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PubMedDate not supplied

Modeling the kinetics of vinyl chloride cometabolism by an ethane-grown Pseudomonas sp.

Pseudomonas sp strain EA1 was isolated under aerobic conditions using ethane as the sole organic carbon and electron donor source, with an observed yield of 0.99 mg total suspended solids/mg ethane (0.85 mg volatile suspended solids / mg ethane) and a maximum specific growth rate of 0.015 d(-1). When grown on ethane, EA1 cometabolizes vinyl chloride (VC) at a maximum rate of 0.350 micromol/mg volatile suspended solids/d and with a half saturation constant of 0.62 microM VC. The rate of VC use by EA1 is twice as high when ethane is also provided, even though consumption of ethane is almost completely inhibited until VC is consumed. The presence of ethane also reduces the total amount of VC cometabolized. A model was developed that adequately describes the batch kinetics of VC cometabolism in the presence and absence of ethane, as well as ethane metabolism in the presence and absence of VC. Terms are included that increase the initial rate of VC use in the presence of ethane (according to the ratio of initial ethane concentration to the half saturation coefficient) but decrease the total amount of VC cometabolized. Parameter estimates for the model were obtained using a step-wise experimental approach, with varying initial concentrations of VC and ethane. Strain EA1 completely dechlorinates VC in the presence and absence of ethane. Measurements of soluble chemical oxygen demand indicate that approximately 50% of the VC consumed is mineralized, with the balance released as soluble, nonchlorinated products. Ethene is not used as a substrate by EA1 but it does inhibit ethane metabolism and VC cometabolism. In mixtures containing all three compounds, more VC is degraded and at a faster rate compared to VC plus ethene. The results suggest that ethane-enhanced biodegradation of VC may contribute to VC removal at the aerobic fringe of groundwater plumes undergoing reductive dechlorination.

Biodegradation, Environmental↗
PubMed1995

Cigarette smoking and ethane exhalation in humans.

The time course of exhaled ethane gas was determined in the alveolar expirate of healthy, fasting smokers and nonsmokers after smoking a cigarette. Baseline ethane was measured by gas chromatography and corrected for background ethane after a 2-min washout using purified air. Ethane was measured immediately after smoking and hourly thereafter. Ethane was highest immediately after smoking, reflecting ethane in cigarette smoke. An exponential decline of ethane in smokers returned ethane to baseline within 3 h. Ethane in nonsmokers also peaked immediately after smoking but returned to baseline by 1 h. Ethane from smokers, measured 3 h after the last cigarette, was compared with ethane from healthy ex-smokers and nonsmokers. Mean (+/- SEM) baseline ethane in smokers was 2.90 +/- 0.52 pmol/min/kg, 1.55 +/- 0.36 pmol/min/kg in ex-smokers and 1.11 +/- 0.26 pmol/min/kg in nonsmokers (p < 0.05). Ethane in two smokers measured before and after a week of oral beta carotene supplementation (60 mg/d) fell by 80 and 35%. We conclude that cigarette smokers have increased baseline ethane in exhaled breath compared with non-smokers. Trials with antioxidant agents are warranted to assess their ability to reduce expired ethane levels.

Breath Tests↗
PubMed1999

Effect of vitamin E on exhaled ethane in cigarette smokers.

STUDY OBJECTIVES: We hypothesized that micronutrient antioxidant intake may be one factor determining the development of significant COPD. Vitamin E was administered to smokers to determine if exhaled ethane was reduced and if ethane correlated with measures of lung function. STUDY DESIGN: Longitudinal placebo lead-in trial with posttreatment observation period. SETTING: Tucson Veterans Affairs Medical Center. PARTICIPANTS: Twenty-nine current stable smokers having no interest in smoking cessation. INTERVENTIONS: Spirometry, exhaled breath ethane measurements, and vitamin E and [-carotene plasma levels followed by 3 weeks of placebo with repeat plasma vitamin levels and ethane measurements; next, 3 weeks of vitamin E (dl-a-tocopherol), 400 IU po bid followed by plasma vitamin levels and breath ethane measurements; finally, 3 weeks without vitamins followed by breath ethane and plasma vitamin levels. RESULTS: Vitamin E treatment did not reduce ethane significantly. Exhaled ethane levels (mean + SD: pm/min/kg) were as follows: baseline, 7.39 + 5.39; after run-in period, 6.86 + 4.09; after vitamin E, 6.36+/-3.02; and final, 7.23+/-4.63. After vitamin E therapy, a significant negative correlation existed between exhaled ethane and FEV1/FVC. Pack-years of smoking at baseline and after vitamin E were significantly associated with ethane exhaled. Initial lung function was not significantly negatively associated with vitamin E-induced changes in exhaled ethane but a negative trend was found. CONCLUSIONS: Vitamin E alone, unlike the combination of vitamins C, E, and beta-carotene, failed to reduced exhaled ethane in cigarette smokers. Exhaled ethane was correlated with pack-years of smoking. Smokers whose ethane values were found to fall the most tended to have better preserved lung function.

Adult↗
PubMed1982

Sulfite-induced lipid peroxidation in chloroplasts as determined by ethane production.

Ethane formation, as a measure of lipid peroxidation, was studied in spinach (Spinacia oleracea L.) chloroplasts exposed to sulfite. Ethane formation required sulfite and light, and occurred with concomitant oxidation of sulfite to sulfate. In the dark, both ethane formation and sulfite oxidation were inhibited. Ethane formation was stimulated by ferric or ferrous ions and inhibited by ethylenediamine tetraacetate. The photosynthetic electron transport modulators, 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU) and phenazine methosulfate, inhibited both sulfite oxidation and ethane formation. Methyl viologen greatly stimulated ethane formation, but had little effect on sulfite oxidation. Methyl viologen, in the absence of sulfite, caused only a small amount of ethane formation in comparison to that produced with sulfite alone. Sulfite oxidation and ethane formation were effectively inhibited by the radical scavengers, 1,2-dihydroxybenzene-3,5-disulfonic acid and ascorbate. Ethanol, a hydroxyl radical scavenger, inhibited ethane formation only to a small degree; formate, which converts hydroxyl radical to superoxide radical, caused a small stimulation in both sulfite oxidation and ethane formation. Superoxide dismutase inhibited ethane formation by 50% when added at a concentration equivalent to that of the endogenous activity. Singlet oxygen did not appear to play a role in ethane formation, inasmuch as the singlet oxygen scavengers, sodium azide and 1,4-diazobicyclo-[2,2,2]-octane, were not inhibitory. These data are consistent with the view that O(2) is reduced by the photosynthetic electron transport system to superoxide anion, which in turn initiates the free radical oxidation of sulfite, and the free radicals produced during sulfite oxidation were responsible for the peroxidation of membrane lipids, resulting in the formation of ethane.

Journal Article↗
PubMed1985

Absence of lipid peroxidation as determined by ethane exhalation in rats treated with 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD).

The exhalation of ethane is widely used as an indicator of in vivo lipid peroxidation. To test the hypothesis that lipid peroxidative events are involved in the toxicity of 2, 3, 7, 8-tetrachlorodibenzo-p-dioxin (TCDD), we administered a lethal dose of TCDD (60 micrograms/kg), IP to male Sprague-Dawley rats (160-180 g) and measured by gas chromatography the exhalation of ethane into the atmosphere of a closed all-glass exposure chamber. TCDD-treated rats exhaled only slightly more ethane than control rats at a single time point 7 days following TCDD administration. Since the exhalation of ethane is the net result of the endogenous production of the gas and its metabolic degradation, the latter was quantified by measuring the clearance of exogenous ethane (initial concentration = 100 ppm) introduced to the atmosphere of the exposure chamber. The clearance of ethane in TCDD-treated rats was markedly decreased, reaching a minimum 7 days following TCDD treatment. Apparently, the slight increase in exhaled ethane was due to an inhibition of ethane metabolism caused by TCDD. However, rats obviously intoxicated and having lost considerable body weight might be impaired in their ability to transport ethane. To bypass this problem we injected ethane (0.2 ml) directly into the rats IP. Here also the metabolic clearance in TCDD-treated rats was diminished. In a further experiment, rats treated with dithiocarb at a dose where ethane metabolism was totally inhibited exhaled more ethane than did TCDD-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Source of ethane in expirate of rats ventilated with 100% oxygen.

Ethane in alveolar expirate may have its source in organs other than the lung and be transported to the lung for elimination. We determined ethane production rates in rats (group I) ventilated with hydrocarbon-free air (HFA) before and after exsanguination. To determine whether the lung is the source of increased ethane production during exposure to 100% O2, we measured ethane in the expirate of nine exsanguinated, Sprague-Dawley rats (group II) mechanically ventilated with HFA and then with 100% O2. In all nine animals, ethane elimination rates on 100% O2 increased compared with HFA values. In five of the nine rats, HFA ventilation was reinstated after O2 (group III). In all five, ethane elimination fell with HFA ventilation compared with the value on 100%. Six rats with circulation intact were ventilated with HFA and then 100% O2 (group IV). Ethane production rate for group IV animals breathing HFA was not significantly different from the exsanguinated animals in group II while ventilated with HFA. The mean increase in ethane production for the group II animals was not significantly different from the group IV animals. Lung slices from four other rats (group V) were incubated in saline at 37 degrees C with FeCl2 (10 mg) added to enhance free radical formation. Paired lung samples from the same rat were incubated with either HFA or 100% O2. Headspace gas was analyzed chromatographically for ethane at 120 min. Mean ethane in the O2 samples was higher than for HFA. Rat lung tissue is the main source of increased ethane production during 100% O2 exposure.

Animals↗
PubMed1999

Ethane: a marker of lipid peroxidation during cardiopulmonary bypass in humans.

The goals of this study were to (1) determine the utility of quantification of ethane as a marker of ischemia-reperfusion during human cardiopulmonary bypass (CPB); and (2) determine, using an animal model for this surgical procedure, whether the mode of surgical approach produced increases the quantity of exhaled ethane. Human CPB was initiated following standard anesthetic and monitoring regimens. Samples of gas were collected at baseline and at multiple defined time points throughout the studies. Ethane was determined using cryogenic concentration and gas chromatography. Sternotomy increased exhaled ethane compared to baseline (p < .007; 5.8 +/- 1.7 vs. 3.0 +/- 0.7 nmol/m2 x min); ethane returned to baseline levels prior to the initiation of CPB. Aortic unclamping produced ethane elevation (p < .05; 2.3 +/- 0.8 vs. 1.5 +/- 0.4 nmol/m2 x min) with the levels being related to a lower cardiac index and a higher systemic vascular resistance post aortic unclamping. Termination of CPB significantly increased ethane levels compared to baseline (p < .002; 4.8 +/- 1.7 vs. 3.0 +/- 0.7 nmol/m2 x min). Independent variables that correlated with increased ethane measurements included a higher arterial blood pH on bypass and the change in hemoglobin pre- and post-CPB. Electrocautery, but not scalpel, incision of the porcine abdominal wall increased ethane levels significantly (p < .02). These results indicate that exhaled ethane may be a valuable marker of lipid peroxidation during and following CPB.

Animals↗
PubMed2005

Exhaled ethane: an in vivo biomarker of lipid peroxidation in interstitial lung diseases.

BACKGROUND: Oxidative stress plays a role in the pathogenesis and progression of interstitial lung disease (ILD). Exhaled ethane is a product of lipid peroxidation that has been proposed as a biomarker of oxidative stress in vivo. OBJECTIVES: To determine whether the exhaled ethane level is elevated in patients with ILD and to compare it with other clinical parameters. METHODS: Breath samples were collected from 34 patients with ILD, including 13 with idiopathic pulmonary fibrosis (IPF), 9 patients with cryptogenic organizing pneumonia, 6 patients with collagen vascular disease-associated interstitial pneumonia, and 6 patients with pulmonary sarcoidosis. Gas samples were obtained at hospital admission and after 3 weeks. After each expired sample was concentrated using a trap-and-purge procedure, the ethane level was analyzed by gas chromatography. RESULTS: Exhaled ethane levels were elevated in ILD patients (n = 34, mean +/- SD, 8.5 +/- 8.0 pmol/dL) compared with healthy volunteers (n = 16, 2.9 +/- 1.0 pmol/dL; p < 0.001). Serial measurements revealed that increase and decrease of ethane levels were largely consistent with the clinical course. Four patients with IPF who had persistently high ethane levels died or deteriorated, whereas those with ethane levels < 5.0 pmol/dL remained stable or improved. Exhaled ethane concentrations were positively correlated with levels of lactate dehydrogenase (Spearman rank correlation coefficient [rs], 0.28, p = 0.026) and C-reactive protein (rs, 0.38, p = 0.025) and were inversely correlated with Pa(O2) (rs, - 0.40, p = 0.0026). Patients showing increased uptake on (67)Ga scintigraphy demonstrated higher ethane levels (n = 19, 7.5 +/- 5.7 pmol/dL) compared with those who did not show increased uptake on scintigraphy (n = 10, 3.0 +/- 2.4 pmol/dL; p < 0.01). CONCLUSIONS: Exhaled ethane is elevated in patients with ILD and is correlated with the clinical outcome, suggesting that it provides useful information about ongoing oxidative stress, and thereby disease activity and severity in ILD.

Adult↗
PubMed1996

NTP Renal Toxicity Studies of Selected Halogenated Ethanes Administered by Gavage to F344/N Rats.

The National Cancer Institute and National Toxicology Program have performed 2-year toxicology and carcinogenesis studies with a number of ethanes substituted with chlorine or bromine. A review of the results of studies with these halogenated ethanes has revealed several consistencies between the pattern of halogen substitution and neoplastic responses in some affected organs. One of these consistencies was the finding of a modest increase in the incidence of renal tubule cell neoplasms in male rats administered penta- or hexachloroethane. Certain aspects of the nephropathy also noted in these studies resembled what is now recognized as a distinct hyaline droplet nephropathy typically associated with the accumulation of alpha[alpha]2&mgr;-globulin in renal tubule cells. In an attempt to determine some of the structure activity relationships involved in the induction of hyaline droplet nephropathy by halogenated ethanes, a series of commercially available ethanes substituted with three or more chlorines, four or more bromines, or a combination of chlorines and fluorines was studied in a short-term renal toxicity assessment in male F344/N rats. All chemicals were administered by gavage in corn oil to groups of five male rats once daily for 21 days. The doses selected for study, 0.62 and 1.24 mmol/kg per day, were based on those used in the 2-year pentachloroethane studies. The following chemicals were evaluated: 1,1,1,2- and 1,1,2,2-tetrachloroethane; pentachloroethane; 1,1,2,2-tetrachloro1,2-difluoroethane; 1,1,1-trichloro-2,2,2-trifluoroethane; 1,2-dichloro-1,1-difluoroethane; 1,1,1-trichloroethane; hexachloroethane; 1,1,1,2-and 1,1,2,2-tetrabromoethane; and pentabromoethane. Evaluations included survival, mean body weight gains, clinical signs, organ weights, urinalysis, and histopathologic examination of the right kidney and liver. The kidneys of rats that showed a difference in renal protein droplet accumulation compared to the controls were evaluated for replicative DNA synthesis by staining for proliferating cell nuclear antigen. For most groups, survival was not affected by chemical treatment; however, all rats administered either dose of 1,1,2,2-tetrabromoethane died by Day 11, and all rats administered 1.24 mmol/kg pentabromoethane, 1,1,1,2-tetrabromoethane, or 1,1,2,2-tetrachloroethane died before the end of the study. Rats receiving 0.62 mmol/kg pentabromoethane gained less weight than the controls, and rats in the 0.62 mmol/kg 1,1,1,2-tetrabromoethane group lost weight during the study. Increased kidney weights and signs of renal toxicity, indicated by urinalysis results, were noted in rats in many of the groups administered halogenated ethanes, but these observations were not always coincident with a diagnosis of hyaline droplet nephropathy. Hyaline droplet nephropathy was observed only in rats receiving penta-, hexa-, or 1,1,1,2-tetrachloroethane. The renal tubule cell labeling index was increased, indicating replicative DNA synthesis, in male rats receiving chemicals that induced hyaline droplet nephropathy as well as in males receiving pentabromoethane or 1,1,2,2-tetrachloroethane and in female negative control rats administered pentachloroethane; thus some of the halogenated ethanes appeared to cause significant renal toxicity not associated with hyaline droplet nephropathy. In summary, of the halogenated ethanes studied, the capacity to induce hyaline droplet nephropathy in male rats was restricted to ethanes containing four or more halogens, and only the chlorinated ethanes were active. If the ability to induce hyaline droplet nephropathy is the determining factor in the induction of renal tubule cell neoplasms by halogenated ethanes, then an absence of kidney neoplasms in male rats would be predicted in the event that 2-year studies were performed with the bromo- or chlorofluoroethanes.

Journal Article↗
PubMed1988

Ethane production by Methanosarcina barkeri during growth in ethanol supplemented medium.

Methanosarcina barkeri strain 227 produced ethane during growth on H2/CO2 when ethanol was added to the medium in concentrations of 89-974 mM; ethane production varied from 14 to 38 nmoles per tube (20 ml gas phase, 5.7 ml liquid) with increasing ethanol concentrations. Cells grown to mid-logarithmic phase (A600 approximately 0.46, protein = 64 micrograms/ml) on H2/CO2, thoroughly flushed with H2/CO2, then exposed to ethanol, produced maximal ethane levels (at 585 and 974 mM ethanol) of about 215 nmoles per tube, with an ethane/methane ratio of 1 x 10(-3). Mid-logarithmic-phase cultures of Methanosarcina barkeri strain Fusaro also produced ethane (up to 20 nmoles per tube) when exposed to ethanol. Cultures of strain 227 growing on methanol in the absence of H2 produced less than or equal to 6 nmoles per tube of ethane when supplemented with ethanol whereas those lacking ethanol but containing H2 and/or methanol produced less than or equal to 1.6 nmoles per tube. Cultures of Methanococcus deltae strains delta LH and delta RC, Methanospirillum hungatei or Methanobacterium thermoautotrophicum produced less than or equal to 5 nmoles ethane per tube when grown in medium containing ethanol. Ethanol concentrations of 177-886 mM were inhibitory to growth of all methanogens examined. Production of ethane by Methanosarcina was inhibited by greater than 62 mM methanol, and both methanogenic inhibitors tested, CCl4 and Br-CH2-CH2-SO3-, inhibited ethane and methane production concurrently. The data suggest that ethanol is converted to ethane by Methanosarcina species using the terminal portion of the methanol-to-methane pathway.

Anaerobiosis↗
PubMed1988

Production of ethane by rats treated with the colon carcinogen, 1,2-dimethylhydrazine.

Ethane was exhaled by rats treated with the colon carcinogen, 1,2-dimethylhydrazine (DMH). At 1 hr, ethane production (mean +/- SD) was 0.2 +/- 0.2 nmol/kg (controls) and 5.2 +/- 1.3, 13.7 +/- 3.4, and 27.7 +/- 9.6, respectively, for DMH injections of 0.15 mmol/kg (20 mg/kg of the dihydrochloride salt), 0.45 mmol/kg, and 1.35 mmol/kg. Rates of ethane evolution tapered off after 2 hr, but persisted for up to 3 hr at the lower dose, and up to 5-6 hr at the higher dose. Although ethane is produced in vivo during lipid peroxidation, experiments with vitamin E, a potent lipid antioxidant, indicated that lipid peroxidation was unlikely to be the source of ethane in DMH-treated rats: pretreatment with vitamin E had no effect on ethane formation from DMH but did suppress ethane production from rats treated with carbon tetrachloride, an inducer of hepatic lipid peroxidation. When rats were injected with 1,2-diethylhydrazine in place of DMH, large amounts of ethane and ethylene were produced (9800 and 5600 nmol/kg/hr). The hydrocarbon gases exhaled by rats may arise from dimerization of methyl radicals (.CH3) generated during the metabolism of DMH, and from ethyl radicals (.CH2CH3) generated during the metabolism of 1,2-diethylhydrazine. Previously, it was shown that methane and ethane are formed from methyl radicals in vitro. Other investigators have observed formation of hydrocarbon gases during the in vitro metabolism of monoalkylhydrazines by microsomes, and ethyl radicals, derived from monoethylhydrazine, have been detected by electron spin-resonance spectroscopy. The results presented here suggest that in vivo metabolism of DMH may produce methyl radicals. Methyl radicals are capable of interacting with biomolecules. Their indiscriminate reaction with tissue constituents may be a contributory factor in DMH-induced carcinogenesis.

1,2-Dimethylhydrazine↗
PubMedDate not supplied

Metabolism of ethane and pentane to carbon dioxide by the rat.

The pulmonary excretion rates of ethane and pentane have been used as indices of lipid peroxidation. This use assumes that exhalation of these hydrocarbons is directly related to their formation rate. This is true only if the elimination (metabolism plus nonpulmonary excretion) of ethane and pentane are constant in the presence of alterations in lipid peroxidation. However, the in vivo metabolic elimination profile for pentane is unknown and it has not been established with certainty that ethane is metabolized in vivo. Radiolabeled [14C]ethane and pentane were used to study the disposition of these hydrocarbons when injected into an enclosed chamber system containing a rat. The ethane and pentane concentrations in chamber air measured as 14C radioactivity were in general agreement with more selective measurements based on GC analysis. Pentane was cleared from chamber air at a much faster rate than ethane. Approximately 50 and 19.8% of the total radioactivity added to the chamber as [14C]pentane or [14c]ethane, respectively, was recovered as carbon dioxide at the end of 8 hr. The fraction of total radioactivity recovered in urine was 7.6 and 1.0% for the pentane and ethane experiments, respectively. These results indicate unequivocally that both ethane and pentane are metabolized in the intact rat.

Animals↗
PubMed2004

Na-montmorillonite hydrates under ethane rich reservoirs: NPzzT and muPzzT simulations.

Na-montmorillonite hydrates in presence of ethane molecules are studied by means of hybrid Monte Carlo simulations in the NP(zz)T and muP(zz)T ensembles. The NP(zz)T ensemble allows us to study the interlaminar distance as a function of water and ethane content. These data show clear plateaus for lower ethane contents and mainly for water contents consistent with the formation of a single water layer. In addition, from this ensemble the structure for some of these interlaminar compositions were analyzed. For systems containing few ethane molecules and water enough to complete a single layer, it was observed that ethane mainly situates close to the interlayer midplane and adopts a nearly parallel arrangement to the clay surface. On the other hand, the muP(zz)T ensemble allows us to determine the interlaminar distance and water-ethane content for any specific reservoir. Here, some important findings are the following: the partial exchange of water by ethane molecules that enhances for decreasing the water vapor pressure; the obtention of a practically constant interlaminar space distance as a function of the water vapor pressure; the conservation of ion solvation shells; the enhancement of the water-ethane exchange for burial conditions; and finally, the incapability for a dehydrated clay mineral to swell in a dry and rich ethane atmosphere.

Journal Article↗
PubMed1995

Effect of the hepatocarcinogenic peroxisome proliferator Wy-14,643 in vivo: no increase in ethane exhalation or hepatic conjugated dienes.

Exhalation of ethane and pentane was used to access lipid peroxidation in rats receiving the hepatocarcinogenic peroxisome proliferator Wy-14,643 at 0.1% in the diet. Wy-14,643 treatment from 23 to 345 days did not increase ethane or pentane exhalation. The lack of an increase in ethane exhalation from rats fed Wy-14,643 was not due to resistance to lipid peroxidation or increased metabolism of ethane since rats fed Wy-14,643 were sensitive to CCl4-induced increases in ethane exhalation and cleared exogenous ethane at rates similar to controls. Difference spectra of hepatic lipids extracted from control and Wy-14,643-treated rats showed peaks at 220 and 275 nm but no defined peak at 240 nm, the wavelength at which conjugated dienes in peroxidized lipids absorb. In contrast, injection of CCl4 ip into control rats produced dose-dependent increases in ethane exhalation at 6.25 to 100 microliters/kg and increases in hepatic conjugated dienes and serum liver enzyme activities at 200 to 1000 microliters/kg. The lack of increased ethane and pentane exhalation in combination with no detectable increase in hepatic conjugated dienes argues against increased hepatic lipid peroxidation in rats receiving a hepatocarcinogenic dose of Wy-14,643.

Alkenes↗
PubMed2006

Patterns of peroxidative ethane emission from submerged rice seedlings indicate that damage from reactive oxygen species takes place during submergence and is not necessarily a post-anoxic phenomenon.

Using ethane as a marker for peroxidative damage to membranes by reactive oxygen species (ROS) we examined the injury of rice seedlings during submergence in the dark. It is often expressed that membrane injury from ROS is a post-submergence phenomenon occurring when oxygen is re-introduced after submergence-induced anoxia. We found that ethane production, from rice seedlings submerged for 24-72 h, was stimulated to 4-37 nl gFW(-1), indicating underwater membrane peroxidation. When examined a week later the seedlings were damaged or had died. On de-submergence in air, ethane production rates rose sharply, but fell back to less than 0.1 nl gFW(-1) h(-1) after 2 h. We compared submergence-susceptible and submergence-tolerant cultivars, submergence starting in the morning (more damage) and in the afternoon (less damage) and investigated different submergence durations. The seedlings showed extensive fatality whenever total ethane emission exceeded about 15 nl gFW(-1). Smaller amounts of ethane emission were linked to less extensive injury to leaves. Partial oxygen shortage (O(2) levels <1%) imposed for 2 h in gas phase mixtures also stimulated ethane production. In contrast, seedlings under anaerobic gas phase conditions produced no ethane until re-aerated: then a small peak was observed followed by a low, steady ethane production. We conclude that damage during submergence is not associated with extensive anoxia. Instead, injury is linked to membrane peroxidation in seedlings that are partially oxygen deficient while submerged. On return to air, further peroxidation is suppressed within about 2 h indicating effective control of ROS production not evident during submergence itself.

Ethane↗
PubMed1980

Ethane production of mouse peritoneal macrophages as indication for lipid peroxidation and the effect of heavy metals.

Mouse peritoneal macrophages cultivated for 24 h produced ethane which is a new index for lipid peroxidation reactions, whereas malondialdehyde (MDA), an alternative method, did not increase. This is explained by the metabolism of MDA by macrophages after addition of MDA, whereas the gaseous ethane added remained constant. This indicates that ethane rather than MDA is a reliable parameter for lipid peroxide formation by macrophages. Divalent heavy metal ions were examined for their effect on ethane formation and on cell viability. Whereas the amount of ethane formed by macrophages in presence of CdCl2 and MnCl2 remained fairly constant, PbCl2 and ZnCl2 resulted in decreased ethane production up to 60%. But with all these metals the viability decreased much more and did not correlate with the ethane formation. With some concentrations of FeCl2 an increased ethane formation was observed which was accompanied by decreased viability of the cells. The results are consistent with the view that heavy metals interfere with the oxygen radical reactions of macrophages, and that viability of macrophages is not closely related to these oxidative reactions.

Animals↗
PubMed1994

Breath ethane generation during clinical total body irradiation as a marker of oxygen-free-radical-mediated lipid peroxidation: a case study.

Total body irradiation (TBI) is used therapeutically for treatment of leukemias and other malignancies of the hemopoietic system. Ionizing radiation produces oxygen free radicals that contribute to cytotoxicity. Breath collected from one patient undergoing therapeutic TBI showed measurable changes in levels of ethane during treatment. Breath ethane is a marker of lipid peroxidation of n-3 fatty acids. The TBI treatment involved 4 days of irradiation. The largest changes in breath ethane occurred on Day 2. The increased levels of breath ethane on Day 2 were correlated to clinical manifestations of toxicity. The correlation of the onset of gastrointestinal side effects with higher levels of breath ethane suggests that breath ethane may be a clinically useful measure of the toxicity of various TBI fractionation treatment protocols currently in use at different medical centers. The levels of breath ethane on the other days of treatment were lower, suggesting that the oxidative-antioxidative balance of the patient may be important in protection against free radical mediated injury. These results for a single patient suggest that breath ethane may be a promising approach to elucidate the role of antioxidants in clinical TBI and should be extended for verification to a larger volunteer patient population.

Adult↗
PubMed1988

Long-term effects of commercial and congeneric polychlorinated biphenyls on ethane production and malondialdehyde levels, indicators of in vivo lipid peroxidation.

Ethane exhalation was increased in male Sprague-Dawley rats following a single intraperitoneal (IP) injection of Aroclor 1254 (500 mg/kg). In the first 2 weeks following Aroclor 1254 treatment, the increase in ethane exhalation was due to an inhibition of metabolism of endogenous ethane rather than to an increase in ethane production. In weeks 3 and 4 following Aroclor 1254 administration, metabolic clearance of ethane returned to and exceeded control levels, while ethane production increased to approximately twice the control rates (day 30). The HPLC determination of in situ hepatic malondialdehyde levels revealed a 2-fold increase in malondialdehyde content on day 30 following the Aroclor 1254 injection. Further, parallel increases in in situ malondialdehyde levels and ethane production rates were also found 30 days following a single IP injection of 3,3',4,4'-tetrachlorobiphenyl, 2,3,4,4',5-pentachlorobiphenyl and 2,2',4,4',5,5'-hexachlorobiphenyl (300 mumol/kg). These effects were not reflected in increased diene conjugation. Redox state of the liver was largely unaffected, as evidenced by the relative concentrations of reduced and oxidized NADPH. However, minor changes in reduced and oxidized glutathione were noted.

Animals↗