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PubMed2001

Microperoxidase 8 catalyzed nitration of phenol by nitrogen dioxide radicals.

Microperoxidase 8 (MP8) is a heme octapeptide obtained by hydrolytic digestion of horse heart cytochrome c. At pH below 9, the heme iron is axially coordinated to the imidazole side chain of His18 and to a water molecule. Replacement of this weak ligand by H2O2 allows the formation of high-valent iron-oxo species which are responsible for both peroxidase-like and cytochrome P450-like activities of MP8. This paper shows that MP8 is able to catalyze the nitration of phenol by nitrite. The reaction requires H2O2 and is inhibited by ligands having a high affinity for the iron, catalase and radical scavengers. This suggests that the nitrating species could be NO2* radicals formed by the oxidation of nitrite by high-valent iron-oxo species. This new activity of MP8 opens a new access to nitro-aromatic compounds under mild conditions and validates the use of this minienzyme to mimick heme peroxidases, especially in the reactions of NO-derived species with biomolecules under oxidative stress conditions.

Animals↗

PubMed2005

Pivotal participation of nitrogen dioxide in L-arginine induced acute necrotizing pancreatitis: protective role of superoxide scavenger 4-OH-TEMPO.

For the first time, a direct sensitive method of *NO(2) detection and measurement in biological material has been established. It is based on the interaction of this radical with the coordination compound of Cr(III) with aminodeoxysugar as biosensor. Our new method makes it possible to precisely assess *NO(2) level in experimental acute necrotizing pancreatitis induced by L-arginine, where oxidative and nitrosative stresses are supposed to play a key role in the pathomechanism of the disease. As much as 20 nmol of *NO(2)/mg protein was detected which correlated with severe deterioration of pancreatic acinar cell ultrastructure. Protective effect of superoxide radical scavenger 4-OH-TEMPO expressed as *NO(2) level decrease confirmed by preserved acinar cell ultrastructure and decreased pancreatic amylase release to blood serum is demonstrated. This study reveals a possible pathomechanism of L-arginine induced acute pancreatitis.

Amylases↗

PubMed1981

Fate of inhaled nitrogen dioxide in isolated perfused rat lung.

The fate of inhaled NO2 was studied with isolated perfused rat lungs. The isolated lungs were exposed to 5 ppm NO2 for 90 min at a ventilation rate of 34 ml/min. The NO2 exposure had no adverse effects on the lungs as judged from their weights, glucose uptake, or lactate production compared to control lungs. Isolated lungs absorbed 36% of ventilated NO2, which was detected in perfusate and lung tissue as NO2- but not NO3-. The NO2- concentration in perfusate increased linearly with time, and after 90 min of ventilation with NO2 and perfusion with erythrocyte-free medium the NO2- accumulation was 6.36 +/- 0.39 micrograms. If perfusate contained 10% erythrocytes, the ventilated NO2 product was mostly NO3- in perfusate but NO2- in lung tissue. Protein solutions absorbed NO2 more effectively than simple salt solutions, but they all yielded mainly NO2- unless erythrocytes were present, when the product was mostly NO3-. The results indicate that absorbed NO2 in the lung is converted predominantly to NO2-, but after its diffusion into the vascular space it is oxidized to NO3- by interactions with erythrocytes.

Absorption↗

PubMed2005

Nitrogen dioxide multiphase chemistry: uptake kinetics on aqueous solutions containing phenolic compounds.

The uptake coefficients of NO2 on aqueous solutions containing guaiacol, syringol and catechol were determined over the pH range from 1 to 13 using the wetted wall flowtube technique. The measured uptake coefficients were used to determine the rate coefficients for the reaction of the physically dissolved NO2 with the neutral and deprotonated forms of phenolic compounds listed above. These organic compounds are ubiquitous not only in biomass burning plumes but also in soils, where they form part of the building blocks of humic acids. The NO2 uptake kinetics on solutions containing guaiacol, syringol or catechol were observed to be strongly pH dependent with uptake coefficients increasing from below 10(-7), under acidic conditions, to more than 10(-5) at pH values above 10. This behaviour illustrates the difference of reactivity between the neutral phenolic species and the phenoxide ions. The corresponding second order rate coefficients were typically observed to increase from 10(5) M(-1) s(-1) for the neutral compounds to a minimum of 10(8) M(-1) s(-1) for the phenoxide ions.

Biomass↗

PubMed1988

Changes in T-lymphocyte subpopulations and natural killer cells following exposure to ambient levels of nitrogen dioxide.

The effects of ambient levels of NO2 on murine splenic T-lymphocyte subpopulations and natural killer cells were investigated. AKR/cum and C57BL/6J mice were exposed, in inhalation chambers, to 0.25 ppm NO2 for 7 wk and 0.35 ppm NO2 for 12 wk, respectively. Monoclonal antibody technology was used in conjunction with fluorescence-activated cell sorter (FACS) analysis to detect quantitative changes in total T-lymphocytes (Thy-1.2-positive), mature T-lymphocytes (Lyt-1-positive), T-helper/inducer lymphocytes (L3T4-positive), T-cytotoxic/suppressor lymphocytes (Lyt-2-positive), and natural killer cells (asialo GM1-positive). Percentages of all T-lymphocyte subpopulations tested and natural killer cells were lower in spleens of mice exposed to NO2 compared to filtered-air controls. This is the first report providing evidence linking alterations in T-lymphocyte subpopulations and natural killer cells to NO2 exposure at ambient levels. Changes in T-lymphocyte subpopulations detected by FACS and correlated to impaired immune function may provide an extremely sensitive means of demonstrating NO2-induced changes in the immune system.

Animals↗

PubMed1998

Personal exposure to nitrogen dioxide in Switzerland. SAPALDIA team. Swiss Study on Air Pollution and Lung Diseases in Adults.

Home indoor and outdoor levels, and personal exposures to NO2 were determined for more than 500 subjects in a subpopulation of SAPALDIA by using passive samplers. The overall personal NO2 average was found to be 27 micrograms m-3, the overall indoor average 21 micrograms m-3 and the overall outdoor average 31 micrograms m-3. Personal NO2 levels ranged between the outdoor and indoor levels, with the exception of study areas with low NO2 concentrations. In the winter, the indoor/outdoor ratios were lower than in the summer. Outdoor NO2 levels were higher in winter. In some study areas, indoor NO2 levels were lower in the winter than in the summer due to reduced ventilation but this was not consistent. Personal NO2 concentrations were very similar during all seasons. Gas-cooking and smoking were important factors for elevated indoor and personal NO2 levels (contribution: 5 micrograms m-3, 2 micrograms m-3, respectively). Personal exposure to NO2 correlated best with the indoor NO2 concentrations.

Adult↗

PubMed1987

Neutrophil recruitment and degranulation during induction of emphysema in the rat by nitrogen dioxide.

Rats exposed to 30 ppm NO2 continuously for 3 to 6 wk developed mild centriacinar air-space enlargement and mild interstitial fibrosis. The emphysematous changes did not become more severe after 6 wk with continued NO2 exposure for as long as 14 additional weeks. Elastase inhibitory capacity (EIC) and the total protein concentration increased acutely in lung lavage fluid, consistent with the histologic evidence of pulmonary edema, then subsided but remained above control levels for the entire exposure period. The ratio of EIC to total protein remained unchanged relative to that in control animals. Neutrophils accumulated in the lung and were recoverable by lavage with the same relative concentration profile as observed for total protein. The average elastase activity per neutrophil in cells recovered from the air space by lung lavage was 60% less than in cells recovered from peripheral blood. This was true for control or NO2-exposed rats. Thus, emphysematous changes in the NO2-exposed rat were accompanied by a marked neutrophil recruitment concomitant with an increased neutrophil elastase burden in the lung, which may have directly contributed to lesion development.

Animals↗

PubMed1985

Effects of short-term exposure to ambient nitrogen dioxide concentrations on human bronchial reactivity and lung function.

Eight normal and 8 asthmatic subjects were exposed to NO2 in a modified body box for plethysmography during 20 min at 0,230,460 and 910 micrograms/m3 on 4 separate days. Bronchial reactivity (histamine inhalation test) was measured after exposure to air alone and to 910 micrograms/m3NO2. Airway resistance (Raw), thoracic gas volume (TGV) and specific airway resistance (SRaw) were measured before, during and after exposure. The bronchial reactivity of the asthmatic subjects increased significantly (p = 0.04) by 20 min exposure to 910 micrograms/m3 NO2. In the non-asthmatic group the airway resistance increased significantly (p = 0.03) after 20 min exposure to 460 micrograms/m3 NO2 and decreased significantly (p = 0.01) after 20 min exposure to 910 micrograms/m3 NO2. In the asthmatic group the trend in airway resistance was the same but not statistically significant. In the latter group TGV was significantly decreased (p = 0.02) during exposure to 910 micrograms/m3 NO2. Short term NO2-exposure in concentrations even below 1000 micrograms/m3 seems to have effects on human bronchial reactivity and lung function.

Adolescent↗

PubMed1976

Time--dose response for nitrogen dioxide exposure in an infectivity model system.

The concentration of NO2 in polluted atmosphere is subject to wide variation, according to peak traffic load, industrial productivity, intensity of sunlight and meteorological conditions. Normally NO2 has a low basal concentration with superimposed spikes when the above conditions are optimal for its production. Thus, it is important to determine the relative importance of a short-term, relatively high concentration of NO2 versus exposure for longer periods of minimal dose levels. This problem was approached experimentally by measuring the effect of NO2 on an animal's resistance to the induction of bacterial pneumonia. The data collected indicate that: (1) in short-term dose-response studies using the same Ct (concentration x time) product of 7, the actual concentration exerts a greater influence on NO2 effect than does the duration of exposure; (2) when concentration is held constant and the time increased, the average difference in mortality from controls can be seen after only 1 hr exposure to 3.5 ppm and after 3 weeks of exposure to 0.5 ppm; and (3) the relative mean survival time at 3.5 ppm for 1 hr was 18--36 hr less than that of the control animals.

Animals↗

PubMed1988

Effects of chlorphentermine and nitrogen dioxide on murine alveolar macrophages.

Male Swiss-Webster mice were treated daily for 14 days with either 120 mg/kg chlorphentermine (CP) to produce pulmonary lipidosis or an equal volume of water. Animals in each treatment group were then exposed by whole-body inhalation to either air or NO2 for 48 h. Immediately following exposure, alveolar macrophages (MPs) were collected from each animal by bronchoalveolar lavage. Assays performed on adherent viable MPs showed some changes in metabolic reduction, phagocytosis, and killing activity. 5'-Nucleotidase activity and yeast phagocytosis and killing assays suggested that CP elicited an increase in phagocytosis over control levels. Although the percentage metabolic reduction and microbicidal killing activities following CP were not increased when compared to controls, absolute reduction and killing (percentage values times total MPs) were significantly increased. These increased functions seemed to be highly dependent on the large increase in the total number of MPs induced by CP. It is possible that the large accumulation of MPs in the airways of the lipidotic lung may help protect the alveolar epithelium from NO2 by quenching free radicals produced during NO2-induced lipid peroxidation.

5'-Nucleotidase↗

PubMed2004

Characterization of indoor air quality using multiple measurements of nitrogen dioxide.

Indoor air quality can be affected by indoor sources, ventilation, decay and outdoor levels. Although technologies exist to measure these factors, direct measurements are often difficult. The purpose of this study was to develop an alternative method to characterize indoor environmental factors by multiple indoor and outdoor measurements. Daily indoor and outdoor NO2 concentrations were measured for 30 consecutive days in 28 houses in Brisbane, Australia, and for 21 consecutive days in 37 houses in Seoul, Korea. Using a mass balance model and regression analysis, penetration factor (ventilation rate divided by the sum of ventilation rate and deposition constant) and source strength factor (source strength divided by the sum of ventilation rate and deposition constant) were calculated using multiple indoor and outdoor measurements. Subsequently, the ventilation rate and NO2 source strength were estimated. Geometric means of ventilation rate were 1.44 air change per hour (ACH) in Brisbane, assuming a residential NO2 deposition constant of 1.05/h, and 1.36 ACH in Seoul, with the measured residential NO2 deposition constant of 0.94/h. Source strengths of NO2 were 15.8 +/- 18.2 and 44.7 +/- 38.1 microg/m3/h in Brisbane and Seoul, respectively. In conclusion, indoor environmental factors were effectively characterized by this method using multiple indoor and outdoor measurements.

Air Pollution, Indoor↗

PubMed1981

Spleen changes in animals inhaling ambient levels of nitrogen dioxide.

The effects of ambient levels of NO2 on the spleens of adult and newborn Swiss Webster (S/W) mice were determined. Spleens were evaluated by the following criteria: (1) spleen weight, expressed as a percent of the body weight (% spleen weight), (2) size of the spleen lymphoid nodules as determined by computed image analysis, (3) spleen cell counts, and (4) histopathologic evaluation. Data for NO2-exposed animals were compared with data for control animals that inhaled filtered air. Totals of 217 control and 217 NO2-exposed animals were studied. After 6 wk of exposure to NO2 at ambient levels (0.35 +/- 0.05 ppm), the following significant changes were observed in the spleens of exposed mice: (1) increase in % spleen weight (p less than 0.0025), (2) increase in size of spleen lymphoid nodules (p less than 0.01), (3) smaller increase in spleen cell number per given weight increment of spleen as determined by correlation coefficients (p less than 0.0125) and linear regression analysis of spleen cell counts, and (4) an apparently greater predominance of red cells in the red pulp. It is concluded that inhalation of NO2 is associated with quantifiable spleen changes, which may prove to be useful indicators for assessing effects of inhaled NO2.

Air↗

PubMed1993

Spin trapping of nitrogen dioxide radical from photolytic decomposition of nitramines.

The photochemical (lambda < 400 nm) decomposition of some monocyclic and polycyclic nitramines produces .NO2, which can be detected in the respective nitramine crystals at 77 K by EPR (electron paramagnetic resonance). In solutions of perdeutero-dimethylsulfoxide (DMSO-d6) the .NO2 produced by photolytic decomposition of dissolved nitramines can be spintrapped by the solvent to give a radical having the structure CD3-(SO2)-(NO.)-CD3. In this article, we examine this reaction for two nitramines: cyclotrimethylenetrinitramine (RDX) and hexanitrohexaazaisowurzitane (HNIW), which are energetic materials. The decay of the spin-adduct radical (I) follows first-order kinetics for both nitramines studied, having a rate constant (k) of congruent to 7.1 x 10(-4) s-1. The net growth in spin concentration of (1) measured from EPR spectra is fitted by a first-order rate equation taking into account the simultaneous competitive decay rate of spin adduct (I). Using the rate data and EPR spin concentration data, the ratio of free .NO2 produced per parent nitramine molecule is estimated as 1:1 for RDX and 4:1 for HNIW. Biological implications of trapping of .NO2 by dimethyl sulfoxide are discussed.

Bridged-Ring Compounds↗

PubMedDate not supplied

Effects of sulfuric acid and nitrogen dioxide on airway responsiveness of the guinea pig.

Hartley guinea pigs were exposed for 1 h to either NO2 gas of H2SO4 aerosol and examined for changes in airway responsiveness to inhaled histamine. Concentrations ranged from 7 to 146 ppm NO2 and 4 to 40 mg/m3 H2SO4. One group of animals exposed to filtered air served as controls. Histamine challenges were performed on unanesthetized animals 2 h before pollutant or air exposure (baseline) and 10 min and 2 and 19 h after exposure. No2-exposed animals had increased histamine sensitivities 10 min after exposure, and the magnitude of the increase was directly dependent on the NO2 concentration. Most of the NO2-exposed animals demonstrated a dramatic return toward baseline values by 2 h after exposure; however, several animals had not returned to baseline by 19 h after exposure. Some animals exposed to H2SO4 developed severe labored breathing during exposure, and major increases in histamine sensitivity were observed only in those animals. These results suggest that both No2 and H2SO4 alter airway sensitivity to histamine, but apparently by different mechanisms. Changes produced by NO2 exposures appeared primarily concentration-dependent, while changes produced by H2SO4 exposures appeared related to dyspnea developed during exposure.

Air Pollutants↗

PubMed1994

Differences in bronchoalveolar cell response to nitrogen dioxide exposure between smokers and nonsmokers.

We have previously reported on the bronchoalveolar inflammatory effects of the common air pollutant NO2 in nonsmokers. In this study, we have investigated these effects in tobacco smokers. Eight young nonbronchitic smokers and, as a reference group, eight healthy life-time nonsmokers were exposed to 3.5 ppm NO2 for 20 min. Bronchoalveolar lavage (BAL) was performed 3 weeks before and 24 h after exposure. The first recovered 20 ml was analysed separately and defined as the bronchial portion (BP), and the following fluid recovered as the bronchoalveolar portion (BAP). Before exposure, the smokers had significantly less CD3+ cells and more alveolar macrophages (AMs) in the BP and the BAP, as well as reduced AM phagocytosis in vitro compared to nonsmokers. After NO2 exposure, the smokers reacted with an increase of AMs and neutrophils in BAP. Nonsmokers reacted with an increase of neutrophils in BP, an increase of lymphocytes in BAP, and a tendency to reduced AM phagocytosis. In summary, young smokers and nonsmokers differed to some extent in their reactions to NO2 exposure. This is probably due to the pre-existing airway inflammation and compensatory mechanisms to oxidant stress in the smokers.

Adult↗

PubMed1981

Possible formation of nitrosamine in guinea pigs following exposure to nitrogen dioxide and dimethylamine.

The possibility of formation of nitrosamine was investigated in animals exposed to a combination of dimethylamine (DMA) and NO2. First, the distribution and covalent binding of DMA and dimethylnitrosamine (DMN) in rats and guinea pigs were determined. The apparent volume of distribution and biological half-life for [14C]-DMA or [14C]DMN did not reveal any species difference. In general, there were no marked differences in accumulation of radioactivity in tissues of guinea pigs and rats 4 h after the administration of DMA, while the guinea pig tissues showed higher accumulation after DMN administration. Nucleic acid fractions prepared from liver and lungs of both species following administration of DMN or DMA in vivo showed much higher covalent binding with DMN than with DMA. Furthermore, the covalent binding of DMN was found to be due to bioactivation, whereas the DMA binding was nonspecific. Since guinea pig liver showed a higher degree of covalent binding than rat liver, this species was used to investigate the possible increase in covalent binding in the presence of NO2 and DMA as a reflection of DMN formation. There was no evidence of enhancement of covalent binding when animals pretreated with [14C]-DMA were exposed for various lengths of time to different concentrations of NO2.

Animals↗

PubMed2001

An evaluation of nitric oxide and nitrogen dioxide absorbers and filters.

The absorbance of NO (5-90 ppm) and NO2 (0.5-4 ppm) by a number of absorbers and filters was assessed via bench testing. All absorbers (Sodasorb, Purafil CP, Purafil Select, Sofnolime, Sofnofil and 50/50 mix of Sofnolime/Sofnofil) except Sodasorb absorbed NO almost completely. Only Sofnolime absorbed NO2 completely while Sodasorb and the Sofnolime/Sofnofil 50/50 mix had absorbances between 47% and 90%. The absorbance of four filters (ILF100, ILF150, ILF200 and HgCONO) as well as Sofnolime and the Sofnolime/Sofnofil 50/50 mix was tested in the expiratory port of a Servo 900C ventilator All absorbers and filters produced a change in ventilator pressures. The HgCONO filter Sofnolime and the Sofnolime/Sofnofil 50/50 mix all absorbed NO. At 80 ppm NO, the HgCONO filter had 100% absorbance for four hours while Sofnolime's absorbance was significantly reduced after one hour. All filters and absorbers tested on the ventilator except the Sofnolime/Sofnofil 50/50 mix and the ILF150 filter absorbed NO2 completely for a period ranging from 90 minutes to four hours. We recommend the HgCONO filter and Sofnolime to absorb both NO and NO2. If absorption of NO2 only is required we recommend the HgCONO, ILF100 or ILF200 filters or the Sofnolime absorber.

Absorption↗

PubMed1983

Relationship between survival times of rats exposed to lethal level of nitrogen dioxide and arylhydrocarbon hydroxylase activity in lungs.

A previous paper has shown that survival times of rats exposed to lethal levels of NO2 were prolonged by administration of enzyme-inducing agents prior to NO2 exposure, and that the survival time of female rats was longer than that of male rats. In order to investigate a mechanism on prolongation of survival times by administration of enzyme-inducing agents and on sex-difference, a relationship between survival times and microsomal enzyme activity in lungs of rats administered enzyme-inducing agents was examined. The survival times of rats exposed to 65 ppm NO2 were prolonged with increase of 3MC doses, and AHH activity in lungs of rats rose with increase of 3MC doses. A significant correlation between the survival time and AHH activity was observed. Induction of AHH activity of female rats administered 3MC was higher than that of male rats. NADPH-dependent cytochrome c reductase activity in lungs of male and female rats did not change with 3MC administration, and a significant relationship between the survival time and NADPH-dependent cytochrome c reductase activity was not observed. These results suggest that cytochrome P1-450 system in lung microsomes may have protective action against the toxicity of NO2.

Animals↗