Nitrogen Oxide Species Research Articles

The Activation of Metabolites of Nitric Oxide Synthase by Metals Is Both Redox and Oxygen Dependent: A New Feature of Nitrogen Oxide Signaling

Nitrite (NO(2)-), N (G)-hydroxy-L-arginine (NOHA), and hydroxylamine (NH(2)OH) are products of nitric oxide synthase (NOS) activity and can also be formed by secondary reactions of nitric oxide (NO). These compounds are commonly considered to be rather stable and as such to be dosimeters of NO biosynthesis. However, each can be converted via metal-catalyzed reactions into either NO or other reactive nitrogen oxide species (RNOS), such as nitrogen dioxide (NO(2)) and nitroxyl (HNO), which have biologic activities distinct from those of the parent molecules. Consequently, certain aspects of tissue regulation controlled by RNOS may be dictated to a significant extent by metal-dependent reactions, thereby offering unique advantages for cellular and tissue regulation. For instance, because many metal-catalyzed reactions depend on the redox and oxygen status of the cellular environment, such reactions could serve as redox indicators. Formation of RNOS by metal-mediated pathways would confine the chemistry of these species to specific cellular sites. Additionally, such mechanisms would be independent both of NO and NOS, thus increasing the lifetime of RNOS that react with NO. Thus metal-mediated conversion of nitrite, NOHA, and NH(2)OH into biologically active agents may provide a unique signaling mechanism. In this review, we discuss the biochemistry of such reactions in the context of their pharmacologic and biologic implications.

A New Wrinkle on Topical Vitamin E and Photo-inflammation: Mechanistic Studies of a Hydrophilic γ-Tocopherol Derivative Compared with α-Tocopherol

The antioxidant function of vitamin E is thought to mediate its photo-protective effects. Cyclooxygenase-2 (COX-2) is an important mediator of early photo-inflammation. Thus, the ability of gamma-tocopherol to inhibit COX-2 activity independently of its antioxidant function raises important questions regarding potential roles that this form of vitamin E plays in photo-protection and skin cancer chemoprevention.

Sodium as the major mediator of NO-induced cell death in cultured hepatocytes

NO has been shown to induce cellular injury via inhibition of the mitochondrial respiratory chain and/or oxidative/nitrosative stress. Here, we studied which mechanism and downstream mediator is responsible for NO toxicity to hepatocytes. When cultured rat hepatocytes were incubated with spermineNONOate (0.01–2 mM) at 2, 5, 21 and 95% O 2 in Krebs-Henseleit buffer (37 °C), spermineNONOate caused concentration-dependent hepatocyte death (lactate dehydrogenase release, propidium iodide uptake) with morphological features of both apoptosis and necrosis. Increasing O 2 concentrations protected hepatocytes from NO-induced injury. Steady-state NO concentrations were lower at higher O 2 concentrations, suggesting formation of reactive nitrogen oxide species. Despite this, the scavenger ascorbic acid was hardly protective. In contrast, at equal NO concentrations loss of viability was higher at lower O 2 concentrations and inhibitors of hypoxic injury, fructose and glycine (10 mM), strongly decreased NO-induced injury. Upon addition of spermineNONOate, the cytosolic Na + concentration rapidly increased. The increase in sodium depended on the NO/O 2 ratio and was paralleled by hepatocyte death. Sodium-free Krebs-Henseleit buffer strongly protected from NO-induced injury. SpermineNONOate also increased cytosolic calcium levels but the Ca 2+ chelator quin-2-AM did not diminish cell injury. These results show that – in analogy to hypoxic injury – a sodium influx largely mediates the NO-induced death of cultured hepatocytes. Oxidative stress and disturbances in calcium homeostasis appear to be of minor importance for NO toxicity to hepatocytes.

Paradoxical coronary microcirculatory constriction during ischemia: a synergic function for nitric oxide and endothelin

A paradoxical microcirculatory constriction has been observed in hearts of patients with ischemia, secondary to coronary stenosis. Here, using the isolated mouse heart (Langendorff), we examined the mechanism of this response, assuming involvement of nitric oxide (NO) and endothelin-1 (ET-1) systems. Perfusion pressure was maintained at 65 mmHg for 70 min (protocol 1), or it was reduced to 30 mmHg over two intervals, between the 20- and 40-min marks (protocol 2) or from the 20-min mark onward (protocol 3). In protocol 1, coronary resistance (CR) remained steady in untreated heart, whereas it progressively increased during treatment with the NO synthesis inhibitor N(G)-nitro-l-arginine methyl ester (L-NAME) (2.7-fold) or the ET(A) antagonist BQ-610 (2.8 fold). The ET(B) antagonist BQ-788 had instead no effect by itself but curtailed vasoconstriction to BQ-610. In protocol 2, hypotension raised CR by 2.2-fold. This response was blunted by reactive oxygen species (ROS) scavengers (mannitol and superoxide dismutase plus catalase) and was converted into vasodilation by l-NAME, BQ-610, or BQ-788. Restoration of normal pressure was followed by vasodilation and vasoconstriction, respectively, in untreated and treated preparations. In protocol 3, CR progressively increased with hypotension in the absence but not presence of L-NAME or BQ-610. We conclude that the coronary vasculature is normally relaxed by two concerted processes, a direct action of NO and ET-1 curtailing an ET(B2)-mediated tonic vasoconstriction through ET(A) activation. The negative feedback mechanism on ET(B2) subsides during hypotension, and the ensuing vasoconstriction is ascribed to ET-1 activating ET(A) and ET(B2) and reactive nitrogen oxide species originating from ROS-NO interaction.

Cancer-preventive anti-oxidants that attenuate free radical generation by inflammatory cells

Active inflammatory leukocytes are a major endogenous source of reactive oxygen and nitrogen oxide species (RONS). We have recently established novel bioassay systems, in which either phorbol ester-stimulated, differentiated HL-60 human leukemia cells or lipopolysaccharide (LPS)-stimulated RAW264.7 murine macrophages were co-cultured with AS52 Chinese hamster ovary cells. Extensive screening of extracts from Asian vegetables and fruits led to the identification of 1'-acetoxychavicol acetate (ACA), auraptene, nobiletin, and zerumbone, all of which were found to be highly anti-mutagenic in the above co-culture systems. Pretreatment of RAW264.7 macrophages with LPS led to the activation of mitogen-activated protein kinases (MAPKs) and Akt, together with the degradation of IkappaB-alpha protein, and the resultant activation of the AP-1, NF-kappaB, and CREB transcription factors. ACA abrogated ERK1/2 and JNK1/2, but not p38 activation, as well as the activation and transcriptional activation of NF-kappaB and CREB, whereas nobiletin allowed phosphorylation of these MAPKs, while it suppressed AP-1, NF-kappaB, and CREB activation. Interestingly, zerumbone did not have any effects on the latter transcription factors, although it did attenuate iNOS mRNA expression. In addition, auraptene suppressed iNOS protein production, but not mRNA expression, implying that it targets the translation step. Our model systems may be useful for identifying potentially anti-carcinogenic inhibitors of RONS generation.

The Biological Chemistry of Nitric Oxide as It Pertains to the Extrapulmonary Effects of Inhaled Nitric Oxide

The chemical properties of nitric oxide (NO) have been studied for over 200 years. However, it is only within the last 20 years that the biological implications of this chemistry have been considered. The classical model of NO action within the vasculature centers on production in the endothelium, diffusion to the smooth muscle, and subsequent activation of guanylate cyclase via binding to its heme iron. In the context of this model, it is difficult to conceptualize extrapulmonary effects of inhaled NO. However, NO possesses complex redox chemistry and is capable of forming a range of nitrogen oxide species and is therefore capable of interacting with a variety of biomolecules. Of particular interest is its reaction with reduced cysteine to form an S-nitrosothiol (SNO). SNOs are formed throughout NO biology and are a post-translational modification that has been shown to regulate many proteins under physiologic conditions. Hemoglobin, which was considered to be solely a consumer of NO, can form SNO in a conformationally dependent manner, which allows for the transport of inhaled NO beyond the realm of the lung. Higher oxides of nitrogen are capable of modifying proteins via nitration of tyrosines, which has been shown to occur under pathologic conditions. By virtue of its redox reactivity, one can appreciate that inhaled NO has a variety of routes by which it can act and that these routes may lead to extrapulmonary effects.

Ab Initio Molecular Dynamics Simulation of NO Reactivity on the CaO(001) Surface

Ab initio molecular dynamics (MD) is used to investigate NO reaction processes on the (001) surface of CaO. A novel path is proposed for the first steps of nitrogen oxides reactivity catalyzed by the CaO surface. The mechanism consists of the formation of anionic dimers, adsorbing on the surface cations, at the expense of oxidized NO species adsorbed on surface anions. The complete charge-transfer process takes place in two steps, producing first monovalent anionic dimers (NO)2- and, later on, divalent anionic dimers (NO)2(2-). These redox processes cause spin quenching and are observed in the short time scale of the ab initio MD simulation at 300 K. The results presented provide a rationalization of a recent electron spin resonance (ESR) investigation indicating that the spectroscopy is silent to most of the nitrogen oxide species adsorbed on CaO powders, despite deposition of paramagnetic NO molecules at room temperature.

Nitroxidation, nitration, and oxidation of a BODIPY fluorophore by RNOS and ROS

BODIPY C11 581/591 (BODIPY11) represents a sensitive probe for quantification of relative antioxidant capacity. However, the mechanism of BODIPY11 fluorescence decay in the presence of reactive oxygen species (ROS) and reactive nitrogen oxide species (RNOS) requires clarification. Azo-initiators provide a continuous source of peroxyl radicals that in simple, aerobic, homogeneous, buffered solution simulate lipid peroxyl radical formation. Inhibition of BODIPY11 fluorescence decay was assayed and quantified for several families of antioxidants, including phenols, NO donors, and thiols. Fluorescence decay of BODIPY11 in these systems demonstrated similar patterns of antioxidant activity to those observed in classical oxygen pressure measurements, and provided a readily applied quantification of antioxidant capacity and mechanistic information, which was analyzed by measurement of induction periods, initial rates, and net oxidation. LC/MS analysis confirmed that peroxyl radical-induced irreversible fluorescence decay of the BODIPY11 fluorophore is due to oxidative cleavage of the activated phenyldiene side chain. The behavior of BODIPY11 towards RNOS was more complex, even in these simple systems. Incubation of BODIPY11 with bolus peroxynitrite or a sydnonimine peroxynitrite source produced a variety of novel products, characterized by LC/MS, derived from oxidative cleavage, nitroxidation, and nitration reactions. The "NO scavenger" PTIO reinforced the antioxidant activity of NO, and inhibited BODIPY11 oxidation induced by the sydnonimine. These observations suggest that BODIPY11 is a well-behaved fluorescence probe for peroxidation and antioxidant studies, but that for study of RNOS even co-application of fluorescence decay with LC/MS measurements requires careful analysis and interpretation.

Synthesis and evaluation of NO-release from symmetrically substituted furoxans

A series of symmetrically substituted dibenzoyl furoxans were synthesized and investigated for their potential to release nitric oxide, which plays a key role in the nervous and cardiovascular systems. Cysteine was employed to promote nitric oxide release from furoxan via the formation of an S-nitrosothiol intermediate. Transition metal ion-mediated S-nitrosocysteine decomposition liberates nitric oxide that, in aqueous aerobic solutions, is converted to reactive nitrogen oxide species. The percent nitric oxide released was quantified colorimetrically by the Griess reagent system.

Single‐particle characterization of four aerosol samples collected in ChunCheon, Korea, during Asian dust storm events in 2002

A single‐particle analytical technique, named low‐Z particle electron probe X‐ray microanalysis (low‐Z particle EPMA), employing an ultrathin window X‐ray detector and enabling the quantitative determination of even low‐Z elements such as C, N, and O, was applied to characterize “Asian dust” samples, collected in ChunCheon, Korea, during four Asian dust storm events on 21 March, 9 April, 17 April, and 11 November in 2002. In this study, it is demonstrated that single‐particle analysis using the low‐Z particle EPMA provides detailed information on various types of chemical species in the samples. The most abundantly encountered particles, both in coarse and fine fractions, are soil‐derived particles such as aluminosilicates and silicon dioxide, except for the sample collected on 11 November 2002, where reacted CaCO3 particles are the most abundantly encountered. All four samples are found to have experienced chemical modifications during long‐range transport because the samples contain a significant number of particles composed of chemical species, such as nitrate and sulfate, which resulted from atmospheric reactions of CaCO3 and sea‐salt particles. This finding implies that CaCO3 and sea‐salt particles reacted with sulfur and nitrogen oxide species during long‐range transport. The sample collected on 11 November 2002 experienced the most extensive chemical modification during its transport. For this sample, the overall relative abundances of reacted CaCO3 and reacted sea‐salt particles are 29.9% and 23.2%, respectively. In addition to the observation of the reacted CaCO3 and sea‐salt particles, reacted K‐containing particles are also encountered in this sample. In this work, it is observed that chemical modification of sea‐salt particles was more extensive than that of CaCO3 particles. By considering the relative abundances of nitrate‐ and sulfate‐containing particles, nitrate formation from CaCO3 and sea‐salt particles in the air is found to be more favorable than sulfate formation.

Present and future acid deposition to ecosystems: The effect of climate change

A global chemistry-transport model has been used to study the deposition of acidic nitrogen and sulphur species in the present day (1990s) and future (2090s). For the oxidised nitrogen species, climate change increases the amount of nitric acid produced and deposited to soils. However, for reduced nitrogen species, both climate change and pollutant emission increases act to convert more ammonia to ammonium sulphate which in turn may result in further acidification of soils. This change occurs via increased aqueous phase oxidation of sulphur dioxide, indicating that the sulphur and reduced nitrogen cycles are closely linked. The modelled acid deposition fluxes have been used with estimates of base cation deposition fluxes to identify areas with excess deposition above the critical loads. These data show an increasing risk of acidification in parts of the USA and South-East Asia. Certain areas, especially in Asia, remain at risk even when higher values of critical loads and base cation deposition fluxes are used.

A mosquito 2-Cys peroxiredoxin protects against nitrosative and oxidative stresses associated with malaria parasite infection

Malaria parasite infection in anopheline mosquitoes induces nitrosative and oxidative stresses that limit parasite development, but also damage mosquito tissues in proximity to the response. Based on these observations, we proposed that cellular defenses in the mosquito may be induced to minimize self-damage. Specifically, we hypothesized that peroxiredoxins (Prxs), enzymes known to detoxify reactive oxygen species (ROS) and reactive nitrogen oxide species (RNOS), protect mosquito cells. We identified an Anopheles stephensi 2-Cys Prx ortholog of Drosophila melanogaster Prx-4783, which protects fly cells against oxidative stresses. To assess function, AsPrx-4783 was overexpressed in D. melanogaster (S2) and in A. stephensi (MSQ43) cells and silenced in MSQ43 cells with RNA interference before treatment with various ROS and RNOS. Our data revealed that AsPrx-4783 and DmPrx-4783 differ in host cell protection and that AsPrx-4783 protects A. stephensi cells against stresses that are relevant to malaria parasite infection in vivo, namely nitric oxide (NO), hydrogen peroxide, nitroxyl, and peroxynitrite. Further, AsPrx-4783 expression is induced in the mosquito midgut by parasite infection at times associated with peak nitrosative and oxidative stresses. Hence, whereas the NO-mediated defense response is toxic to both host and parasite, AsPrx-4783 may shift the balance in favor of the mosquito.

Discriminating formation of HNO from other reactive nitrogen oxide species

Nitroxyl (HNO) exhibits unique pharmacological properties that often oppose those of nitric oxide (NO), in part due to differences in reactivity toward thiols. Prior investigations suggested that the end products arising from the association of HNO with thiols were condition-dependent, but were inconclusive as to product identity. We therefore used HPLC techniques to examine the chemistry of HNO with glutathione (GSH) in detail. Under biological conditions, exposure to HNO donors converted GSH to both the sulfinamide [GS(O)NH 2] and the oxidized thiol (GSSG). Higher thiol concentrations generally favored a higher GSSG ratio, suggesting that the products resulted from competitive consumption of a single intermediate (GSNHOH). Formation of GS(O)NH 2 was not observed with other nitrogen oxides (NO, N 2O 3, NO 2, or ONOO −), indicating that it is a unique product of the reaction of HNO with thiols. The HPLC assay was able to detect submicromolar concentrations of GS(O)NH 2. Detection of GS(O)NH 2 was then used as a marker for HNO production from several proposed biological pathways, including thiol-mediated decomposition of S-nitrosothiols and peroxidase-driven oxidation of hydroxylamine (an end product of the reaction between GSH and HNO) and N G-hydroxy- l-arginine (an NO synthase intermediate). These data indicate that free HNO can be biosynthesized and thus may function as an endogenous signaling agent that is regulated by GSH content.

Catalytic activity of dispersed CuO phases towards nitrogen oxides (N2O, NO, and NO2)

A systematic reactivity study of N2O, NO, and NO2 on highly dispersed CuO phases over modified silica supports (SiO2–Al2O3, SiO2–TiO2, and SiO2–ZrO2) has been performed. Different reaction paths for the nitrogen oxide species abatement were studied: from direct decomposition (N2O) to selective reductions by hydrocarbons (N2O, NO, and NO2) and oxidation (NO to NO2). The oxygen concentration, temperature, and contact time, were varied within suitable ranges in order to investigate the activity and in particular the selectivity in the different reactions studied. The support deeply influenced the catalytic properties of the active copper phase. The most acidic supports, SiO2–Al2O3 and SiO2–ZrO2, led to a better activity and selectivity of CuO for the reactions of N2O, NO, and NO2 reductions and N2O decomposition than SiO2–TiO2. The catalytic results are discussed in terms of actual turnover frequencies starting from the knowledge of the copper dispersion values.

Involvement of reactive nitrogen oxides for acquisition of metastatic properties of benign tumors in a model of inflammation-based tumor progression

The cells of a weakly tumorigenic and non-metastatic murine fibrosarcoma (QR-32) are converted into highly malignant tumors (acquiring metastatic potential) once they have grown in vivo after being co-implanted with gelatin sponge which induces inflammation. In the present study, we examined whether nitric oxide (NO) is involved in the inflammation-based tumor progression by administrating a specific inhibitor to inducible nitric oxide synthase, aminoguanidine (AG). First, we co-implanted 1 x 10(5) QR-32 cells with gelatin sponge (10 x 5 x 3 mm piece) into a subcutaneous space in C57BL6 mice. Administration of AG in drinking water (1%) had started 2 days before the tumor implantation and continued until the termination of the experiment. The incidence of tumor formation and the tumor growth did not differ between AG-treated group and -untreated group. On day 28, we excised the arising tumors to establish culture cell lines for evaluation of their acquisition of metastatic phenotype in other normal mice. Metastasis incidence and the number of metastatic colonies were significantly reduced in the tumor cell lines obtained from AG-treated mice compared to those from non-treated mice (p < 0.05). Immunohistochemical analysis demonstrated that inducible nitric oxide synthase and nitrotyrosine in the inflamed lesion were reduced in the AG-administered mice. However, intensity of 8-hydroxy-2-deoxyguanosine was not different between the groups. These results showed that nitric oxide and its reactive nitrogen oxide species cooperatively play a pivotal role in the progression of benign tumor cells in inflamed lesions.

Detection of N‐nitrosomelatonin and other N‐nitrosotryptophan derivatives by transnitrosation of APF and DAF‐2

S-nitrosothiols can be analyzed with some simple detection procedures and this fact strongly accelerated the understanding of the biological impact of S-nitrosothiols. Unfortunately, such simple analytic methods are presently missing for low molecular weight N-nitrosotryptophan derivatives like N-nitrosomelatonin (NOMela). Here we demonstrate that commercially available primary aromatic amines, i.e. aminophenylfluorescein (APF) and 4,5-diaminofluorescin (DAF-2), can be used for a quantitative determination of NOMela. Under optimized conditions (e.g. pH 11) of the assays, the lifetime of N-nitrosotryptophan derivatives is largely prolonged and the reactivity of S-nitrosothiols with aromatic amines can be safely ignored. The influence of reactive nitrogen oxide species like N2O3 is additionally limited at the alkaline pH and may be further decreased by working under hypoxic conditions. As a result of these optimal conditions, the APF assay has a detection limit for NOMela of about 25 nm but this assay fails to detect protein-bound N-nitrosotryptophan residues. The DAF-2 assay, however, might be used for a qualitative analysis of such residues. Due to the high efficacy of the APF assay it is safely demonstrated that in regard to peroxynitrite, N2O3 is about 50-fold more effective in nitrosating melatonin at physiological pH.

Neurotoxicity of nitroxyl: Insights into HNO and NO biochemical imbalance

Nitroxyl anion (NO −), and/or its conjugate acid, HNO, may be formed in the cellular milieu by several routes under both physiological and pathophysiological conditions. Since experimental evidence suggests that certain reactive nitrogen oxide species can contribute significantly to cerebral ischemic injury, we investigated the neurotoxic potential of HNO/NO − using Angeli's salt (AS), a spontaneous HNO/NO −-generating compound. Exposure to AS resulted in a time- and concentration-dependent increase in neural cell death that progressed markedly following the initial exposure. Coadministration of the donor with Tempol (1 mM), a one-electron oxidant that converts NO − to NO, prevented its toxic effect, as did the concomitant addition of Fe(III)TPPS. Media containing various chelators, catalase, Cu/Zn superoxide dismutase, or carboxy-PTIO did not ameliorate AS-mediated neurotoxicity, ruling out the involvement of transition metal complexes, H 2O 2, O 2 −, and NO, respectively. A concentration-dependent increase in supernatant protein 3-nitrotyrosine immunoreactivity was observed when cultures were exposed to AS under aerobic conditions, an effect lost in the absence of oxygen. A bell-shaped curve for augmented AS-mediated nitration was observed with increasing Fe(III)TPPS concentration, which contrasted with its linear effect on abating cytotoxicity. Finally, addition of glutamate receptor antagonists, MK-801 (10 μM) and CNQX (30 μM) to the cultures abrogated toxicity when given during, but not following, AS exposure; as did pretreatment with the exocytosis inhibitor, tetanus toxin (300 ng/ml). Taken together, our data suggest that under aerobic conditions, AS toxicity is initiated via HNO/NO − but progresses via secondary excitotoxicity.

An Electrochemically Driven and Electrochemically Regenerated NOx Trap

Absorption traps are used in a wide variety of different applications to prevent potentially harmful chemicals from entering the environment and/or from coming into contact with sensitive downstream equipment. Many of the materials in use cannot be regenerated so that concerns relating to sustainable usage and environmentally acceptable disposal are important; in other cases, regeneration can only be accomplished with relative difficulty. Herein we describe a new principle that can be used to address both these issues. A key application where chemical traps have found widespread use is in the control of NOx emissions generated by fuel-efficient automotive engines which, by reducing the atmospheric CO2 burden, can significantly mitigate the impact of road transport on global warming. Unfortunately, such engines produce much higher concentrations of nitrogen oxides (NOx) than conventional gasoline engines [1] with attendant adverse impact on human health and the environment. As a consequence, conventional “three-way” catalytic converters are inadequate and a post-converter NOx trap is required. These traps consist of an alkaline-earth component (usually barium) that is able to store NOx species as various nitrates and nitrites under the oxygen-rich conditions typical of “lean” engine operation. Precious metals, usually platinum, are also used as they aid in the uptake of NOx by providing sites for the adsorption and catalytic oxidation of NO to NO2. To restore the trap the engine is momentarily switched to “rich operation”, generating a large concentration of reducing species that cause reduction of the adsorbed nitrate/nitrite species to nitrogen thus regenerating the active BaO/BaCO3 component. A disadvantage of this procedure is that relatively high temperatures ( 900 K) are required for complete regeneration. Although the current generation of NOx traps is very effective when run under these conditions, a number of significant problems remain, especially the need for regular high-temperature excursions, the requirement of periodic rich engine operation (which partially defeats the object of lean operation), and susceptibility to poisoning by sulfur compounds present in the fuel. Herein we report a novel electrochemically driven NOx trap that can operate effectively over a range of temperatures and can be regenerated as required in a controlled manner, without the requirement for temperature excursions or changes in gas-phase composition. Although NOx trapping is used herein to illustrate the technique, the general method employed could be applicable in a wide variety of different applications, including, for example, removal oxides of carbon and sulfur. The trap consists of a thin porous layer of a precious metal (Pt, Pd, or Rh) deposited onto the surface of a solid electrolyte wafer that is biased to deliver the active species to the metal surface where it encounters the adsorbed NOx. We used sodium and potassium ionic conductors although a variety of other solid electrolytes could be used, depending on the application. NOx-trapping and trap-regeneration measurements were performed in a well-mixed microreactor operated at atmospheric pressure and described in detail elsewhere. X-ray photoelectron spectroscopy (XPS) measurements were carried out with a VG ADES 400 spectrometer system and in situ infrared spectroscopy measurements were performed with a Perkin Elmer GX2000 spectrometer utilizing a Harrick Refractor Reactor specular reflection accessory. The performance of the trap is illustrated in Figure 1 which shows the effects of 1) electrochemically trapping NOx

Single-Particle Characterization of Four “Asian Dust” Samples Collected in Korea, Using Low-Z Particle Electron Probe X-ray Microanalysis

A single-particle analytical technique, named low-Z particle electron probe X-ray microanalysis (low-Z particle EPMA), employing an ultrathin window X-ray detector and enabling the quantitative determination of even low-Z elements such as C, N, and O, is applied to characterize "Asian Dust" samples, collected in ChunCheon, Korea, during four Asian Dust storm events on March 7, 2000, April 7, 2000, March 22, 2001, and May 17, 2001. In this study, it is demonstrated that single-particle analysis using the low-Z particle EPMA provides detailed information on various types of chemical species in the samples. The most abundantly encountered particles, both in coarse and fine fractions, are aluminosilicates. The relative abundances of those particles on the basis of their size are different between the four Asian Dust samples. The sample collected on March 7, 2000 did not experience any chemical modification during its transport because the sample does not contain particles of chemical species that result from atmospheric reactions. The sample collected on April 7, 2000 contains both genuine and reacted sea-salt particles. The genuine sea-salts are in the form of a mixture of NaCl and MgCl2 entrained during their passage over the Yellow Sea. The reacted sea-salts particles are encountered very much in fine fraction. The sample collected on March 22, 2001 shows somewhat significant chemical modification both for CaCO3 and sea-salts particles. For this sample, a significant number of reacted CaCO3 and sea-salt particles, such as those containing nitrate and/or sulfate, are encountered, implying that CaCO3 and sea-salts particles have reacted with sulfur or nitrogen oxide species during their long-range transport. The sample collected on May 17, 2001 experienced the most extensive chemical modification during its transport. In addition to the observation of the extensively reacted CaCO3 and sea-salt particles, reacted K2CO3 particles are also extensively encountered in this sample, which implies that K2CO3 species should be regarded as an additional important chemical species in the study of the chemical modification of Asian Dust particles during long-range transport.

Thermochemistry of reactive nitrogen oxide species and reaction enthalpies for decomposition of ONOO − and ONOOH

The standard enthalpies of formation ( Δ H f 298 ∘ ) of a set of 16 biologically relevant reactive nitrogen oxide species were calculated using CBS-Q, CBS-QB3, CBS-APNO, G3 and G3X levels of theory. The G3 method gives the smallest mean absolute deviation of 5.1 kJ mol −1, compared with available experimental ( Δ H f 298 ∘ ) values. Enthalpies of three reactions related to decomposition of ONOO − and ONOOH were also examined with various levels of theory. Large discrepancies are found for thermochemical results involving ONOO − using the CBS-APNO and CBS-RAD methods. This is due to the use of inadequate geometry predicted by the QCISD theory.