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PubMedDate not supplied

Biochemical changes in humans upon exposure to nitrogen dioxide while at rest.

The biological response to controlled exposures of nitrogen dioxide (NO2) was studied in 19 human subjects exposed to 0.2 ppm NO2 for 2 hr and compared to 15 control subjects exposed to filtered air for 2 hr. Seven biochemical blood parameters, including glutathione, red blood cell glutathione reductase, 2,3-diphosphoglycerate, methemoglobin, vitamin E, complement C2, and IgA were measured prior to exposure, immediately after exposure, and 22 hr following exposure. The only variable that showed significant change due to NO2 exposure was glutathione. Glutathione is known to protect the erythrocyte from oxidative stress. The increase in glutathione observed upon exposure to NO2 may be a protective reaction of the erythrocyte to meet the oxidative stress.

2,3-Diphosphoglycerate↗

PubMed1986

Mutagenicity of the photochemical reaction products of pyrene with nitrogen dioxide.

The mutagenicity of the photochemical reaction products of pyrene with nitrogen dioxide (NO2) and the mutagens in them were investigated for the interpretation of their biological significance as genetoxic hazards of polycyclic aromatic hydrocarbons (PAHs) in airborne particles. Samples extracted from the photochemical reaction products of pyrene with NO2 diluted with air using a high-pressure mercury lamp were mutagenic for Salmonella typhimurium strains TA97 and TA98 in the absence of S9 mix, with a trend to detoxification in the presence of the metabolic system. The mutagens in the crude samples extracted from their products, which were fractionated by normal-phase high-performance liquid chromatography (HPLC) on a column of Nucleosil 100-30 with n-hexane-benzene as an eluting solution, were analyzed by HPLC, mass spectrometry and Fourier transform infrared (FT-IR) spectrometry. Based on these results, it was recognized that 1-nitropyrene (1-NP), 1,3-dinitropyrene (1,3-DNP), 1,6-dinitropyrene (1,6-DNP) and 1,8-dinitropyrene (1,8-DNP) was formed by the photochemical reaction of pyrene with NO2. The yield of DNPs peaked at 2-3 h irradiation.

Chromatography, High Pressure Liquid↗

PubMed1999

DNA strand breaks caused by exposure to ozone and nitrogen dioxide.

The present study demonstrates that exposure to ozone (O3) and nitrogen dioxide (NO2) can cause DNA single-strand breaks in alveolar macrophages. Three-month-old male Sprague-Dawley rats, specific pathogen free, were exposed to either 1.2 ppm NO2 or 0.3 ppm O3 alone or a combination of these two oxidants continuously for 3 days. The control group was exposed to filtered room air. The oxidant effects were substantiated by determining total and differential cell counts, lactate dehydrogenase activity, and total soluble protein in bronchoalveolar lavage. DNA damage was measured as single-strand breaks by alkaline elution assay. The results showed that, relative to control, NO2 exposure did not cause any significant change in the parameters studied. Exposure to O3 and combined exposure to NO2 and O3 caused significant changes in all parameters studied except cell viability. The rates of elution (Kc) of single-strand DNA from polycarbonate filter for O3 exposure and combined exposure were 73 and 79% faster than that of the control, respectively. The amounts of DNA single-strand breaks caused by O3 and combined exposure were significantly greater than the amounts detected for the NO2-exposed and control groups.

Animals↗

PubMed1998

Nitrogen dioxide compromises defence functions of the airway epithelium.

The effect of nitrogen dioxide (NO2) exposure on airway epithelial defence functions, such as ciliary activity, mucociliary transport velocity and junctional barrier function, remains to be elucidated. Our study investigates the effect of 24-h exposure to 3.0 ppm of NO2 on the airway epithelial defence functions in the healthy rabbit. Fifty-two healthy rabbits were exposed to 3.0 ppm of NO2 (NO2 group) or pure air (control group) for 24 successive hours in exposure chambers. After completion of the exposure sequence, the ciliary activity in the trachea was examined by a photoelectric method, the mucociliary transport velocity in the trachea by an endoscopic method and epithelial permeability of the trachea to fluorescein isothiocyanate-dextrans (FD-70s; molecular weight: 70,000 daltons) by an in vitro tracheal sac method. In the NO2 group, all epithelial defence functions, including ciliary activity, mucociliary transport velocity and epithelial permeability were significantly inferior to those in the control group. Although there was considerable overlap in the parameters examined between the two groups, approximately two-thirds of the animals were susceptible to 24-h exposure to 3 ppm of NO2. Dysfunction of both the junctional barrier and the mucociliary system could allow easier entry of allergen molecules to the airway parenchyma, where immunocomponent cells exist. NO2 might be involved to some extent in the clinical manifestation of airway allergic disorders through epithelial dysfunction.

Air Pollutants↗

PubMed1990

Personal and indoor/outdoor nitrogen dioxide exposure assessments of 23 homes in Taiwan.

Indoor and outdoor nitrogen dioxide (NO2) concentrations of 23 homes from two areas in Taiwan, the city of Taipei and a rural village in central Taiwan, were measured concurrently from December 1987 to January 1988. NO2 measurements were carried out by Palmes tube for one week and filter badges for two days. In Taipei, the mean NO2 concentrations outdoors, in the kitchens, in the livingrooms, and in the bedrooms were 40.1 ppb, 34.4 ppb, 32.1 ppb, and 29.7 ppb for one week, and were 25.7 ppb, 25.6 ppb, 22.6 ppb, and 20.5 ppb for two days. In the village of central Taiwan, the corresponding concentrations were 23.5 ppb, 24.5 ppb, 20.4 ppb, and 17.5 ppb for one week, and 20.3 ppb, 24.7 ppb, 18.8 ppb, and 15.4 ppb for two days. The NO2 concentrations of all microenvironments in Taipei were significantly higher than those in the village of central Taiwan. The outdoor NO2 concentrations were significantly higher than the indoor NO2 concentrations in Taipei. The NO2 measurements in the kitchens were higher than all other measurements indoors and outdoors in the village of central Taiwan. The houses which used natural gas as cooking fuel had slightly higher indoor NO2 concentrations than the houses which used LPG as cooking fuel in Taipei city. Cement houses had slightly higher indoor NO2 concentrations than brick houses. The mean of housewives' exposures was 30.8 ppb in Taipei and 19.9 ppb in the village of central Taiwan. The explanation power of the housewife's exposure to NO2 was 72% by the time weighted-average model and 70% by the simple linear regression model.

Air Pollutants↗

PubMed1984

In-vivo nitrosation of amines in mice by inhaled nitrogen dioxide and inhibition of biosynthesis of N-nitrosamines.

Inhalation of nitrogen dioxide (NO2) by mice administered orally morpholine (MOR) or dimethylamine (DMA) resulted in the biosynthesis of N-nitrosomorpholine (NMOR) or N-nitrosodimethylamine (NDMA), respectively, as determined by the analysis of frozen whole-mouse powder, using gas chromatography with a Thermal Energy Analyzer detector. Significant levels of NMOR were detected following exposure of mice to 0.38 mg/m3 NO2 for 0.5 h (26 ng NMOR/mouse) and there was a two-fold increase when NO2 exposure was extended to 4 h. NMOR levels also increased in a time-dependent manner at 28.4 and 47.3 mg/m3 NO2 exposure levels, reaching a maximum of 450 and 725 ng NMOR/mouse, respectively, at 4 h. Oral administration of sodium ascorbate (50-250 mg), ammonium sulfamate (50-100 mg) or DL-alpha-tocopherol (67-167 mg) immediately after MOR or DMA, but prior to NO2 exposure, significantly inhibited both NMOR and NDMA biosynthesis, sulfamate being the most effective (greater than 90% NMOR and NDMA inhibition), followed by ascorbate (83-90% NMOR and 58-90% NDMA inhibition) and alpha-tocopherol (22-42% NMOR and 46-69% NDMA inhibition). Low levels of NDMA were found in untreated control mice (less than 13 ng/mouse) and in most samples of commercially obtained animal feed (10-15 micrograms/kg); NMOR, however, was not detectable or was detected in negligible amounts in these cases. Various control experiments indicated that most of the recovered nitrosamine resulted from in-vivo nitrosation in mice, with only up to 1-2% of NMOR and approximately 10% of NDMA yields being attributed to artefact formation, possibly during work-up of the mouse-powder samples.

Animals↗

PubMed1996

Generation of glycolaldehyde from guinea pig airway epithelial monolayers exposed to nitrogen dioxide and its effects on sodium pump activity.

Pulmonary injury from nitrogen dioxide (NO2) may in part be related to the generation of aldehydic compounds, which bind with cellular proteins and subsequently impair or inhibit cell function. We examined the generation of aldehydes from guinea pig tracheobronchial epithelial (GPTE) cell monolayers exposed to NO2. With the use of dinitrophenylhydrazine (DNP) to derivatize aldehydic compounds, glycolaldehyde, a two carbon alpha-hydroxyaldehyde, was identified in elevated levels in the basolateral fluid from monolayers exposed to NO2. DNP-glycolaldehyde levels were 81.2 +/- 2.7 and 234.0 +/- 42.6 nM in response to a 1-hr exposure to 1 and 5 ppm NO2, respectively, as compared to an air-control value of 20.3 +/- 6.8 nM. Taking into account dilution and reactivity, cellular glycolaldehyde levels could have reached as high as 3 mM for the 60-min exposure period (i.e., 0.05 mM/min). The effects of exogenous glycolaldehyde on GPTE ouabain-sensitive basolateral 86Rb uptake (an index of Na+,K(+)-ATPase activity) were examined and compared with the actions of NO2 exposure. Bolus addition of glycolaldehyde to the basolateral fluid at concentrations > or = 5 mM led to an inhibition of ouabain-sensitive 86Rb uptake, while lower concentrations had no effect. the effects of exogenous glycolaldehyde differ from NO2 exposure, which led to a sustained elevation of ouabain-sensitive 86Rb uptake with presumed generation of glycolaldehyde at a continuous low level. Glycolaldehyde does not appear to play a significant role in the acute alterations of sodium pump activity, suggesting that the NO2-induced changes in Na+,K(+)-ATPase activity of GPTE monolayers probably are further mediated by other lipid peroxidation products/oxidation processes yet to be identified.

Acetaldehyde↗

PubMed1989

Effect of methylprednisolone on nitrogen dioxide (NO2)-induced pulmonary edema in guinea pigs.

The treatment of nitrogen dioxide (NO2)-induced lung edema is controversial. In addition, mechanisms and patterns of interstitial edema formation in this form of increased permeability edema are unclear. To ascertain if methylprednisolone (MP) is effective in the therapy of NO2-induced edema, we exposed 108 unaesthetized guinea pigs, in groups of 12, to 277-448 ppm.hr NO2: in 60, we administered MP just before, and in 48 immediately after exposure. In each group, half the animals were randomly assigned to receive 30 mg/kg MP ip, and the other half saline. Mortality rates and lung water with wet weight/dry weight (W/D) ratios were calculated. Alveolar edema, periarterial interstitial edema, and NO2-induced bronchiolitis were graded semiquantitatively by light microscopy from freeze-substituted middle (ML) and lower lobes (LL). We found NO2 produced an exposure-dependent increase in lung water (R = 0.70, p less than 0.01). Treatment with MP preexposure produced a fourfold reduction mortality, and and a significant fall in W/D ratios and in alveolar and interstitial edema. No difference in the degree of acute bronchiolitis was found between treated and untreated animals, although ML had significantly more inflammation than LL. Treatment with MP immediately after NO2 was ineffective since mortality rates, W/D ratios, and alveolar and interstitial edema were not lower in the treated animals; there was significantly more intestitial edema in the middle lobes of the latter. Both LL and ML had equally abundant alveolar edema, but LL had significantly more interstitial edema, supporting our previous findings that in NO2-induced edema interstitial fluid accumulation follows alveolar flooding, with interlobar discrepancies probably due to differences in lung volume or in ventilation.

Animals↗

PubMed1982

Childhood respiratory illness and the home environment. II. Association between respiratory illness and nitrogen dioxide, temperature and relative humidity.

The relation of respiratory illness to nitrogen dioxide (NO2), temperature and relative humidity in homes with a gas cooker was investigated in five and six year old children living in an urban area of the northern England. NO2 was measured for one week in the child's bedroom and living room of each home, and temperature and relative humidity were measured in the bedroom only. Information on respiratory conditions experienced by the child and characteristics of the home was collected in a self-administered questionnaire completed by the child's mother. Access was gained to 183 homes (54.3% of 337) where only gas was used for cooking. Complete information was obtained for 179 (93.7%) of 191 children who lived in the 183 homes. After allowing for the effects of age, sex, social class, and number of cigarette smokers in the home and temperature or relative humidity, no statistically significant relation was found between the prevalence of having one or more respiratory conditions and weekly average levels of NO2 in the bedroom (range 4.7 to 160.8 ppb) or living room (range 9.0 to 292.2 ppb). However, the prevalence of having one or more respiratory conditions tended to be highest in homes with high levels of NO2 and lowest in homes with low levels, consistent with earlier findings. A significant positive association was found between the prevalence of respiratory conditions and relative humidity (p less than .05). A harmful effect on health from NO2 cannot be totally dismissed but if it exists it is weak and difficult to detect in small samples of children.

Air Pollutants↗

PubMed1991

Effects of nitrogen dioxide exposure on pulmonary function and airway reactivity in normal humans.

Nitrogen dioxide (NO2) is a product of combustion that has become recognized as a significant component of indoor air in some homes. Despite extensive study, it remains unresolved whether exposures to low levels of NO2 affect airway function or reactivity. These studies were designed to assess effects of various levels and patterns of NO2 exposure on pulmonary function and airway reactivity in normal humans. Normal volunteers screened for the absence of airway hyperreactivity were exposed for 3 h in an environmental chamber to purified air or NO2, separated by at least 2 wk, according to three protocols: (1) continuous 0.60 ppm NO2, (2) baseline 0.05 ppm NO2 with intermittent peaks of 2.0 ppm, and (3) continuous 1.5 ppm NO2. Subjects exercised for 10 min of each 30 min at a level sufficient to result in a minute ventilation near 40 L/min. Pulmonary function was measured before, during, and after exposure. Airway reactivity to increasing doses of carbachol was assessed 30 min after exposure. NO2 did not directly alter pulmonary function in any of the exposure protocols. In addition, airway reactivity was not altered by continuous exposure to 0.60 ppm or intermittent peaks of 2.0 ppm NO2. In contrast, continuous exposure to 1.5 ppm NO2 resulted in a greater fall in FVC and FEV1 in response to carbachol than after exposure to air (percent decrease in FVC: 1.5% after air, 3.9% after NO2, p less than 0.01). We conclude that for subjects without airway hyperreactivity, exposure to 1.5 ppm NO2 for 3 h increases airway reactivity, whereas repeated 15-min exposures to 2.0 ppm NO2 do not alter airway reactivity.

Adult↗

PubMed2002

Interference of a short-term exposure to nitrogen dioxide with allergic airways responses to allergenic challenges in BALB/c mice.

Nitrogen dioxide (NO(2)) is a common indoor and outdoor air pollutant whose role in the induction of asthma is unclear. We investigated the effects of NO(2) on the development of asthma-like responses to allergenic challenge in BALB/c mice. Ovalbumin (OVA)-immunized mice were intranasally challenged with OVA or saline solution just before starting a 3 h exposure to 5 or 20 ppm NO(2) or air. Twenty parts per million of NO(2) induced a significant increase of bronchopulmonary hyperreactivity in OVA-challenged mice and of permeability according to the fibronectin content of the bronchoalveolar lavage fluid (BALF) 24 h after exposure, as compared with air or 5 ppm NO(2). Eosinophilia (cell counts in the BALF and eosinophil peroxidase of lung tissue) was detected at 24 and 72 h with similar levels for air and 20 ppm NO(2), whereas a marked reduction was unexpectedly observed for 5 ppm NO(2). At 24 h, interleukin-5 in the BALF was markedly reduced at 5 ppm compared with 20 ppm NO(2) and was also more intense for 20 ppm NO(2) than for the air group. In contrast to specific IgG1 titers, anti-OVA IgE titers and interleukin-4 in the BALF were not affected by NO(2) exposure. Irrespective of the concentration of NO(2), OVA-challenged mice did not develop late mucosal metaplasia compared with those exposed to OVA-air. These results indicate that a short exposure to NO(2) can exacerbate or inhibit some features of the development of allergic disease in mice and may depend on the concentration of pollutant.

Air Pollutants↗

PubMed1989

A selective decrease in the xenobiotic metabolizing activity of rat lungs by nitrogen dioxide exposures.

Groups of male Wistar rats were continuously exposed to nitrogen dioxide (NO2) ranging from 1.2 to 15 ppm for 1 or 2 weeks to examine the dose-effect relationship between NO2 and the xenobiotic metabolizing activity of lung microsomes. The lung cytochrome P-450 decreased significantly after 1-week exposures to 10 and 15 ppm NO2 and showed a decreasing tendency after 2-week exposures to 6-10 ppm NO2. On the other hand, the cytochrome b5, NADPH-cytochrome P-450 reductase and NADH-cytochrome b5 reductase of lung microsomes were increased concomitant with increase in microsomal proteins during 2-week exposures to 6-10 ppm NO2. These results show that the lung cytochrome P-450 decreases preferentially upon exposure to NO2 at higher concentrations. The coumarin hydroxylase activity was the most sensitive to NO2 exposures among activities metabolizing 4 kinds of xenobiotics examined. The coumarin hydroxylase activity was decreased in a dose-dependent fashion to 67-10% of the control level by 2-week exposures to 1.2-6 ppm NO2 and became negligible at 10 ppm NO2. The 7-ethoxycoumarin O-deethylase activity was also decreased to 82-56% of the control level by 2-week exposures to 1.2-6 ppm NO2 and became a constantly reduced level at 10 ppm NO2. The benzo[a]pyrene hydroxylase activity was decreased by exposures to NO2 above 10 ppm, and the benzphetamine N-demethylase activity also decreased during 2-week exposures to 6-10 ppm NO2. These results indicate that exposures to NO2 above 1.2 ppm cause a consistent and preferential reduction in the activities of coumarin hydroxylase and 7-ethoxycoumarin O-deethylase of lung microsomes in a dose-dependent manner.

7-Alkoxycoumarin O-Dealkylase↗

PubMed2001

The relationship between low level nitrogen dioxide exposure and child lung function after cold air challenge.

BACKGROUND: Nitrogen dioxide (NO(2)) or home gas appliance use has been inconsistently associated with adverse respiratory outcomes in childhood. OBJECTIVES: (i) To examine the contribution of home gas appliance type and personal NO(2) exposure. (ii) To examine the relationship between NO(2) exposure and child lung function and respiratory history. (iii) To assess whether these relationships vary by house dust mite sensitization status. METHODS: A cross-sectional survey of 344 children (71% of the eligible group) with a mean age of 9.1 years from four randomly selected schools in the Australian Capital Territory from July to September 1999. Study measurements included a parental questionnaire, NO(2) exposure by passive gas samplers, skin prick testing for 10 aeroallergens and lung function at rest and after cold air challenge. RESULTS: Total NO(2) exposure was low with a mean concentration of 10.1 ppb. No associations were found between NO(2) exposure or gas appliance use and asthma, wheeze or baseline lung function. Personal NO(2) exposure was associated with a reduction in forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) after cold air challenge (adjusted difference - 0.12% (- 0.23% to - 0.01%) per 1 ppb increase). After exclusion of children who had home heating changed because of asthma, gas heater use was also significantly associated with a reduction in this measure (adjusted difference - 2.0% (- 3.7% to - 0.2%)). There was some evidence that these reductions were greater among the non-mite-sensitized children. CONCLUSIONS: The effect of low-level NO(2) exposure on these respiratory outcomes was not marked. The possible effect of low-level NO(2) exposure on non-specific bronchial reactivity requires confirmation. Future studies on NO(2) and respiratory health should include measures of house dust mite sensitization and bronchial hyper-responsiveness.

Air↗

PubMed2000

Antioxidant and inflammatory response after acute nitrogen dioxide and ozone exposures in C57Bl/6 mice.

Ozone (O(3)) and nitrogen dioxide (NO(2)) are highly reactive and toxic oxidant pollutants. The objective of this study is to compare chemokine, cytokine, and antioxidant changes elicited by acute exposures of O(3) and NO(2) in a genetically sensitive mouse. Eight-week-old C57Bl/6J mice were exposed to 1 or 2.5 ppm ozone or 15 or 30 ppm NO(2) for 4 or 24 h. Changes in mRNA abundance in lung were assayed by slot blot and ribonuclease protection assay (RPA). Messages encoding metallothionein (Mt), heme oxygenase I (HO-I), and inducible nitric oxide synthase (iNOS) demonstrated increased message abundance after 4 and 24 h of exposure to either O(3) or NO(2). Furthermore, increases in message abundance were of a similar magnitude for O(3) and NO(2). Messages encoding eotaxin, macrophage inflammatory protein (MIP)-1alpha, and MIP-2 were elevated after 4 and 24 h of exposure to 1 ppm ozone. Interleukin-6 was elevated after 4 h of exposure to ozone. After 4 h of 2.5 ppm ozone exposure, increased mRNAs of eotaxin, MIP-1alpha, MIP-2, Mt, HO-I, and iNOS were elevated to a higher magnitude than were detected after 1 ppm ozone. Monocyte chemoattractant protein (MCP-1) was elevated following 15 ppm NO(2) exposure. After 4 h of 30 ppm NO(2) exposure, messages encoding eotaxin, MIP-1alpha, MIP-2, and MCP-1 were elevated to levels similar to those detected after ozone exposure. Our results demonstrate a similar antioxidant and chemokine response during both O(3) and NO(2) exposure. Induction of these messages is associated with the duration and concentration of exposure. These studies suggest that these gases exert toxic action through a similar mechanism.

Administration, Inhalation↗

PubMed1991

Effects of 0.60 PPM nitrogen dioxide on circulating and bronchoalveolar lavage lymphocyte phenotypes in healthy subjects.

Nitrogen dioxide (NO2) is a common oxidant air pollutant. Animal studies have suggested that NO2 exposure causes a decrease in the numbers of some splenic lymphocyte subtypes and impairs lymphocyte-dependent immune responses. To investigate whether ambient levels of NO2 alter circulating and bronchoalveolar lavage fluid (BALF) human lymphocytes, we studied five healthy nonsmoking adult volunteers. In each subject, blood and bronchoalveolar lavage fluid was obtained and then, more than 2 weeks later, volunteers were exposured to 0.60 ppm NO2 for 2 hr with intermittent light to moderate exercise on 4 separate days within a 6-day period. We measured standard tests of pulmonary function (airway resistance, thoracic gas volume, maximal expiratory flow) and had the subjects rate the severity of respiratory symptoms before and after each NO2 exposure. Circulating and BALF lymphocytes were labeled with fluorochrome-conjugated monoclonal antibodies to human lymphocyte antigens and a flow cytometer was used to count lymphocyte subtypes. Neither any single day's exposure nor all four exposures caused a change in symptoms or in the results of tests of pulmonary function. The total number of circulating lymphocytes obtained after NO2 exposure was slightly greater than at baseline (1792 +/- 544 vs 1598 +/- 549 cells/mm3 at baseline; P = not significant) but the proportions of lymphocyte subtypes did not differ. In the BALF obtained after NO2 exposure and in the baseline state, the total number of lymphocytes and the percentages of T cells (CD 3), B cells (CD 20), T cytotoxic-suppressor cells (CD 8), T helper-inducer cells (CD 4), and large granular lymphocytes (CD 57) also did not differ after NO2 exposure. A slightly but significantly greater proportion of natural killer cells (CD 16) was found in the BALF obtained after NO2 exposure (7.2 +/- 3.1 vs 4.2 +/- 2.4% of total lymphocytes). We conclude that repeated exposures of healthy nonsmoking adults to 0.60 ppm NO2 are not associated with clinically significant symptoms, changes in airway caliber, or alterations in circulating and BALF lymphocyte subtypes. We suggest that brief, daily exposures to NO2 at levels higher than those achieved in urban atmosphere are unlikely to provoke acute respiratory impairment in healthy, nonsmoking adults.

Adult↗

PubMed1993

Effect of nitrogen dioxide inhalation on surfactant phosphatidylcholine synthesis in rat alveolar type II cells.

After exposure of rats to NO2 (10 ppm, 72 h) type II pneumocytes were isolated and compared to cells from control animals in order to determine whether nitrogen dioxide inhalation affects surfactant phospholipid synthesis. (1) Exposed cells contained more DNA, protein and phospholipid than type II cells from controls. (2) Choline kinase, CTP: cholinephosphate cytidylyltransferase, and cholinephosphotransferase showed higher specific activities in the exposed cells. (3) In correspondence with this finding, the incorporation rates of choline into intermediate metabolic products were also higher in the NO2-exposed cells. (4) The pool sizes of the intermediate metabolic products of the CDP-choline-pathway for the synthesis of phosphatidylcholine were also higher in the cells isolated from exposed animals. This suggests that acute nitrogen dioxide exposure leads to an enhanced phospholipid synthesis that may be responsible for the higher amount of phospholipid detectable in lung lavage.

Administration, Inhalation↗

PubMed2005

Chemical modification of a porous silicon surface induced by nitrogen dioxide adsorption.

The effect of gaseous and liquid nitrogen dioxide on the composition and electronic properties of porous silicon (PS) is investigated by means of optical spectroscopy and electron paramagnetic resonance. It is detected that the interaction process is weak and strong forms of chemisorption on the PS surface, and the process may be regarded as an actual chemical reaction between PS and NO(2). It is found that NO(2) adsorption consists in forming different surface nitrogen-containing molecular groups and dangling bonds of Si atoms (P(b)-centers) as well as in oxidizing and hydrating the PS surface. Also observed are the formation of ionic complexes of P(b)-centers with NO(2) molecules and the generation of free charge carriers (holes) in the volume of silicon nanocrystals forming PS.

Journal Article↗

PubMed1986

Inhibition by amines indicates involvement of nitrogen dioxide in autocatalytic oxidation of oxyhemoglobin by nitrite.

Oxidation of oxyhemoglobin by nitrite is characterized by a lag period followed by an autocatalytic phase. The oxidation can be inhibited by the addition of morpholine, piperidine, triethanolamine or triethylamine (6 mM each). These amines are known to react with nitrogen dioxide to yield nitrosamine. Unexpectedly, aniline or aminopyrine (120 microM each) markedly inhibited the oxidation. These compounds, but not the other amines given above, inhibited the peroxide compound formation from methemoglobin and hydrogen peroxide. The results establish that, during the oxidation, the peroxide compound is generated and converts nitrite into nitrogen dioxide by its peroxidatic activity, resulting in an autocatalytic phase.

Amines↗