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PubMed1992

Synergistic interaction of nitrogen dioxide and ozone on rat lungs: acute responses.

Rats were exposed for 6 hr per day to either ozone alone (0.2-0.8 ppm), nitrogen dioxide (NO2) alone (3.6-14.4 ppm), or to combinations of these two oxidant air pollutants. Their response was quantified by changes in the total protein content of lung lavage supernatants or by changes in the content of specific cell types in the lung lavage pellets. A concentration-dependent synergistic response was observed when rats were exposed to the combination of ozone and NO2. Apparent threshold concentrations for the observation of synergistic interaction between ozone and NO2 were assay specific, with epithelial cell content of lung lavage fluid being the most sensitive parameter evaluated, showing positive interaction (greater than additive response) at the lowest concentrations tested. Concurrent exposure to ozone and NO2 was necessary to elicit greater than additive responses; no such interactions were seen upon sequential exposure to ozone or NO2 in either order of presentation. Based upon apparent disappearance rates of ozone in the chambers during exposure of rats to ozone and NO2, we modelled the predicted outcomes based upon the assumption that the two oxidant gases were reacting to form nitrogen pentoxide (N2O5) in the chambers. Agreement between predicted concentrations of ozone and NO2 and those actually observed was excellent. Based upon such modelling estimates and our acute toxicological data, we conclude that synergistic toxicologic interactions between ozone and NO2 are found only at concentrations very much higher than would be encountered in environmental or occupational settings. It remains to be determined whether there are any chronic toxicological responses to exposure to combinations of ozone and NO2 at concentrations below the thresholds for observing acute responses.

Administration, Inhalation↗

PubMed1998

Determinants of nitrogen dioxide concentrations in indoor ice skating rinks.

OBJECTIVES: The combination of poor ventilation and fuel-powered ice resurfacers has resulted in elevated nitrogen dioxide (NO2) concentrations in many indoor ice skating rinks. This study examined the factors influencing concentrations and the effects of various engineering controls in ice rinks with different resurfacer fuels. METHODS: Indoor NO2 concentrations were measured in 19 enclosed ice skating rinks over 3 winters by means of passive samplers, with 1-week average measurements during the first winter pilot study and single-day working-hour measurements in the final 2 winters. Personal exposures to drivers also were assessed during the last winter. RESULTS: Rinks in which propane-fueled resurfacers were used had a daily mean indoor NO2 concentration of 206 ppb, compared with 132 ppb for gasoline-fueled and 37 ppb for electric-powered resurfacers. Engineering controls, such as increased ventilation and resurfacer tuning, reduced NO2 concentrations by 65% on average, but outcomes varied widely, and concentrations increased in subsequent months. CONCLUSIONS: Electric ice resurfacers, increased ventilation, or emission control systems are recommended to protect the health of workers and patrons, with surveillance programs proposed to track implementation and maintain an observer effect.

Air Pollutants, Occupational↗

PubMed2005

Feasibility study of preparation and certification of reference materials for nitrogen dioxide and sulfur dioxide in diffusive samplers.

This paper presents the results of a feasability study for the preparation and certification of reference materials (RMs) for nitrogen dioxide (NO(2)) and sulfur dioxide (SO(2)) in diffusive samplers. RMs for NO(2) were prepared by exposure to gas mixtures in a chamber while the RMs for SO(2) were prepared by liquid spiking. Certification of RMs for NO(2) was found feasible with a certified uncertainty of 5.8% and a proposed shelf life of 5 years. The uncertainty was calculated with contribution from the homogeneity of preparation, stability and transport of the CRMs and from an external verification of the certified value. To reach 5.8% of uncertainty, the contribution of the differences between the results of analysis by ion chromatography and colorimetry must be eliminated. It is proposed to solve this by pre-extracting the samplers with water before analysis. The results of this study indicate that the samplers are stable for at least two years before and after exposure when stored in a refrigerator. By contrast, the certification of RMs for SO(2) was found to not be feasible due to instability problems. This instability was attributed to reaction of sulfate on the walls of the samplers. Alternatively, the preparation of RMs by simultaneous exposure to SO(2) and NO(2) has been tested. Satisfying homogeneities has been reached both for NO(2) and SO(2).

Air Pollutants↗

PubMedDate not supplied

The relationship between inhalation of nitrogen dioxide, the immune system, and progression of a spontaneously occurring lymphoma in AKR mice.

The effects of exposure to an ambient level of nitrogen dioxide (NO2) on the development and progression of the spontaneous T-cell lymphoma in AKR/cum mice are evaluated. The animals were exposed to 0.25 ppm +/- 0.05 ppm NO2 for 7 hr/day, 5 days/week for up to 181 days. Following exposure periods of 37, 71, 111, 141, and 181 days, the extent of lymphoma was determined microscopically in histologic sections of the thymus, spleen, lymph nodes, lung, and liver. In addition, T-lymphocyte subpopulations were quantitated by flow cytometry. The results indicate that the development and progression of lymphoma in mice was influenced by intermittent inhalation of NO2. The lymphoma was detectable earlier in control animals and the survival of the NO2-exposed group was significantly higher. The T-lymphocyte subpopulations were significantly lower in NO2-exposed animals following 37 and 181 days of NO2 exposure. The T-helper/inducer (CD4+) lymphocytes were adversely affected to the greatest extent, explaining in part the more aggressive behavior of the lymphoma in the control animals. Most importantly, these studies provide additional evidence that in vivo exposure to a level of NO2 commonly encountered in polluted metropolitan areas adversely affects cells of the immune system. In the case of the AKR mouse, the adverse effect of NO2 on CD4+ cells manifested itself by retarding development and progression of the spontaneous lymphoma. Our data suggest that this neoplasm may be dependent on growth factors such as interleukin 2, produced by CD4+ lymphocytes in the early stages.

Air Pollutants↗

PubMed1997

Nitrogen dioxide exposure enhances asthmatic reaction to inhaled allergen in subjects with asthma.

We investigated whether exposure to a low level (490 micrograms/m3) of nitrogen dioxide (NO2) affects bronchial responsiveness to allergen and enhances allergen-induced increase in airway responsiveness to histamine. Eighteen subjects with asthma and allergy to pollen were exposed at rest to either purified air or NO2 for 30 min followed 4 h later by an allergen inhalation challenge. Responsiveness to histamine was measured the day after. Lung function during NO2 exposure and allergen challenge was measured by plethysmography and after exposure by a portable spirometer hourly. The order of exposure to NO2 and air was randomized and separated by at least 2 wk. The asthmatic reaction during the late phase was enhanced by NO2, and peak expiratory flow after allergen challenge was on average 6.6% lower (p = 0.02) after NO2 than after air exposure. The number of subjects having a late asthmatic reaction (fall in FEV1 > 15%) was seven after air and 10 after NO2 (NS). Peripheral blood samples were analyzed for differential cell counts before and after NO2/allergen and serum levels of eosinophil cationic protein (ECP). NO2 effect on lung function was neither associated with an increase in eosinophil numbers nor with ECP levels. NO2 did not affect lung function before allergen challenge, early asthmatic reaction, and allergen-induced increase in responsiveness to histamine. These results indicate that short exposure to an ambient level of NO2 followed several hours later by allergen inhalation enhances allergen-induced late asthmatic reaction.

Administration, Inhalation↗

PubMed1999

Nitric oxide and nitrogen dioxide concentrations during in vitro high-frequency oscillatory ventilation.

PURPOSE: The purpose of this study was to measure nitric oxide (NO) and nitrogen dioxide (NO2) concentrations, at various ventilatory settings and sampling sites, during in vitro inhaled NO and high-frequency oscillatory ventilation therapy [iNO-HFOV]. MATERIALS AND METHODS: We used a high-frequency oscillatory ventilator (model 3100A, SensorMedics, Yorba Linda, CA), a test lung (model VT-2A Ventilator Tester, Bio-Tek Instruments, Inc., Winooski, VT), nitric oxide delivery and NO/NO2 monitoring (Pulmonox II, Pulmonox, Tofield, Canada), and scavenging systems in this study. The ventilator frequency, amplitude, and inspired oxygen concentration were systematically changed at a fixed flow of NO. The concentrations of NO and NO2, sampled at four sites, were determined by an electrochemical method (Pulmonox II). The NO and NO2 concentrations were measured at the proximal part of the inspiratory limb (site 1), near the Y-piece (site 2), the carina of the test lung (site 3), and the bellows of the test lung (site 4). RESULTS: The concentration of NO decreased significantly (P < .001) from the proximal port (site 11 of the inspiratory circuit (86.16 +/- 0.38 ppm) through the lung bellows (site 4) (70.08 +/- 0.23 ppm). The concentration of NO2 increased significantly (P < .001) from site 1 (3.25 +/- 0.04 ppm) through site 4 (19.4 +/- 0.19 ppm). However, the total concentration of NO + NO2 (NOx) remained unchanged at both site 1 and site 4. Increasing the frequency and amplitude of the ventilator significantly altered NO and NO2 concentrations. The NO2 concentration increased significantly (P < .0001) from 5.6 ppm to 18.1 ppm at site 4 when the fraction of inspired oxygen was increased from 0.25 to 0.93. The NO2 concentration also increased significantly (P < .0001) from 0.6 ppm to 18.7 when NO concentrations were independently increased from 12 ppm to 80 ppm. CONCLUSIONS: During HFOV, the concentrations of NO and NO2 vary between sampling sites and also are influenced by the frequency, amplitude, and inspired oxygen concentration. NO2 concentrations in the lung were significantly increased above commonly accepted toxic concentrations during ventilation with high concentrations of NO (80 ppm) and high fractional concentrations of oxygen. The excessive increase in NO2 concentration at the "alveolar" level in our test lung model warrants confirmation in an in vivo model.

Analysis of Variance↗

PubMed1983

Altered atrial responses to drugs after acute exposure to nitrogen dioxide and/or ethanol.

The responses of atria isolated from four groups of rats: (a) control (air/H2O) and test animals treated with (b) 5 PPM nitrogen dioxide NO2 for 72 hours, (NO2/H2O), (c) 10% ethanol (ET) in water for 13 days, (air/ET), or (d) combination of NO2 and ET (NO2/ET). Isolated atria were tested with norepinephrine and dose response curves determined. The chronotropic responses among groups were not different. However, there were significant differences when tested with pilocarpine and to lesser extent to increased calcium concentration in the bathing medium. Ethanol and/or NO2 attenuates parasympathetic activity possibly by altering receptor numbers or activity. The changes in calcium activity may result from altered calcium channel activity. This data indicates that acute exposure to NO2, ET and/or the interaction between these agents can alter cardiac activity.

Animals↗

PubMed1978

Influence of 0.5 ppm nitrogen dioxide exposure of mice of macrophage congregation in the lungs.

The lungs of 12 mice, half of which were exposed to continuous 0.5 ppm nitrogen dioxide for 3 weeks, were explanted in culture, and the instances of macrophage congregation were quantitated according to numbers of target cells involved, categories of congregation from three to 11 or more, numbers of macrophages participating in each category for the total cultures, and the influence of delaying explantation for 24 and 96 hr. A total of 9042 macrophages and 2140 epithelial and spindle target cells were counted in the outgrowths from 306 explants. The incidence of macrophage congregation (or numbers of target cells) was greater for the cultures from the NO2-exposed animals, both with respect to total incidences between groups (p leads to) and the 0-hr (p less than 0.001) and 24-hr (p less than 0.01) culture subgroups. In addition, the values for T3 to T6 macrophage congregation were individually and consistently greater for the exposed animal group. Postmortem interval stress at 96 hr appeared to result in large colonies, but they were reduced greatly in number. Also the incidence of macrophage congregation fell by 28% as compared to 0-hr and 24-hr subgroups.

Animals↗

PubMed1987

Mucus protection and airway peroxidation following nitrogen dioxide exposure in the rat.

In the current study, biochemical measures of lipid peroxidation following 4-h inhalation exposure to 76 mg/m3 (40 ppm) nitrogen dioxide were correlated with measures of deposition and tissue antioxidant levels in the nasal cavity and the trachea of the Fischer rat. In addition, respiratory-tract mucus samples were collected via esophageal cannulation and nasopharyngeal lavage over known time periods, and were analyzed for phospholipid (PL) content to provide an index of the unsaturated lipids (UL) that they may contain. UL are thought to be important in the scavenging of oxidants by the mucous lining layer. Nasal deposition efficiency, as measured in the surgically isolated upper respiratory tract under unidirectional flow conditions, averaged 25%, corresponding to an absolute deposition rate of 41 nmol/min. Vitamin E levels averaged 1.7, 5.9, and 0.7 nmol/mumol PL in nasal, tracheal, and pulmonary tissues, respectively. The level in the trachea was significantly (p less than 0.005) higher than in the other tissues. As estimated from the increase in lavage PL content over 1 h, the overall mucous PL transport rate was less than 0.013 nmol/min, suggesting the PL of the mucous lining layer could not offer significant protection against the inhaled NO2. Conjugated dienes were detected in two of four pooled nasal tissue samples. Thiobarbituric acid-reactive material levels in tracheal tissues were significantly elevated over control levels by NO2 (p less than 0.05). Thus, despite the relatively high vitamin E levels, 4-h NO2 exposure appeared to result in lipid peroxidation in the trachea and, perhaps, in the nasal airways of the rat, a result that correlated with the apparent lack of oxidant-scavenging species in the mucus lining these airways.

Animals↗

PubMed1996

Nitrogen dioxide exposure increases airway contractile response to histamine by decreasing histamine N-methyltransferase activity in guinea pigs.

To determine the mechanism responsible for nitrogen dioxide (NO2)-induced airway hyperresponsiveness, we examined the effects of NO2 exposure on the contractile response to histamine and the level of histamine N-methyltransferase (HMT) activity, a histamine-degrading enzyme, in guinea pig trachea in vitro. Guinea pigs were divided into seven groups. Each group received continuous NO2 exposure (2.0 ppm) for either 2, 6, 12, 24, 48, or 96 h. The remaining group did not receive NO2 exposure (control). HMT activity in trachea was decreased from the control value of 70.3 +/- 7.7 pmol/min/mg protein to 34.6 +/- 6.7 pmol/min/mg protein by 12 h exposures of NO2. However, 24 and 48 h exposures of NO2 did not significantly alter HMT activity. In contrast, HMT activity exceeded the control value by 96 h exposures of NO2 (85.5 +/- 5.1 pmol/min/mg protein). Twelve hour exposures of NO2 shifted the concentration-response curves to histamine to lower concentrations and significantly reduced the median effective concentration (EC50) of histamine (log M) from the control value of -5.16 +/- 0.09 to -6.15 +/- 0.14 (P < 0.01). In contrast, the EC50 concentration of histamine (log M) increased from the control value of -5.20 +/- 0.10 to -4.90 +/- 0.11 by 96 h exposures of NO2 (P < 0.05). However, NO2 exposure did not alter the contractile response to acetylcholine. Morphologically, tracheal epithelial cells had vacuoles after 12 h exposures of NO2, but denudation of the epithelium did not occur during this experiment. In situ hybridization for HMT mRNA demonstrated that the level of HMT mRNA increased dominantly in tracheal epithelial cells after 96 h exposures of NO2. The present results indicated that the decrease in the level of HMT activity in the trachea was closely associated with the increase in the airway contractile response to histamine, suggesting that NO2-induced transient airway hyperresponsiveness to histamine is due to the decreased capacity of histamine catabolism in airway.

Animals↗

PubMed1991

Effect of nitrogen dioxide on sulfhydryl groups in the central nervous system of guinea pigs.

Two groups of male guinea pigs were exposed to 5 and 10 p.p.m. nitrogen dioxide, 2 hr daily for 35 consecutive days, respectively. The third group, exposed to clean room air, was used as control. Total, free and protein bound sulfhydryl groups were estimated in the cerebral hemisphere cerebellum, midbrain and spinal cord. Significant decrement in total and protein bound sulfhydryl groups and increment in free sulfhydryl groups have been observed. Interestingly, dose-related statistically significant alterations in various CNS regions have been detected.

Animals↗

PubMed2003

Tetrahydrobiopterin prevents nitration of tyrosine hydroxylase by peroxynitrite and nitrogen dioxide.

Tyrosine hydroxylase (TH) is the initial and rate-limiting enzyme in the synthesis of the neurotransmitter dopamine. TH is inhibited and nitrated at tyrosine residues in vitro by the reactive nitrogen species peroxynitrite and nitrogen dioxide (NO2) and in vivo by drugs that damage dopamine neurons. Tetrahydrobiopterin, which is the essential cofactor for TH and is concentrated in dopamine neurons, completely blocks nitration of tyrosine residues in TH caused by peroxynitrite or NO2. Various tetrahydro- and dihydro-analogs of tetrahydrobiopterin, including 6,7-dimethyl-tetrahydropterin, 6-methyl-tetrahydropterin, 6-hydroxymethyl-tetrahydropterin, tetrahydropterin, 7,8-dihydrobiopterin, 7,8-dihydroxanthopterin, and sepiapterin, also prevent nitration of tyrosines caused by the reactive nitrogen species. Biopterin and pterin, the fully oxidized forms of the pterin molecule, fail to block peroxynitrite- or NO2-induced nitration of TH. Reduced pterins prevent neither the inhibition of TH activity nor cysteine modification caused by peroxynitrite or NO2, despite blocking tyrosine nitration. However, dithiothreitol prevents and reverses these effects on TH of tetrahydrobiopterin and reactive nitrogen species. Using an enhanced green fluorescent protein-TH fusion construct as a real-time reporter of intracellular tyrosine nitration, tetrahydrobiopterin was found to prevent NO2-induced tyrosine nitration in intact cells but to leave TH activity inhibited. These results indicate that tetrahydrobiopterin prevents the tyrosine-nitrating properties of peroxynitrite and NO2. Tetrahydrobiopterin-derived radical species formed by reaction with reactive nitrogen species may account for inhibition of TH via mechanisms that do not involve tyrosine nitration.

Animals↗

PubMed1995

Concentration- and time-dependent increase in specific airway resistance after induction of airway hyperresponsiveness by subchronic exposure of guinea pigs to nitrogen dioxide.

In the present study utilizing male Hartley guinea pigs, we investigated (1) the concentration and time dependency of the effects of subchronic exposure to nitrogen dioxide (NO2) on airway responsiveness and (2) the concentration and time dependency of the effects on specific airway resistance under room air (SRaw0). Animals were exposed to filtered air, 0.06, 0.5, 1.0, 2.0, or 4.0 ppm NO2 for 6 and 12 weeks (24 hr/day). Airway responsiveness and SRaw0 were determined 1 week before the beginning of exposure at 10 weeks of age and on the day of termination of the exposure. Our results revealed that (1) subchronic exposure to NO2 induces airway hyperresponsiveness, both concentration and time dependently, (2) such exposure also induces an increase in SRaw0, both concentration and time dependently, and (3) subsequent to the airway hyperresponsiveness induced by NO2 is an increase in the SRaw0. Therefore, NO2 could be a potent risk factor for alteration of pulmonary function and airway responsiveness.

Administration, Inhalation↗

PubMed1988

Nitrogen-dioxide-induced emphysema in rats. Lack of worsening by beta-aminopropionitrile treatment.

We evaluated the effect of beta-aminopropionitrile (beta APN) on the nitrogen dioxide (NO2) animal model of emphysema. Rats maintained on a beta APN-supplemented or a regular diet were exposed to 30 ppm NO2 for intervals ranging from 1 to 8 wk. Emphysema development was assessed by histologic evaluation and by changes in lung volume and mean linear intercept values. Evidence of pathologic changes were also documented by clinical and radiographic findings of osteolathyrism. The induction of centriacinar emphysema was attributed specifically to NO2 exposure. Neither the severity of the emphysema nor the time course of its development was altered by the beta APN-supplemented diet. These findings are in marked contrast to those observed with the exogenous elastase model of the disease, and they suggest that elastin synthesis and repair may not modulate elastin destruction in the NO2 model of emphysema.

Aminopropionitrile↗

PubMed1988

Laboratory study of asthmatic volunteers exposed to nitrogen dioxide and to ambient air pollution.

Adult volunteers with moderate to severe asthma (N = 59) underwent dose-response studies to assess their reactivity to nitrogen dioxide (NO2) in otherwise clean air. Exposure concentrations were 0.0 (control), 0.3 and 0.6 ppm. A subgroup (N = 36) also underwent exposures to Los Angeles area ambient air at times when NO2 pollution was expected. Concentrations of NO2 during ambient exposures were 0.086 +/- 0.024 ppm (mean +/- s.d.). All exposures took place in a movable chamber/laboratory facility. Each study lasted 2 hr, with alternating 10 min periods of exercise (mean ventilation rate 40 L/min) and rest. Lung function was measured prior to exposure and after 10 min, 1 hr and 2 hr of exposure. Symptoms were recorded prior to exposure, during exposure and for 1 week afterward. In some subjects bronchial reactivity to cold air was measured 1 hr after the end of exposure and again 24 hr later. Different exposure conditions were presented in randomized order, 1 week apart. No pollutant exposure produced statistically significant changes in lung function, symptoms, or bronchial reactivity, relative to clean air. Ambient air exposures produced the largest (still nonsignificant) mean changes in some lung function tests. Given the physiological and atmospheric variability, negative statistical results do not rule out a small unfavorable effect of ambient pollution on lung function. If any such effect occurred, it was not likely caused by NO2. Statistical results remained negative when the analysis was restricted to the 20 subjects with most severe lung dysfunction. In conclusion at least in the Los Angeles area, sensitivity to ambient concentrations of NO2 is not common, even among adult asthmatics with moderate to severe disease.

Adult↗

PubMed2000

Medical devices; anesthesiology devices; classification of nitric oxide administration apparatus, nitric oxide analyzer, and nitrogen dioxide analyzer. Food and Drug Administration, HHS. Final rule.

The Food and Drug Administration (FDA) is classifying the nitric oxide administration apparatus, nitric oxide analyzer, and nitrogen dioxide analyzer into class II (special controls). The special control that will apply to these devices is a guidance document. The agency is taking this action in response to a petition submitted under the Federal Food, Drug, and Cosmetic Act (the act) as amended by the Medical Device Amendments of 1976 (the amendments), the Safe Medical Devices Act of 1990, and the Food and Drug Administration Modernization Act of 1997. The agency is classifying these devices into class II (special controls) in order to provide a reasonable assurance of the safety and effectiveness of the devices.

Equipment Safety↗

PubMedDate not supplied

Improving accuracy of the chemiluminescent analyser for measurement of nitric oxide and nitrogen dioxide in respired gas.

OBJECTIVE: The aim of this study was to improve the accuracy of the chemiluminescent analyser in the measurement of nitric oxide (NO) and nitrogen dioxide (NO2) in both dry and humidified gas mixtures containing oxygen (O2) in varying concentrations. This work was performed because initial attempts to determine rate constants for the decay of NO and rates of formation of NO2 were unsuccessful. METHODS: Equations were developed by which the raw output signal of the analyser could be corrected for errors arising from variations in sensitivity of the analysis cell, degree of conversion of NO2 to NO and degradation of NO to nitrogen (N2) in the converter prior to analysis. Once correction factors were derived from calibration, the analyser was used to measure rate of decay of 40 ppm nitric oxide in both dry and humidified gases containing either 21%, 60% or 100% O2 in N2. RESULTS: Correction factors obtained from calibration corrected falls in sensitivity to a maximum of 28%, variations in degree of conversion of NO2 to NO from 62-96% and degradation of NO from 2-8% in the converter before analysis depending on O2 concentration and humidification. When the calibrated machine was used to measure decay of NO, an excellent fit (r2 > 0.95) with a hyperbolic function was obtained confirming that rate of decay is proportional to oxygen O2 concentration and square of NO concentration. A rate constant per unit O2 concentration of 9.40E-10 ppm(-2) min(-1) for humidified gas was significantly higher than 8.27E-10 ppm(-2) min(-1) for "dry" gas (P = 0.008) at 22 degrees C. Rise in NO2 predicted from the "wet" rate constant achieved 3ppm in 65 seconds with 40 ppm NO in 100% oxygen and 107 sec. in 60% oxygen. CONCLUSION: This study indicates that for accurate analysis of NO and NO2 concentrations in airway gases a rigorous calibration of the instrument for the conditions applying in the experiment is mandatory. Once this is achieved the instrument is capable of precise analysis of both gases.

Calibration↗

PubMed1975

Nitrogen dioxide and the erythrocyte redox state.

Normal human erythrocytes were exposed for two hours at 38 C to an atmosphere of air containing variable concentrations of nitrogen dioxide, in order to detect any primary cytoplasmic effect of NO2 on the calculated oxidation-reduction (redox) ratio ([NAD+]/[NADH]) of a mitochondria-free cell. Substantial increases in the redox ratio were noted only when NO2 concentrations exceeded 15 ppm. In the range of 15 to 500 ppm NO2, the increase in the redox ratio significantly correlated with the NO2 concentration (r=.71; p less than .01). Intracellular to extracellular anion distribution ratios for chloride, lactate, and pyruvate were similar in NO2 and non-NO2 exposed cells, suggesting absence of a substantial hemolytic effect. These data identify a direct cytoplasmic NO2-induced biochemical change that may be mediated by a mechanism other than lipid peroxidation. Alteration of hemoglobin or NAD-NADH-dependent enzyme activity is suggested.

Cell Fractionation↗