Possible Role Of NO Research Articles

The mechanism of NO and N2O decomposition catalyzed by short-distance Cu(I) pairs in Cu-ZSM-5: A DFT study on the possible role of NO and NO2 in the [Cu[sbnd]O[sbnd]Cu]2+ active site reduction

The reactivity between NO and the oxidized form of a short-distance dinuclear Cu-ZSM-5 catalyst (ZCu2O) was investigated. ZCu2O, which contains the [CuOCu]2+ bridge coordinated at the opposite T11 positions of the M6 ring of ZSM-5, is obtained by the spin-forbidden decomposition of N2O on the reduced form of the catalyst, ZCu2, with an activation energy of about 18 kcal mol−1. The further addition of NO to the [CuOCu]2+ unit of ZCu2O occurs in the doublet state without activation energy and gives NO2. After desorption, which requires 39.9 kcal mol−1, NO2 decomposes on a second ZCu2O site, giving NO again and O2. Three reaction paths were defined for the latter reaction, with activation energies ranging from about 30 to 42–43 kcal mol−1. Final O2 desorption is endothermic. The effect of enthalpy and Gibbs free energy contributions at 298.15 and at 773 K was also shown and discussed. According to the present calculations, the [CuOCu]2+ bridge can easily be broken by reaction with NO but the desorption and further decomposition of NO2 are characterized by energetics which make the above mechanism slower than the spin-allowed decomposition of N2O on similar sites, already reported in the literature. The above conclusions were based on a kinetic analysis according to the Energetic Span Model.

Cardioprotective effect of Angiotensin (1-7) on myocardial infarction: Possible role of Nitric oxide and prostaglandins.

Objective: to detect the possible cardioprotective effect of Ang-(1-7) in rat model of MI; Also, possible role of NO and PGs in this probable cardioprotective effect of Ang- (1-7) was studied. Methods: Rats were divided randomly into 6 groups (8 rats each): Group I : Control group:, Group II: rats received S.C isoprenaline at a dose of 150 mg/kg/day on two consecutive days with an interval of 24 hours between applications, Group III: rats received Ang (1-7) (576μg/kg/day) S.C for 6 days after induction of MI ,Group IV: in which rats received Ang (1-7) (576μg/kg/day)+ L-NAME in the drinking water (80 mg/l) for 6days after induction of MI ,Group V: in which rats received Ang (1-7) (576μg/kg/day) +Indomethacin 5 mg/kg/day IP for 6 days after induction of MI ,Group VI: in which rats received both Ang-(1-7)+ L- NAME and Indomethacinat dose mentioned previously. Biochemical, histopathologial , and ECG changes were studied Results: ISO –MI group exhibited a significant rise in serum cardiac enzymes and disturbed lipid profile, increased myocardial damage score and Caspase3 expression when it is compared to the normal group (p<0.001). ECG changes of rat revealed elevation ST segment, QT interval prolongation, decrease QRS duration and voltage, and accelerated heart rate. Ang-(1-7) caused significant improvement in the studied parameters ,while co-infusion of L-NAME and or indomethacin prevent this effect of Ang-(1-7) .Combined L-NAME and indomethacin produce more deleterious effect than separate administration of them. Conclusion: Ang-(1-7) is considered one of the cardioprotective components of RAS .NO and PGs mediate the action of Ang-(1-7) and they may have an additive effect.

24S-hydroxycholesterol suppresses neuromuscular transmission in SOD1(G93A) mice: A possible role of NO and lipid rafts

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by the initial denervation of skeletal muscle and subsequent death of motor neurons. A dying-back pattern of ALS suggests a crucial role for neuromuscular junction dysfunction. In the present study, microelectrode recording of postsynaptic currents and optical detection of synaptic vesicle traffic (FM1-43 dye) and intracellular NO levels (DAF-FM DA) were used to examine the effect of the major brain-derived cholesterol metabolite 24S-hydroxycholesterol (24S-HC, 0.4 μM) on neuromuscular transmission in the diaphragm of transgenic mice carrying a mutant superoxide dismutase 1 (SODG93A). We found that 24S-HC suppressed spontaneous neurotransmitter release and neurotransmitter exocytosis during high-frequency stimulation. The latter was accompanied by a decrease in both the rate of synaptic vesicle recycling and activity-dependent enhancement of NO production. Inhibition of NO synthase with L-NAME also attenuated synaptic vesicle exocytosis during high-frequency stimulation and completely abolished the effect of 24S-HC itself. Of note, 24S-HC enhanced the labeling of synaptic membranes with B-subunit of cholera toxin, suggesting an increase in lipid ordering. Lipid raft-disrupting agents (methyl-β-cyclodextrin, sphingomyelinase) prevented the action of 24S-HC on both lipid raft marker labeling and NO synthesis. Together, these experiments indicate that 24S-HC is able to suppress the exocytotic release of neurotransmitter in response to intense activity via a NO/lipid raft-dependent pathway in the neuromuscular junctions of SODG93A mice.

NITRIC OXIDE MEDIATED NEURODEGENERATION IN PARKINSON’S DISEASE

ABSTRACTNitric oxide (NO) is an endogenous molecule which functions as a neurotransmitter, hormone, free radical, etc. NO has been found to regulate the releaseof neurotransmitters, synaptic transmission, cell death, etc. NO is involved in the pathogenesis of various neuropsychiatric and neurodegenerativedisorders. NO plays a key role in cellular apoptosis and neuronal degeneration. Parkinson’ disease (PD) is a neurodegenerative disorder characterizedby motor dysfunction that can be seen in the patients suffering from PD. The motor dysfunction is due to the progressive degeneration of dopaminergicneurons in mid brain. Dopamine (DA) is highly reactive molecule and is prone to the oxidation very much. The oxidation of DA is accompanied bythe production of the reactive oxygen species that activates microglia cells. Upon activation, microglia cells cause the upregulation of inducible NOsynthase, the enzyme involved in the production of NO. NO thus plays a key role in the neurodegeneration process implicated in PD. Thus, the aim ofthe present manuscript is to describe the possible role of NO in PD.Keywords: Dopamine, Neuromelanin, Nitric oxide, Parkinson.

Evaluation of protein pattern changes in roots and leaves of Zea maysplants in response to nitrate availability by two-dimensional gel electrophoresis analysis

BackgroundNitrogen nutrition is one of the major factors that limit growth and production of crop plants. It affects many processes, such as development, architecture, flowering, senescence and photosynthesis. Although the improvement in technologies for protein study and the widening of gene sequences have made possible the study of the plant proteomes, only limited information on proteome changes occurring in response to nitrogen amount are available up to now. In this work, two-dimensional gel electrophoresis (2-DE) has been used to investigate the protein changes induced by NO3- concentration in both roots and leaves of maize (Zea mays L.) plants. Moreover, in order to better evaluate the proteomic results, some biochemical and physiological parameters were measured.ResultsThrough 2-DE analysis, 20 and 18 spots that significantly changed their amount at least two folds in response to nitrate addition to the growth medium of starved maize plants were found in roots and leaves, respectively. Most of these spots were identified by Liquid Chromatography Electrospray Ionization Tandem Mass Spectrometry (LC-ESI-MS/MS). In roots, many of these changes were referred to enzymes involved in nitrate assimilation and in metabolic pathways implicated in the balance of the energy and redox status of the cell, among which the pentose phosphate pathway. In leaves, most of the characterized proteins were related to regulation of photosynthesis. Moreover, the up-accumulation of lipoxygenase 10 indicated that the leaf response to a high availability of nitrate may also involve a modification in lipid metabolism.Finally, this proteomic approach suggested that the nutritional status of the plant may affect two different post-translational modifications of phosphoenolpyruvate carboxylase (PEPCase) consisting in monoubiquitination and phosphorylation in roots and leaves, respectively.ConclusionThis work provides a first characterization of the proteome changes that occur in response to nitrate availability in leaves and roots of maize plants. According to previous studies, the work confirms the relationship between nitrogen and carbon metabolisms and it rises some intriguing questions, concerning the possible role of NO and lipoxygenase 10 in roots and leaves, respectively. Although further studies will be necessary, this proteomic analysis underlines the central role of post-translational events in modulating pivotal enzymes, such as PEPCase.

Changes in ATP content in cerebellar granule cells during hyperstimulation of glutamate receptors: Possible role of NO and nitrite ions

In primary 7-8-day culture of cerebellar granule cells, glutamate exposure (100 microM, 10-240 min) induced a 60-30% drop in ATP level; during the postglutamate period ATP level completely recovered after 24 h. Inhibition of NO-synthase with L-NAME during glutamate application resulted in less pronounced decrease in ATP level immediately after its application and had no effect on ATP recovery after 24 h. It was found that hyperstimulation of glutamate receptors elevates concentration of NO products (nitrites and nitrates), while NO2(-) ions can increase ATP content.

Nitric Oxide Modulates Tissue Plasminogen Activator Release in Normotensive Subjects and Hypertensive Patients

We evaluated the possible role of NO in modulating tissue plasminogen activator (t-PA) release in the forearm microcirculation of normotensive subjects and hypertensive patients. Essential hypertensive patients are characterized by endothelial dysfunction because of a reduced NO availability and also show an impaired t-PA release. In healthy volunteers and essential hypertensive patients, we studied local t-PA release and forearm blood flow changes (strain-gauge plethysmography) induced by intrabrachial administration of acetylcholine (0.45 and 1.5 microg/100 mL/min) and of sodium nitroprusside (0.5 and 1.0 microg/100 mL/min), an endothelium-dependent and -independent agonist, respectively. Acetylcholine was also repeated in the presence of intra-arterial infusion of the NO synthase inhibitor N(G)-monomethyl-l-arginine (100 microg/100 mL/min). In normotensive subjects, vasodilation to acetylcholine was blunted by N(G)-monomethyl-l-arginine. In these subjects, acetylcholine infusion induced a significant, dose-dependent increase in net forearm t-PA release. N(G)-monomethyl-l-arginine significantly reduced basal t-PA release, as well as acetylcholine-induced t-PA release. In essential hypertensive patients, vasodilation to acetylcholine was reduced as compared with controls and resistant to N(G)-monomethyl-l-arginine. In contrast to what was observed in healthy control subjects, in hypertensive patients, acetylcholine had no effect on t-PA release. Similarly, N(G)-monomethyl-l-arginine failed to modify either the tonic or the agonist-induced t-PA release. Both tonic and agonist-induced release of NO are directly involved in t-PA release by endothelial cells. Essential hypertension, characterized by a reduction in tonic and stimulated NO availability, is also associated with impaired capacity of t-PA release, suggesting a major role of impaired NO availability in worsening both vasodilation and t-PA release.

Nitric oxide and central antihypertensive drugs: one more difference between catecholamines and imidazolines.

NO is known to be involved in the peripheral and central regulation of the cardiovascular function. It plays a neuromodulatory role via a direct action on presynaptic nerve terminals, stimulating the release of gamma-aminobutyric acid, glutamate, and norepinephrine. Our aim was to study the possible role of NO in the cardiovascular effects of the central antihypertensive drugs clonidine, rilmenidine, and alpha-methyl-norepinephrine (alpha-MNA). Sites and mechanisms of the hypotensive action of these drugs were different; clonidine and rilmenidine acted on imidazoline receptors in the nucleus reticularis lateralis, whereas alpha-MNA acted upon alpha(2)-adrenoceptors in the nucleus tractus solitarius. The influence of N:(G)-nitro-L-arginine, an NO synthase inhibitor, on the central hypotensive effects of these drugs was investigated in pentobarbital-anesthetized rabbits. The intracisternal (IC) administration of alpha-MNA (30 microg/kg) induced hypotension (79+/-2 versus 103+/-4 mm Hg) and bradycardia (222+/-8 versus 278+/-4 bpm) (P:<0.05) (n=5). Clonidine (0.07 microg/kg IC) also induced hypotension (69+/-5 versus 99+/-4 mm Hg) and bradycardia (266+/-7 versus 306+/-10 bpm) (P:<0.05) (n=5). In addition to clonidine, rilmenidine (1 microg/kg IC) induced hypotension (64+/-4 versus 97+/-4 mm Hg) and bradycardia (264+/-11 versus 310+/-4 bpm) (P:<0.05) (n=5). Pretreatment with N:(G)-nitro-L-arginine (900 microg/kg IC) completely prevented the hypotensive effect of alpha-MNA but influenced the cardiovascular effects of neither clonidine nor rilmenidine. These results confirm that imidazoline drugs, such as clonidine, rilmenidine, and the catecholamine alpha(2)-adrenoceptor agonist alpha-MNA, have distinct mechanisms of action.

Evidence for the function of the free radical gas — nitric oxide (NO•) — as an endogenous maturation and senescence regulating factor in higher plants

The hypothesis that endogenously-produced nitric oxide (NO•) gas is a natural plant growth regulator was experimentally tested. Experimentation encompassed a wide spectrum of both climacteric and non-climacteric varieties of fruits, flowers, vegetables and legume sprout species. Specific NO• probe monitoring of both vegetative and generative plant organs revealed that temporal progress of maturation and senescence goes hand in hand with a significant decrease of NO• emission. Conversely, exogenous application of the gas either by direct fumigation in an O2-free atmosphere or by means of NO• releasing biochemicals such as N-tert-butyl-α-phenylnitrone and 3 morpholinosyl-nonimine, markedly delayed senescence and maturation. NO• decrease was moreover stoichiometrically related to ethylene upsurge, this phenomenon also being geared to ethylene increment under short-term heat stress. Furthermore, a classic foliage expansion bioassay indicated a concentration-dependent growth effect evidenced as a typical growth regulator-like response where low concentrations promote, and high concentrations inhibit growth. Regarded together, experimental data lends support to the possible role of NO• as a natural senescence-delaying plant growth regulating agent acting primarily, but not solely, by down regulating ethylene emission.

Evidence for the involvement of nitric oxide in the inhibitory effect of GSPYFVamide on Helix aspersa central neurones

Intracellular recordings were made from neurones E-8, E-16 and E-13a in the visceral ganglion of Helix aspersa. GSPYFVamide inhibits the activity of these neurones and the role of a second messenger system in this inhibition was investigated. 8-Bromo-cGMP, 100 μM was found to potentiate this inhibition while ODQ, 100 μM, an inhibitor of guanylyl cyclase, almost completely blocked GSPYFVamide-induced inhibition. Four NO donors sodium nitroprusside, 100 μM, sodium nitrite, 1 mM, SNOG, 50 μM, and SNAP, 10–50 μM, all potentiated the GSPYFVamide-induced inhibition. L-NAME, 100–1000 μM, a competitive inhibitor of NOS, blocked the GSPYFVamide-induced inhibition. In some cases recovery was only partial. The possible role of NO in modulating the inhibitory response to GSPYFVamide is discussed.

Gender differences of inducible nitric oxide production in SJL/J mice with experimental autoimmune encephalomyelitis

We identified gender related differences of inducible nitric oxide synthase (iNOS) expression and NO production in mice with experimental autoimmune encephalomyelitis (EAE). When myelin basic protein-specific T-lymphocytes derived from female mice were transferred, the female recipients developed more severe EAE and expressed higher levels of iNOS and NO than male recipients. When the T-lymphocytes derived from males were transferred, severe EAE was induced in neither female nor male recipients and neither iNOS nor NO were detectable. These data show an association between NO production and EAE severity, suggesting a possible role of NO in the pathogenesis of EAE.

In vivo inactivation of phosphotyrosine protein phosphatases by nitric oxide

The effect of NO on phosphotyrosine protein phosphatases (PTPases) has been investigated in vivo. NO production is induced in interferon-γ and lipopolyaccharide stimulated RAW-264.7 macrophages as indicated by the increase of NO 2 − in the medium. Our results demonstrate an inhibition of p-nitrophenylphosphatase activity as a consequence of macrophages activation. Under the described experimental conditions, most of the hydrolysis of p-nitrophenylphosphate can be ascribed to the action of cellular PTPases. The presence of N G - monomethyl- l-arginine , a specific inhibitor of NO synthase decreases the inactivation rate of both membrane-bound and soluble PTPases. This evidence further confirms the ability of NO to inactivate PTPases and suggests a possible role of NO in the regulation of cellular processes involving this class of phosphatases.

Regulation of inducible nitric oxide production by cytokines in human thyrocytes in culture.

We now report on the induction and modulation of NO production by cytokines in primary cultures of human thyrocytes and the effect of NO on iodine organification by human open thyroid follicles in the process of thyroid hormone biosynthesis. Although unstimulated thyrocytes produced little NO (measured as nitrite), interleukin-1 alpha or beta (IL-1 alpha/beta) substantially increased NO formation. Interferon-gamma (IFN-gamma) by itself failed to stimulate NO formation but markedly increased the IL-1-stimulated NO production. Tumor necrosis factor-alpha alone did not induce NO production but did so slightly in the presence of IFN-gamma. Induction of NO formation by thyrocytes upon stimulation with IL-1 alpha + IFN-gamma was accompanied by the synthesis of tetrahydrobiopterin (BH4), an obligatory cofactor of NOS. Coinduction of NO and BH4 synthesis in thyrocytes was preceded by coexpression of messenger RNAs for NOS and GTP cyclohydrolase I (GTPCH), the rate-limiting enzyme for de novo synthesis of BH4. NO synthesis was prevented by an inhibitor of GTPCH, 2,4-diamino-6-hydroxypyrimidine, and this inhibition was completely reversed by administration of sepiapterin, a substrate for BH4 synthesis via pterin salvage pathway. In contrast to IFN-gamma, some cytokines such as interferon-alpha, IL-4, and transforming growth factor-beta 1 inhibited the IL-1-induced NO production. Finally, a possible role of NO on thyroid hormone synthesis was investigated. Iodine organification by human open thyroid follicles was inhibited by two kinds of NO donor but not by cell permeable cyclicGMP analog. Thus, cytokines such as IL-1, IL-1/IFN-gamma, and tumor necrosis factor-alpha/IFN-gamma stimulate human thyrocytes to produce NO; this process can be modulated by other cytokines and coregulated with a cofactor BH4 biosynthesis, and resulting NO may affect cell function including thyroid hormone synthesis.

Effect of nitric oxide on renin secretion. II. Studies in the perfused juxtaglomerular apparatus

To examine the possible role of NO in macula densa control of renin secretion, we examined the effects of varying NO availability on renin release in the isolated perfused rabbit juxtaglomerular apparatus (JGA). Gradual increments of luminal Na/Cl concentration ratio (mM/mM) from 26/7 over 46/27, 66/47, to 86/67 caused a progressive decrease in renin secretion from (as log of nano-Goldblatt hog units vs. time, i.e., log nGU/min) 1.09 +/- 0.34 to 0.46 +/- 0.24 log nGU/min, with the greatest change occurring at the first concentration step. The presence of 0.7 mM N omega-nitro-L-arginine (NNA), an NO synthase inhibitor, in the luminal fluid significantly reduced renin secretion at the lowest Na/Cl concentration ratio to 0.65 +/- 0.32 log nGU/min (P < 0.01 compared with control). Renin secretion at the higher Na/Cl concentration ratios was not significantly affected by NNA compared with control. In contrast to these results, the addition of the NO donor nitroprusside (1 mM) to the bath caused a reduction in renin secretion from 1.0 +/- 0.39 to 0.47 +/- 0.46 log nGU/min (P < 0.05), an effect that was reversed by bath addition of 0.01 mM methylene blue. Similarly, addition of L-arginine (0.7 mM) to the bath reduced renin secretion from 0.99 +/- 0.37 to 0.81 +/- 0.38 log nGU/min (P < 0.01), whereas addition of L-arginine to the luminal fluid increased renin secretion from 0.85 +/- 0.43 to 1.94 +/- 0.46 log nGU/min (P < 0.05). The stimulatory effect of luminal L-arginine was reversed by the luminal addition of NNA.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of nitric oxide in control of prolactin release by the adenohypophysis.

Nitric oxide synthase-containing cells were visualized in the anterior pituitary gland by immunocytochemistry. Consequently, we began an evaluation of the possible role of NO in the control of anterior pituitary function. Prolactin is normally under inhibitory hypothalamic control, and in vitro the gland secretes large quantities of the hormone. When hemipituitaries were incubated for 30 min in the presence of sodium nitroprusside, a releaser of NO, prolactin release was inhibited. This suppression was completely blocked by the scavenger of NO, hemoglobin. Analogs of arginine, such as NG-monomethyl-L-arginine (NMMA, where NG is the terminal guanidino nitrogen) and nitroarginine methyl ester, inhibit NO synthase. Incubation of hemipituitaries with either of these compounds significantly increased prolactin release. Since in other tissues most of the actions of NO are mediated by activation of soluble guanylate cyclase with the formation of cyclic GMP, we evaluated the effects of cyclic GMP on prolactin release. Cyclic GMP (10 mM) produced an approximately 40% reduction in prolactin release. Prolactin release in vivo and in vitro can be stimulated by several peptides, which include vasoactive intestinal polypeptide and substance P. Consequently, we evaluated the possible role of NO in these stimulations by incubating the glands in the presence of either of these peptides alone or in combination with NMMA. In the case of vasoactive intestinal polypeptide, the significant stimulation of prolactin release was augmented by NMMA to give an additive effect. In the case of substance P, there was a smaller but significant release of prolactin that was not significantly augmented by NMMA. We conclude that NO has little effect on the stimulatory action of these two peptides on prolactin release. Dopamine (0.1 microM), an inhibitor of prolactin release, reduced prolactin release, and this inhibitory action was significantly blocked by either hemoglobin (20 micrograms/ml) or NMMA and was completely blocked by 1 mM nitroarginine methyl ester. Atrial natriuretic factor at 1 microM also reduced prolactin release, and its action was completely blocked by NMMA. In contrast to these results with prolactin, luteinizing hormone (LH) was measured in the same medium in which the effect of nitroprusside was tested on prolactin release, there was no effect of nitroprusside, hemoglobin, or the combination of nitroprusside and hemoglobin on luteinizing hormone release. Therefore, in contrast to its inhibitory action on prolactin release NO had no effect on luteinizing hormone release. Immunocytochemical studies by others have shown that NO synthase is present in the folliculostellate cells and also the gonadotrophs of the pituitary gland. We conclude that NO produced by either of these cell types may diffuse to the lactotropes, where it can inhibit prolactin release. NO appears to play little role in the prolactin-releasing action of vasoactive intestinal polypeptide and substance P, but mediates the prolactin-inhibiting activity of dopamine and atrial natriuretic factor.

Role of nitric oxide in neurally induced pancreatic exocrine secretion in pigs.

Formation of NO, enzymatically catalyzed by NO synthases in both endothelial cells and autonomic nerves, seems to explain some noncholinergic nonadrenergic tissue reactions. We studied the possible role of NO in vagally induced pancreatic exocrine secretion using isolated perfused porcine pancreas (n = 11) with intact vagus nerve (VN) supply. Electrical stimulation of the VN (8 Hz, 10 mA) and infusions of vasoactive intestinal polypeptide (VIP, 2 x 10(-9) M) were carried out before and after addition to the perfusate of the NO synthase inhibitors N omega-nitro-L-arginine methyl ester (L-NAME, 10(-4) M) or NG-nitro-L-arginine (L-NNA, 10(-5) M) with and without further addition of L-arginine (10(-3) M). We also studied the effects of L-arginine alone and of sodium nitroprusside (10(-4) M). In all experiments VN and VIP caused a profuse exocrine secretion (43 +/- 7 and 44 +/- 11 times basal secretion). The inhibitors increased vascular resistance approximately twofold but had no effect on the vascular relaxation caused by VIP and VN. The exocrine fluid response to VN was reduced to 19 +/- 5 and 4.7 +/- 1.8% (L-NAME and L-NNA), and response to VIP was reduced to 54 +/- 12 and 35 +/- 13%. Protein and bicarbonate outputs largely paralleled flow rate. Addition of L-arginine (no effects alone) to L-NAME restored the responses to VN (to 100 +/- 21% of controls) and increased VIP responses (to 65 +/- 11%).(ABSTRACT TRUNCATED AT 250 WORDS)

Expression of nitric oxide synthase in kidney macula densa cells.

The distribution of nitric oxide synthase (NOS), the enzyme by which NO is generated from L-arginine, was investigated in rat kidney. The indirect immunofluorescence technique using a polyclonal antibody against type I NOS was applied, followed by the histochemical NADPH diaphorase staining technique on the same sections in order to demonstrate the enzymatic activity of NOS. Macula densa cells were strongly stained by both techniques, demonstrating abundant NOS in the cytoplasm of these cells. In addition, these findings were confirmed by nonradioactive in situ hybridization, thus demonstrating the corresponding messenger RNA in macula densa cells as well. Our findings provide the morphological basis for a possible role of NO as a mediator substance in signal transfer from distal tubular fluid to glomerular arterioles.

Comment [on “Possible role of NO3 in the nighttime chemistry of a cloud” by William L. Chameides

Journal of Geophysical Research: AtmospheresVolume 91, Issue D13 p. 14569-14570 CommentariesFree Access Comment [on “Possible role of NO3 in the nighttime chemistry of a cloud” by William L. Chameides] Michael Mozurkewich, Michael MozurkewichSearch for more papers by this author Michael Mozurkewich, Michael MozurkewichSearch for more papers by this author First published: 20 December 1986 https://doi.org/10.1029/JD091iD13p14569Citations: 21AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL No abstract is available for this article. References Berdnikov, V. M., N. M. Bazhin, Oxidation-reduction potentials of certain inorganic radicals in aqueous solutions, Engl. Transl., Russ. J. Phys. Chem., 44, 395– 398, 1970. Chameides, W. L., The photochemistry of a remote marine stratiform cloud, J. Geophys. Res., 89, 4379– 4755, 1984. Chameides, W. L., Possible role of NO3 in the nighttime chemistry of a cloud, J. Geophys. Res., 91, 5331– 5337, 1986. Klaning, U. K., K. Sehested, J. Holcman, Standard Gibbs energy of formation of hydroxyl in aqueous solution: Rate constants for the reaction ClO2− + O3 = O3− + ClO2, J. Phys. Chem., 89, 760– 763, 1985. Lee, Y.-N., S. E. Schwartz, Reaction kinetics of nitrogen dioxide with liquid water at low partial pressure, J. Phys. Chem., 85, 840– 848, 1981. Schwartz, S. E., Gas- and aqueous-phase chemistry of HO2 in liquid water clouds, J. Geophys. Res., 89, 11589– 11598, 1984. Schwartz, S. E., J. E. Freiberg, Mass-transport limitation to the rate of reaction of gases in liquid droplets: Application to oxidation of SO2 in aqueous solutions, Atmos. Environ., 15, 1129– 1144, 1981. Schwarz, H. A., H. J. Bielski, Reactions of HO2 and O2 — with iodine and bromine and the I2 — and I atom reduction potentials, J. Phys. Chem., 90, 1445– 1448, 1986. Schwarz, H. A., R. W. Dodson, Equilibrium between hydroxyl radicals and thallium(II) and the oxidation potential of OH(aq), J. Phys. Chem., 88, 3643– 3647, 1984. Citing Literature Volume91, IssueD1320 December 1986Pages 14569-14570 ReferencesRelatedInformation

Reply [to “Comment on ‘Possible role of NO3 in the nighttime chemistry of a cloud’ by William L. Chameides”

Journal of Geophysical Research: AtmospheresVolume 91, Issue D13 p. 14571-14572 Commentaries Reply [to “Comment on ‘Possible role of NO3 in the nighttime chemistry of a cloud’ by William L. Chameides”] W. L. Chameides, W. L. ChameidesSearch for more papers by this author W. L. Chameides, W. L. ChameidesSearch for more papers by this author First published: 20 December 1986 https://doi.org/10.1029/JD091iD13p14571Citations: 14AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume91, IssueD1320 December 1986Pages 14571-14572 RelatedInformation

Possible role of NO3 in the nighttime chemistry of a cloud

The NO3 radical in the aqueous phase is a strong oxidizing agent which reacts rapidly with a wide variety of inorganic and organic species. Within nighttime clouds the production of gaseous NO3 from the reaction of NO2 with O3 followed by heterogeneous scavenging of NO3 by cloud droplets can represent a significant source of these reactive radicals to cloud water. Model calculations indicate that in addition to leading to the production of NO3− in cloud water, this aqueous‐phase source of NO3 can, under the appropriate conditions and depending upon the values for a number of uncertain rate constants, have a significant impact upon the rate of conversion of SO2 to H2SO4.