to ONOO Ϫ formation and suppression of respiration. Electron paramagnetic resonance oximetry was used to measure O2 consumption rates of bovine aortic ECs sheared (10 dyn/cm 2 , 30 min) at 5%, 10%, or 21% O2 or left static at 5% or 21% O2. Respiration was inhibited to a greater extent when ECs were sheared at 21% O2 than at lower PO2 or left static at different PO2. Flow in the presence of an endothelial NO synthase (eNOS) inhibitor or a ONOO Ϫ scavenger abolished the inhibitory effect. EC transfection with an adenovirus that expresses manganese superoxide dismutase in mitochondria, and not a control virus, blocked the inhibitory effect. Intracellular and mitochondrial O2 ⅐ Ϫ production was higher in ECs sheared at 21% than at 5% O2, as determined by dihydroethidium and MitoSOX red fluorescence, respectively, and the latter was, at least in part, NO-dependent. Accumulation of NO metabolites in media of ECs sheared at 21% O2 was modestly increased compared with ECs sheared at lower PO2, suggesting that eNOS activity may be higher at 21% O2. Hence, the hyperoxia of in vitro EC flow studies, via increased NO and mitochondrial O2 ⅐ Ϫ production, leads to enhanced ONOO Ϫ formation intramitochondrially and suppression of respiration. shear stress; endothelium; mitochondria; reactive oxygen species MITOCHONDRIA ARE THE SUBCELLULAR organelles for the production of cellular energy, but they also activate intracellular signaling pathways that modulate cell proliferation or promote cell cycle arrest and apoptosis by oxidative or nitrosative reactions. These reactions are regulated by the matrix concentration of nitric oxide (NO), which diffuses to the mitochondria from the cytosolic NO synthase (NOS) isoforms and is thought to be produced also locally by a mitochondrial NOS variant (11). In rat heart, skeletal muscle and liver mitochondria (15,57,58), isolated rat hearts (59), and whole animals (68), NO at physiological concentrations binds reversibly and in competition with oxygen (O 2 ) to the reduced binuclear center Cu B /a 3 of cytochrome-c oxidase (complex IV) of the electron transport chain (ETC) and inhibits mitochondrial O 2 uptake. At slightly higher concentrations, NO oxidizes ubiquinol of ubiquinolcytochrome c reductase (complex III) to increase unstable ubisemiquinone, which, by univalent electron transfer to O 2 , produces the reactive O 2 species (ROS) superoxide (O 2 ⅐ Ϫ ) (57, 58). O 2 ⅐ Ϫ generated from that location is released both into the matrix and intermembrane space (51), where it is dismutated to hydrogen peroxide (H 2 O 2 ) by manganese superoxide dismutase (MnSOD) and copper zinc SOD (CuZ...

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Section: Discussionmentioning

confidence: 95%

Endothelial cell respiration is affected by the oxygen tension during shear exposure: role of mitochondrial peroxynitrite

Jones¹,

Han²,

Presley³

et al. 2008

American Journal of Physiology-Cell Physiology

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“…Many have questioned the relevance of nitrosation via NO autoxidation, reasoning that sufficient levels of NO cannot be achieved in vivo to satisfy the rate-limiting step for N 2 O 3 formation, which is second order in [11][12][13][14][15][16][17][18][19][20]. In contrast to NO autoxidation, the reaction between NO and superoxide (O 2 Ϫ ) is first order in both reactants and occurs at near diffusion control (21-24).…”

mentioning

confidence: 99%

Focusing of nitric oxide mediated nitrosation and oxidative nitrosylation as a consequence of reaction with superoxide

Espey

Thomas

Miranda

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

160

138

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The impact of nitric oxide (NO) synthesis on different biological cascades can rapidly change dependent on the rate of NO formation and composition of the surrounding milieu. With this perspective, we used diaminonaphthalene (DAN) and diaminofluorescein (DAF) to examine the nitrosative chemistry derived from NO and superoxide (O 2 ؊ ) simultaneously generated at nanomolar to low micromolar per minute rates by spermine͞NO decomposition and xanthine oxidasecatalyzed oxidation of hypoxanthine, respectively. Fluorescent triazole product formation from DAN B iosynthesis of nitrogen monoxide (NO) from nitric-oxide synthase (NOS)-catalyzed oxidation of L-arginine can lead to selective formation of NO adducts on protein residues, which modulates homeostatic metabolism and affects numerous pathophysiologic responses. N-nitrosamines and S-nitrosothiols are typically formed via donation of a nitrosonium equivalent (NO ϩ ) from dinitrogen trioxide (N 2 O 3 ) to the nucleophilic residue (1). The function of many proteins has been altered by nitrosation in vitro including caspases (2, 3), glyceraldehyde-3-phosphate dehydrogenase (4), the N-methyl-D-aspartate receptor (5, 6), O 6 -methylguanine-DNA-methyltransferase (7, 8), ras (9) and the ryanodine receptor (10).The mechanism through which these modifications may occur in biological systems is a subject of debate. Many have questioned the relevance of nitrosation via NO autoxidation, reasoning that sufficient levels of NO cannot be achieved in vivo to satisfy the rate-limiting step for N 2 O 3 formation, which is second order in [11][12][13][14][15][16][17][18][19][20]. In contrast to NO autoxidation, the reaction between NO and superoxide (O 2 Ϫ ) is first order in both reactants and occurs at near diffusion control (21-24). Much emphasis has been placed on the product of this reaction, peroxynitrite (ONOO Ϫ ), as an important mediator of oxidation and nitration (23)(24)(25)(26)(27)(28). In this study, we tested the hypothesis that ONOO Ϫ may also serve as an intermediary in a pathway leading to formation of NO adducts (e.g., N-nitrosamines, S-nitrosothiols) in vivo.The results suggest that these moieties may be produced through both nitrosation and oxidative nitrosylation dependent mechanisms, which are strongly influenced by the relative rates of NO and O 2 Ϫ formation. Buffer pH (7.4) and temperature (37°C) were confirmed before each experiment because of the major influence these parameters have on the rate of spermine͞NO decomposition (t 1/2 ϭ 42 min). Rates of NO release were determined by measuring oxymyoglobin oxidation (582 nm, ϭ 9,100 M Ϫ1 ⅐cm Ϫ1 ) in PBS solution containing DTPA and HX (HX buffer, ref. 32). Oxymyoglobin was prepared by reducing myoglobin (500 M; Sigma) in water with excess sodium dithionite (Fluka) followed by passage through a Sephadex G-25 column (PD-10; Amersham Pharmacia). Steady-state NO concentrations were also assessed by using a NO selective electrode (World Precision Instruments, Sarasota, FL) controlled by a DUO18 amplifier. Peak ampl...

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“…It must be oxidized first to form nitrosative agents, such as N 2 O 3 . Because of the slow rate of the third-order reaction of NO with O 2 (k Ϸ4ϫ10 6 mol/L Ϫ2 per second), 17,18 the formation of N 2 O 3 and eventually RSNO should depend primarily on the local concentration of NO and the molecular environment. Indeed, strong acceleration of NO oxidation occurs within lipid membranes 19 and hydrophobic pockets of plasma proteins 20 that effectively sequester NO from the aqueous phase.…”

mentioning

confidence: 99%

Control of Plasma Nitric Oxide Bioactivity by Perfluorocarbons

et al. 2004

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Background-Perfluorocarbons (PFCs) are promising blood substitutes because of their chemical inertness and unparalleled ability to transport and upload O 2 and CO 2 . Here, we report that PFC emulsions also efficiently absorb and transport nitric oxide (NO). Methods and Results-Accumulation of NO and O 2 in PFC micelles results in rapid NO oxidation and generation of reactive NO x species. Such micellar catalysis of NO oxidation leads to formation of vasoactive S-nitrosothiols (RSNO) in vitro and in vivo as detected electrochemically. The efficiency of PFC-mediated S-nitrosation depends on the amount of PFC in aqueous solution. The optimal PFC concentration that produced the maximum level of RSNO was Ϸ1% (vol/vol). Larger PFC amounts were progressively less efficient in generating RSNO and functioned simply as NO sink. These results explain the characteristic hemodynamic effects of PFCs. Intravenous bolus application of PFC (0.14 g/kg, Ϸ1% vol/vol) to Wistar-Kyoto rats decreased mean arterial pressure significantly (Ϫ10 mm Hg over 40 minutes). PFC-induced hypotension could be further stimulated (Ϫ17 mm Hg over 140 minutes) by exogenous thiols (cysteine and glutathione). In contrast, a larger amount of PFC (1 g/kg, Ϸ7% vol/vol) exhibited a strong hypertensive effect (11 mm Hg over 40 minutes). Conclusions-The present study reveals a physiologically significant pool of endogenous plasma NO and underscores the crucial role of the circulating hydrophobic phase in modulating its bioactivity. The results also establish PFC as a conceptually new pharmacological tool for various cardiovascular complications associated with NO imbalance.

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Kinetics of the Reaction of Nitric Oxide with Oxygen in Aqueous Solutions

Cited by 277 publications

References 15 publications

Endothelial cell respiration is affected by the oxygen tension during shear exposure: role of mitochondrial peroxynitrite

Endothelial cell respiration is affected by the oxygen tension during shear exposure: role of mitochondrial peroxynitrite

Focusing of nitric oxide mediated nitrosation and oxidative nitrosylation as a consequence of reaction with superoxide

Control of Plasma Nitric Oxide Bioactivity by Perfluorocarbons

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