SEARCH · PubMed Health

Results for “NITROGEN DIOXIDE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources

PubMed1994

Damage of amino acids and proteins induced by nitrogen dioxide, a free radical toxin, in air.

Damage of amino acids and proteins induced by nitrogen dioxide, a free radical toxin in polluted air, was investigated. When nitrogen dioxide (30-90 ppm) in air was exposed to a solution of an amino acid at pH 7.5 for several hours, tryptophan and tyrosine were damaged. Degradation of tryptophan was accompanied by formation of a nitroindole derivative. Decrease of tyrosine was accompanied by formation of 3-nitrotyrosine and fluorescent dityrosine. When nitrogen dioxide was exposed to a solution of bovine serum albumin, human gamma-globulin and bovine eye lens alpha-crystallin, the proteins were crosslinked by nondisulfide bonds. Tryptophan and tyrosine residues in the proteins were extensively decreased, and significant amounts of 3-nitrotyrosine and fluorescent dityrosine were formed. The modification of the proteins with nitrogen dioxide in air may have toxicological significance. Because fluorescent dityrosine is detected in a wide variety of natural proteins, nitrogen dioxide may play a role in its occurrence in natural proteins.

Air Pollutants↗

PubMed1989

Nitrogen dioxide and respiratory infection: pilot investigations.

Laboratory and human studies have raised concern that exposure to nitrogen dioxide may increase the frequency and severity of respiratory infections in children and adults. Cooking with a natural-gas-fueled stove exposes a home's residents to short-term peaks of nitrogen oxides and to higher average levels of nitrogen oxides than are measured in homes with electric stoves. We have designed a longitudinal study of infants to determine if nitrogen dioxide exposure from cooking stoves increases the incidence or severity of respiratory infections during the first 18 months of life. Pilot investigations for the longitudinal study were conducted from 1984 through 1986. This report provides the results of the pilot investigations. The first study, conducted in 1984 and 1985, was designed to document (1) that appropriate subjects could be recruited; (2) that nitrogen dioxide concentrations in Albuquerque homes were in the range of interest; (3) that an infant's personal exposure to nitrogen dioxide could be estimated; and (4) that a valid, feasible approach for surveillance could be implemented. To accomplish these goals, the families of infants were recruited at two Albuquerque hospitals, and their homes were monitored for nitrogen dioxide using a passive sampling tube. With this approach, we successfully recruited 147 households; monitoring for nitrogen dioxide showed substantially higher levels in homes with gas stoves than in homes with electric stoves, as previously found in other U.S. cities. More detailed investigations in a sample of the homes showed that personal exposures of the infants, who did not attend day care, could be satisfactorily estimated by room concentrations. We also demonstrated that mothers would complete a daily calendar-diary on respiratory symptoms and provide information every two weeks on illnesses occurring since the previous surveillance call. The second pilot study, conducted in 1986, was designed to refine the system for illness surveillance. Additional goals were to test further the methods for exposure assessment and to evaluate recruitment of subjects through pediatric practices. We recruited 75 infants and followed them over a four-month period. Information from the surveillance system was compared with the clinical assessments of the project's nurse practitioner and the subjects' physicians, and with the results of viral cultures. We also evaluated biweekly versus weekly surveillance calls. Overall, the results of the second pilot study documented that a surveillance system for respiratory illness that incorporates calendar-diaries and biweekly telephone calls is a feasible, relatively unbiased, and sensitive method for studying respiratory illness in a large population of infants. We also found that subjects could be successfully recruited through a pediatric practice.(ABSTRACT TRUNCATED AT 400 WORDS)

Cohort Studies↗

PubMedDate not supplied

Longitudinal distribution of ozone absorption in the lung: effects of nitrogen dioxide, sulfur dioxide, and ozone exposures.

Investigators used an ozone bolus inhalation method to study the effects of continuous exposure to ozone, nitrogen dioxide, and sulfur dioxide on ozone absorption in the conducting airways of human lungs. Healthy, young nonsmokers (6 males, 6 females) were exposed on separate days for 2 h to air containing 0.36 ppm nitrogen dioxide, 0.75 ppm nitrogen dioxide, 0.36 ppm sulfur dioxide, or 0.36 ppm ozone. Every 30 min, the subject interrupted exposure for approximately 5 min, during which he or she orally inhaled five ozone boluses-each in a separate breath. Investigators targeted penetration of the boluses distal to the lips in the 70-130-ml range, which corresponded to the lower conducting airways. The authors computed the change in absorption resulting from exposure (delta lambda) by comparing the amount of each ozone bolus that was absorbed with a corresponding value obtained prior to exposure. Results indicated that ozone exposure caused delta lambda to decrease relative to air exposure (p < .01), whereas both nitrogen dioxide and sulfur dioxide exposures caused an increase in delta lambda that was not significantly different from air exposure. This resulted, at least in part, to an artifact caused by preexposure to ozone boluses. The authors concluded that exposure of the lower conducting airways to nitrogen dioxide or sulfur dioxide increased their capacity to absorb ozone because more of the biochemical substrates that are normally oxidized by ozone were made available. During continuous ozone exposure, this excess of substrate is depleted and the absorption of ozone boluses decreases.

Absorption↗

PubMed1990

[The effect of quiet breathing of nitrogen dioxide and sulfur dioxide on the sensitivity of the respiratory tract to hyperventilation of sulfur dioxide].

In 14 patients with an oversensitive bronchial system (non-smokers), we investigated the question as to whether quiet breathing in a nitrogen dioxide or sulphur dioxide atmosphere would modify the sensitivity of the airways to sulphur dioxide. On three consecutive days, over a period of 30 minutes at rest, the patients breathed either filtered air or an atmosphere containing 0.25 ppm nitrogen dioxide, or 0.5 ppm sulphur dioxide. There then followed isocapnic hyperventilation of 0.75 ppm sulphur dioxide in increasing ventilation steps of 3 minutes duration each. On three other experimental days, in 7 patients, a stepwise hyperventilation of filtered air was carried out. Quiet breathing of nitrogen dioxide or sulphur dioxide resulted in no obstruction of the airways. The ventilation required to achieve a doubling of the specific airway resistance (PV100SRaw) during hyperventilation of sulphur dioxide was, on average, 46.5, 37.7 and 45.4 l/min after inhalation of filtered air, nitrogen dioxide and sulphur dioxide, respectively. Following nitrogen dioxide, PV100SRaw was significantly smaller (p less than 0.01 than following filtered air or sulphur dioxide. During hyperventilation of filtered air, the average PV100SRaw was 58.2, 51.8 and 55.7 l/min, respectively. We conclude that in non-smokers with an hypersensitive bronchial system, the inhalation of nitrogen dioxide can bring about an increase in the obstructive reaction to sulphur dioxide, without itself leading to an obstruction of the airways; in contrast, sulphur dioxide does not modify the degree of sensitivity.

Adult↗

PubMed1991

Effect of 0.25 ppm nitrogen dioxide on the airway response to methacholine in asymptomatic asthmatic patients.

In asthmatic patients, short-term exposure to nitrogen dioxide at low concentrations has been reported to result in a nonuniform airway response to various bronchoconstrictive stimuli. We therefore investigated in 11 patients with mild and stable asthma with normal baseline airway tone the effect of 0.25 ppm nitrogen dioxide on the airway response to methacholine. On 2 separate days, the subjects inhaled either 0.25 ppm nitrogen dioxide or filtered air (sham) during 20 min of tidal breathing followed by 10 min of bicycle exercise at room temperature (mean exercise ventilation 30 L/min). Methacholine inhalation tests were performed 1 h after the end of exercise to determine the methacholine concentration necessary to increase SRaw by 100% (PC100SRaw). On a third day, a methacholine challenge was done without previous exposure (control). Mean (SEM) exercise-induced increase of SRaw was 80 (24) % after sham and 82 (25) % after nitrogen dioxide, which was not significantly different (p greater than 0.10). PC100SRaw did not differ on the 3 occasions, geometric mean values (variability of mean) being 0.41 (1.6). 0.41 (1.6), and 0.46 (1.5) mg/ml after sham, nitrogen dioxide, and control, respectively (p less than 0.10). We therefore conclude that in patients with mild and stable asthma short-term exposure to 0.25 ppm nitrogen dioxide during rest and exercise does not increase methacholine responsiveness 1 h after exposure.

Adolescent↗

PubMed2001

Measurements of nitrogen dioxide in Greenland using Palmes diffusion tubes.

Measurements of nitrogen dioxide using the Palmes diffusion tubes in Uummannaq, Aasiaat, and Nuuk. all located along the west-coast of Greenland, have demonstrated that the levels of pollution at the most heavily impacted sites are comparable to levels in much larger towns in Denmark. The highest concentrations were, in general, observed near sites influenced by car traffic (peak concentrations of up to 16 ppbv), medium concentrations were observed in the residential areas (2 6 ppbv), and very low levels were found at the background locations in the town outskirts (1-2 ppbv). Observations of nitrogen dioxide concentrations less than 0.1 ppbv at a remote site, Akia, 25 km from Nuuk, indicate that, compared to local sources, long-range transport of nitrogen dioxide is not important in western Greenland.

Air Pollution↗

PubMedDate not supplied

Nitrogen dioxide exposure and urinary excretion of hydroxyproline and desmosine.

The relationship between average and peak personal exposure to nitrogen dioxide and urinary excretion of hydroxyproline and desmosine was investigated in a population of preschool children and their mothers. Weekly average personal nitrogen dioxide exposures for subjects who resided in homes with one or more potential nitrogen dioxide source (e.g., a kerosene space heater, gas stove, or tobacco smoke) ranged between 16.3 and 50.6 ppb (30.6 and 95.1 micrograms/m3) for children and between 16.9 and 44.1 ppb (12.8 and 82.9 micrograms/m3) for mothers. In these individuals, the hydroxyproline-to-creatinine and desmosine-to-creatinine ratios were unrelated to personal nitrogen dioxide exposure--even though continuous monitoring documented home nitrogen dioxide concentration peaks of 100-475 ppb lasting up to 100 h in duration. Significantly higher hydroxyproline-to-creatinine and desmosine-to-creatinine ratios were observed in children, compared with mothers (p < .001 and .003, respectively).

Adult↗

PubMed1990

[Effect of nitrogen dioxide on exercise-induced bronchial asthma and the sensitivity of the respiratory tract to methacholine].

In patients with bronchial asthma, airway hyperreactivity may be further increased by exposure to low concentrations of nitrogen dioxide. We studied the effect of inhaled nitrogen dioxide in 11 patients with bronchial asthma who presented with normal lung function values. On two different days, 20 min tidal breathing of either filtered air or 0.25 ppm nitrogen dioxide was followed by bicycle exercise (average minute ventilation 30 l/min). One hour after the end of exercise, we performed a methacholine provocation challenge and determined PC100SRaw. The methacholine provocation challenge was repeated on another day (control day). Mean (SEM) SRaw increased by 79.8 (23.8) % and 82.4 (24.9) % after breathing of filtered air and nitrogen dioxide during exercise, respectively (n.s.). Mean (SEM) PC100SRaw was 0.409 (0.205), 0.407 (0.201) and 0.455 (0.181) mg/ml after breathing of filtered air, nitrogen dioxide and on the control day, respectively (n.s.). We conclude that in mild asthmatics short-term exposure to 0.25 ppm nitrogen dioxide does not enhance airway responsiveness to exercise or methacholine.

Adult↗

PubMed1988

Photochemical formation of mutagenic compounds from alkenes and ozone or nitrogen dioxide.

In order to investigate the possible formation of mutagenic compounds from alkenes emitted in ambient air, laboratory experiments were performed with Salmonella typhimurium strain TA100 in a small-scale flow-through exposure system. The reaction time for mixtures of alkenes with ozone or nitrogen dioxide was 40 minutes, and the exposure time for bacteria was 6 hours. Ozone gave rise to a small mutagenic effect in combination with 1,3-butadiene or vinyl chloride, with and without ultraviolet (UV) irradiation, but not in combination with ethene or propene. Nitrogen dioxide gave rise to a mutagenic effect in combination with propene, 1,3-butadiene, or vinyl chloride, but only after UV irradiation. The mutagenic activity was highest with butadiene and seemed to be dose-related to the concentration of nitrogen dioxide. Nitrogen dioxide with ethene did not produce a mutagenic effect. A mixture of ethene, propene, and butadiene, tested with ozone or nitrogen dioxide with UV irradiation, did not potentiate each other's mutagenic effect.

Alkenes↗

PubMedDate not supplied

Personal exposure to nitrogen dioxide pollution and effect on plasma antioxidants.

We conducted a cross-sectional epidemiological study to evaluate personal exposure to nitrogen dioxide and its effect on blood antioxidants. Personal exposure of 107 volunteers was assessed for 14 d with passive monitors. We excluded heavy smokers (> 10 cigarettes/d) from the study. Sociodemographic and environmental data, as well as beta-carotene intake, were recorded. We mainly attributed the mean nitrogen dioxide personal exposure (31.9 +/- 12.7 microg/m3 [0.017 ppm or 0.70 microM/m3]) (R2 = 0.75) to residence site in the city, time spent in urban traffic, and use of gas stoves. The correlation between nitrogen dioxide exposure and blood antioxidant concentration was weak; in addition, the correlation coefficients for men and women were inconsistent. Nonetheless, we found some evidence of an interaction between carotene intake and nitrogen dioxide exposure: a significantly lower plasma beta-carotene level was evident among subjects who consumed < or = 4.5 mg/jour of carotene and who were exposed to nitrogen dioxide levels that exceeded 40 microg/m3 (0.021 ppm or 0.87 microM/m3) of nitrogen dioxide.

Adult↗

PubMed1994

The reaction of low levels of nitrogen dioxide with methyl linoleate in the presence and absence of oxygen.

The reaction of methyl linoleate with low levels of nitrogen dioxide in a carrier gas, such as helium or air, at nitrogen dioxide concentrations ranging from 2 to 228 ppm was studied and the products formed were monitored. In both aerobic and anaerobic conditions, low concentrations of nitrogen dioxide reacted with methyl linoleate predominantly to form allylic products. When a 1:1 mixture of methyl palmitate/methyl linoleate was layered over an aqueous buffer and a nitrogen dioxide stream was passed from underneath, so that the stream passed through the aqueous layer before contacting the organic layer, allylic products again predominated. In the absence of air, the allylic products consisted of allylic nitro and nitrite, derivatives of linoleate, whereas in the presence of air, allylic hydroperoxides were the principal products. The findings suggest that fatty acids with doubly allylic hydrogen atoms react preferentially by a hydrogen atom abstraction reaction rather than by the addition of nitrogen dioxide to a double bond.

Fatty Acids↗

PubMed2004

Nitrogen dioxide air pollution near ambient levels is an atherogenic risk primarily in obese subjects: a brief communication.

Ambient exposure to nitrogen dioxide, a critical air pollutant in developed countries, is positively associated with cardiovascular mortality and morbidity. Although its cardiovascular effects are predominantly shown in patients with high risk of atherogenesis, no studies have elucidated whether daily exposure to nitrogen dioxide air pollution enhances atherogenic metabolisms, primarily in obese subjects who are susceptible to atherogenesis and subsequent cardiovascular diseases. We used male Otsuka Long-Evans Tokushima Fatty (OLETF) rats as obese subjects and Long-Evans Tokushima (LETO) rats as nonobese controls. The animals were continuously exposed to nitrogen dioxide at a concentration of 0, 0.16, 0.8, or 4.0 ppm from 8 weeks of age through 32 weeks. At 40 weeks of age, levels of body weight, triglyceride, and total cholesterol were significantly greater in the OLETF rats than in the LETO rats. A ratio of high-density lipoprotein (HDL) to total cholesterol was significantly smaller in the former than in the latter. In the LETO rats, nitrogen dioxide exposure significantly decreased only the levels of HDL as compared with clean air exposure. In the OLETF rats, however, nitrogen dioxide exposure at a concentration of 0.16 ppm significantly elevated triglyceride concentration and decreased the ratio of HDL to total cholesterol as well as the levels of HDL. Nitrogen dioxide air pollution near ambient levels is an atherogenic risk primarily in obese subjects.

Air Pollution↗

PubMed1989

Rural concentrations of nitrogen dioxide pollution throughout Wales.

Monitoring of nitrogen dioxide was carried out at over 50 rural sites in Wales throughout 1986. All sites were chosen so as to be remote from any local sources of NO(2) and the values obtained were deemed to be minimum values for the different regions. Measurements were made using a diffusion tube technique which aimed to give mean concentrations of NO(2) for 2-week exposure periods. The results obtained have been used to generate pollution maps to show mean monthly levels of NO(2) for rural environments throughout Wales. It is apparent that levels of NO(2) are generally higher during the winter months. In addition, annual mean concentrations of the pollutant are greatest in the north-eastern and south-eastern parts of Wales with the lowest levels being found along the western coast. The work marks the completion of the first national survey of nitrogen dioxide pollution in Wales. The data are discussed in terms of the potential threat rural concentrations of NO(2) pose to crops and natural vegetation.

Journal Article↗

PubMed1999

Formation of nitrogen dioxide from nitric oxide and their measurement in clinically relevant circumstances.

Therapy with inhaled nitric oxide in oxygen requires adequate monitoring of nitric oxide and nitrogen dioxide. The characteristics of chemiluminescence and electrochemical measurement techniques were determined by analysis of continuously flowing gas mixtures and comparisons with traceable gas standards. Gas mixtures were also diluted with mass flow controllers and in addition created in ventilator breathing systems. Factors influencing the formation of nitrogen dioxide were defined. Both techniques accurately measured nitric oxide (10-80 parts per million, ppm) and nitrogen dioxide (0.5-5 ppm) in normoxic and hyperoxic (90% oxygen) gas in the studied ranges. Nitrogen dioxide in hyperoxic gas had three origins: (1) from the premixing point of nitric oxide in nitrogen, (2) as a result of the mixing process, and (3) from post-mixing and time-dependent continuous formation of nitrogen dioxide in oxygen. We conclude that adequate monitoring is possible and that factors affecting nitrogen dioxide generation can be defined.

Electrochemistry↗

PubMed1991

Mechanisms of nitrogen dioxide toxicity in humans.

These studies were undertaken to evaluate short-term respiratory effects and identify markers of nitrogen dioxide toxicity during exposures designed to approximate realistic conditions. With the development of bronchoalveolar lavage as a clinical investigative technique, the evaluation focused on the assessment of effects induced at the alveolar level. The exposure protocols were designed to assess the duration of nitrogen dioxide-induced effects and determine exposure-response relationships. Groups of normal, nonsmoking volunteers of both sexes between the ages of 18 and 40 years, without airway hyperreactivity, constituted the study population. The exposure protocols required a total of three to five days for each subject, depending on the timing of bronchoalveolar lavage. Subjects were exposed to nitrogen dioxide or air for three hours in a double-blind, randomized fashion in a 45-m3 environmental chamber, with intermittent exercise sufficient to quadruple minute ventilation. Pulmonary function was measured during and after exposure, and airway reactivity to carbachol was assessed before and after exposure. Lavaged cells were examined for their capacity to inactivate influenza virus and secrete IL-1 in vitro. Cell-free lavage fluid was analyzed for total protein, albumin, alpha 2-macroglobulin, arylsulfatase, and alpha 1-protease inhibitor. The studies were undertaken in three phases, each of approximately one year's duration. In Phase 1, 15 subjects were exposed to a background concentration of 0.05 parts per million2 (ppm) nitrogen dioxide and to three 15-minute peaks of 2.0 ppm, and underwent bronchoalveolar lavage 3.5 hours after nitrogen dioxide exposure. During Phase 2, 8 subjects were exposed to continuous 0.60 ppm nitrogen dioxide and underwent bronchoalveolar lavage 18 hours later. Finally, in Phase 3, 15 subjects were exposed to continuous 1.5 ppm nitrogen dioxide and underwent bronchoalveolar lavage 3.5 hours after exposure. No significant symptomatic or pulmonary function changes could be detected in response to any of the nitrogen dioxide exposures. However, a small but significant increase in airway reactivity was observed in normal subjects after exposure to 1.5 ppm nitrogen dioxide. Following the highest dose of carbachol (10 mg/mL), the forced expiratory volume in one second decreased 7.5 +/- 1.1 percent after nitrogen dioxide exposure compared to 4.8 +/- 1.1 percent after exposure to air (p less than 0.05). No symptoms were induced in any of the groups by the carbachol exposures. Analyses of cells recovered by bronchoalveolar lavage during all three phases revealed no differences in total cell recovery, cell viability, or differential cell counts.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

PubMedDate not supplied

Effects of nitrogen dioxide on elastin and collagen contents of lung.

Male Syrian hamsters were exposed to 30 +/- 5 ppm nitrogen dioxide for 22 hr daily for 3 wk. Nitrogen dioxide-exposed hamsters sacrificed at various times during the 3 wk exposure showed a general loss of body weight and an increased dry lung weight when compared with the controls, which were housed in a similar, but nitrogen dioxide-free environment. Analysis of total lung collagen and total lung elastin revealed a net decrease in the moieties within 4 and 10 days, respectively, following commencement of nitrogen dioxide exposure. Total lung collagen returned toward pre-exposure levels by the 14th day of nitrogen dioxide exposure. Total lung elastin did not return toward normal until termination of nitrogen dioxide exposure. Recovery in room air for 3 wk following 21 days of nitrogen dioxide exposure restored the total pulmonary collagen and elastin to valutin and collagen degradation and synthesis differ during and after nitrogen dioxide exposure. Lung collagen loss was observed earlier and was restored to normal values during the continuation of nitrogen dioxide exposure. Lung elastin loss occurred later and persisted during the entire period of exposure but returned to normal after exposure was terminated.

Animals↗

PubMed1983

Estimating human exposure to nitrogen dioxide: an indoor/outdoor modeling approach.

Adverse health consequences associated with human exposure to nitrogen dioxide are well documented. In order for policymakers to assess health risks and implement appropriate control strategies, accurate information is required concerning (1) the number of people exposed, (2) the severity and patterns of exposure, and (3) the health-related effects of exposure. In the past, data from central monitoring sites have been used to establish air pollution exposures. However, it is now recognized that people spend much of their time indoors or in areas away from fixed monitors where pollutant concentrations may be drastically different. An attempt to provide a more realistic estimate of nitrogen dioxide exposures is made. A simple deterministic model is developed, relating exposure to background ambient levels, indoor values, and human activities. Ambient and indoor parameters are derived from monitoring programs in six U.S. cities. Results suggest indoor nitrogen dioxide concentrations in private dwellings vary primarily with outdoor levels and type of cooking fuel, but are also affected by factors such as air-exchange rates and strength of indoor sources. Estimates of population exposures are obtained by combining observed distributions of nitrogen dioxide concentrations from outdoor and indoor settings with information about number of people and time spent in each microenvironment.

Air Pollution↗

PubMed1999

Nitration of unsaturated fatty acids by nitric oxide-derived reactive nitrogen species peroxynitrite, nitrous acid, nitrogen dioxide, and nitronium ion.

Reactive nitrogen species derived from nitric oxide are potent oxidants formed during inflammation that can oxidize membrane and lipoprotein lipids in vivo. Herein, it is demonstrated that several of these species react with unsaturated fatty acid to yield nitrated oxidation products. Using HPLC coupled with both UV detection and electrospray ionization mass spectrometry, products of reaction of ONOO- with linoleic acid displayed mass/charge (m/z) characteristics of LNO2 (at least three products at m/z 324, negative ion mode). Further analysis by MS/MS gave a major fragment at m/z 46. Addition of a NO2 group was confirmed using [15N]ONOO- which gave a product at m/z 325, fragmenting to form a daughter ion at m/z 47. Formation of nitrated lipids was inhibited by bicarbonate, superoxide dismutase (SOD), and Fe3+-EDTA, while the yield of oxidation products was decreased by bicarbonate and SOD, but not by Fe3+-EDTA. Reaction of linoleic acid with both nitrogen dioxide (*NO2) or nitronium tetrafluoroborate (NO2BF4) also yielded nitrated lipid products (m/z 324), with HPLC retention times and MS/MS fragmentation patterns identical to the m/z 324 species formed by reaction of ONOO- with linoleic acid. Finally, reaction of HPODE, but not linoleate, with nitrous acid (HONO) or isobutyl nitrite (BuiONO) yielded a product at m/z 340, or 341 upon reacting with [15N]HONO. MS/MS analysis gave an NO2- fragment, and 15N NMR indicated that the product contained a nitro (RNO2) functional group, suggesting that the product was nitroepoxylinoleic acid [L(O)NO2]. This species could form via homolytic dissociation of LOONO to LO* and *NO2 and rearrangement of LO* to an epoxyallylic radical L(O)* followed by recombination of L(O)* with *NO2. Since unsaturated lipids of membranes and lipoproteins are critical targets of reactive oxygen and nitrogen species, these pathways lend insight into mechanisms for the formation of novel nitrogen-containing lipid products in vivo and provide synthetic strategies for further structural and functional studies.

Chromatography, High Pressure Liquid↗