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PubMed1977

Effect of dietary vitamin E on expiration of pentane and ethane by the rat.

An analytical method for the measurement of hydrocarbon gases in the breath of rats is described. The method was used to follow the expiration in rat breath of in vivo formed scission products of hydroperoxides. The major products are pentane from the linoleic acid family and ethane from the linolenic acid family. Rats were fed 0, 11 or 40 i.u. vitamin E acetate/kg diet for 7 wk starting at age 21 days. Data obtained by gas chromatographic analysis of breath samples were analyzed by the Mann-Whitney nonparametric U-test. This statistical analysis showed that pentane evolved by the group of rats not supplemented with vitamin E was significantly higher during the period 1-7 wk than that evolved by either of the two supplemented groups of rats. Ethane from the nonsupplemented group was significantly higher than that from the group supplemented with 40 i.u. vitamin E/kg of diet by 5 wk, and significantly high than both supplemented groups by 6 wk. By 7 wk, pentane production was tenfold greater in the non-supplemented group, and ethane was about twofold greater. There was no significant difference between the groups supplemented with 11 and 40 i.u. vitamin E/kg diet for either ethane or pentane. This new technique, which measures scission products from in vivo lipid peroxidation, promises to be useful for application to many experimental areas where lipid peroxidation is expected or known to occur.

Administration, Oral↗
PubMed1978

Ethane and ethylene formation by mitochondria as indication of aerobic lipid degradation in response to wounding of plant tissue.

During aerobic incubation of potato slices or potato mitochondria at acidic pH, ethane and ethylene in a ratio of approx. 50 : 1 are generated from an endogenous substrate. Both ethane and ethylene production are stimulated by the addition of alpha-linolenic acid. Ethane formation from linolenic acid is a radical mechanism dependent on oxygen and is not significantly influenced by mitochondrial electron transport. Ethane production may represent a sensitive marker for membrane damage.

Chloroplasts↗
PubMed1986

Inverse relationship of ethane or n-pentane and malondialdehyde formed during lipid peroxidation in rat liver microsomes with different oxygen concentrations.

When we incubated rat liver microsomes with ferrous ions and an NADPH-regenerating system, ethane and n-pentane formation increased correspondingly with decreasing concentrations of oxygen in the atmosphere above the incubation, whereas malondialdehyde increased with increasing oxygen concentrations up to a plateau. At very low oxygen concentrations - 100% helium as atmosphere, but presumably traces of oxygen were present in the microsomes - ethane and n-pentane formation were maximal and dependent on the concentrations of ferrous ions, in the case of ethane, a peak being reached at about 20 microM Fe2+, whereas n-pentane continuously increased with increasing concentrations of Fe2+. It is suggested that the inverse relationship of ethane or n-pentane and malondialdehyde is due to two different reaction sequences of microsomal lipid peroxidation with different oxygen sensitivities.

Animals↗
PubMed1983

Drug-induced lipid peroxidation in mice--V. Ethane production and glutathione release in the isolated liver upon perfusion with acetaminophen.

Isolated liver from phenobarbital-induced male mice was perfused using infusions of cytochrome c pulses as quality control of the system. Livers spontaneously evolved 1.1 pmoles ethane g-1 liver min-1, exogenous pentane disappeared with 0.6 pmoles g-1 min-1. Infusion of 0.26 mmoles/l. FeCl2 led to immediate ethane production followed later on by lactate dehydrogenase release from the liver. Infusion of acetaminophen resulted in hepatic ethane production at drug concentrations greater than 0.1 mmoles/l. A maximum effect was observed at 2 mmoles/l. of acetaminophen infused while higher concentrations, up to 10 mmoles/l. delayed ethane release although they enhanced the rate of glutathione depletion. This glutathione efflux decreased from 12 nmoles/g-1 min-1 observed after perfusion of medium alone to 2.9 nmoles/g-1 min-1 when AAP was infused. The slope of the pseudo first order depletion kinetics depended on the acetaminophen concentrations. This glutathione release represents the perisinusoidal portion of the total efflux measured here independently from the biliary secretion. The results show that in agreement with the in vivo findings acute intoxication of liver with high doses of this drug lead to lipid peroxidation, while in vitro an apparent antioxidative effect was measured. The implications for drug screening are probably important.

Acetaminophen↗
PubMed1983

Inhibition of ethanol- and aldehyde-induced release of ethane from isolated perfused rat liver by pargyline and disulfiram.

Acute addition of ethanol or acetaldehyde to the isolated, perfused rat liver leads to an increase in ethane and n-pentane release. These volatile hydrocarbons are known to originate from the peroxidation of polyunsaturated fatty acids. The effects are half-maximal at 0.5 mM ethanol or 20 microM acetaldehyde in the entering perfusate. Propionaldehyde and benzaldehyde are also able to elicit ethane release. Pargyline and disulfiram, inhibitors of aldehyde oxidation, inhibited the extra ethane release in all cases. The inhibitory effect of pargyline is suppressed during addition of metyrapone. The study indicates that the oxidation of acetaldehyde and not of ethanol itself is the step responsible for increased ethane formation by the perfused rat liver during ethanol infusion.

Acetaldehyde↗
PubMedDate not supplied

Ethane formation of isolated rat hepatocytes due to carbon tetrachloride.

Isolated rat hepatocytes incubated aerobically formed measurable amounts of ethane, a parameter for lipid peroxidation. This ethane formation increased several-fold due to carbon tetrachloride (CCl4) depending on its concentration. Cell damage as measured by trypan blue uptake and lactate dehydrogenase release poorly correlated with ethane formation. Ethane was not metabolized, whereas malondialdehyde (MDA), when added to isolated hepatocytes, decreased very rapidly. The results indicate that rather than MDA is a reliable parameter for lipid peroxidation occurring in isolated hepatocytes, and that a simple relationship between CCl4-induced lipid peroxidation and cell damage is not existing in isolated hepatocytes.

Animals↗
PubMed1999

A practical and reliable method for measuring ethane and pentane in expired air from humans.

We describe a method for the collection of expired air and further document the performance of our analytical technique that is used to measure ethane and pentane simultaneously. Four minutes of breathing hydrocarbon-free air before collection effectively removed high concentrations of residual ambient ethane and pentane from the lungs, with washout times up to 30 min resulting in no further reductions in breath hydrocarbons. Mean (+/-SE) exhalation rates (pmol/kg b.wt./min) in 11 subjects were 2.4 +/- 0.6 for ethane and 1.5 +/- 1.3 for pentane. Total intraindividual variability in exhalation rates (as percent coefficient of variation, %CV), measured from 4 subjects on at least 6 different days, was greater for pentane (44% CV) than for ethane (29% CV). Analytical variability contributed 6% to the total %CV. Advantages of the method are described, and reasons for the large variability in values reported in the literature are discussed.

Adult↗
PubMed2000

Methods for measuring ethane and pentane in expired air from rats and humans.

Numerous studies in animals and humans provide evidence that ethane and pentane in expired air are useful markers of in vivo lipid peroxidation. The measurement of breath hydrocarbons, being noninvasive, is well suited for routine use in research and clinical settings. However, the lack of standardized methods for collecting, processing, and analyzing expired air has resulted in the use of a wide variety of different methods that have yielded highly disparate results among investigators. This review outlines the methods that we have developed and validated for measuring ethane and pentane in expired air from rats and humans. We describe the advantages of these methods, their performance, as well as potential errors that can be introduced during sample collection, concentration, and analysis. A main source of error involves contamination with ambient-air ethane and pentane, the concentrations of which are usually much greater and more variable than those in expired air. Thus, it appears that the effective removal of ambient-air hydrocarbons from the subject's lungs before collection is an important step in standardizing the collection procedure. Also discussed is whether ethane or pentane is a better marker of in vivo lipid peroxidation.

Animals↗
PubMed2005

Direct observation of surface ethyl to ethane interconversion upon C2H4 hydrogenation over Pt/Al2O3 catalyst by time-resolved FT-IR spectroscopy.

Time-resolved FT-IR spectra of ethylene hydrogenation over alumina-supported Pt catalyst were recorded at 25 ms resolution in the temperature range of 323-473 K using various H2 concentrations (1 atm total gas pressure). Surface ethyl species (2870 and 1200 cm(-1)) were detected at all temperatures along with the gas-phase ethane product (2954 and 2893 cm(-1)). The CH3CH2Pt growth was instantaneous on the time scale of 25 ms under all experimental conditions. At 323 K, the decay time of surface ethyl (122 +/- 10 ms) coincides with the rise time of ethane (144 +/- 14 ms). This establishes direct kinetic evidence for surface ethyl as the relevant reaction intermediate. Such a direct link between the temporal behavior of an unstable surface intermediate and the final product in a heterogeneous catalytic system has not been demonstrated before. A fraction (25%) of the asymptotic ethane growth at 323 K is prompt, indicating that there are surface ethyl species that react much faster than the majority of the CH3CH2Pt intermediates. The dispersive kinetics is attributed to the varying strength of interaction of the ethyl species with the Pt surface caused by heterogeneity of the surface environment. At 473 K, the majority of ethyl intermediates are hydrogenated prior to the recording of the first time slice (24 ms), and a correspondingly large prompt growth of ethane is observed. The yield and kinetics of the surface ethylidyne are in agreement with the known spectator nature of this species.

Aluminum Oxide↗
PubMed1983

Ethane release during metabolism of aldehydes and monoamines in perfused rat liver.

Infusion of aldehyde such as acetaldehyde, propionaldehyde or benzaldehyde to perfused rat liver leads to an increase in hepatic ethane production. Half-maximal effect was obtained with about 20 microM acetaldehyde, a concentration range found in plasma during ethanol metabolism. Compounds which metabolically generate aldehydes such as monoamines (benzylamine, phenylethylamine) as substrates for monoamine oxidase or ethanol as substrate for alcohol dehydrogenase [A. Müller and H. Sies (1982) Biochem. J. 206, 153-156] are also able to elicit ethane release. Results obtained with inhibitors of hepatic aldehyde metabolism (pargyline or cyanamide) or of monamine oxidase (pargyline or tranylcypromine) suggest that metabolism of the aldehydes is required for ethane production. Radical scavenging by the addition of the flavonoid, cyanidanol, or by pretreatment with vitamin E (alpha-tocopherol) abolished ethane release, in agreement with lipid peroxidation as a source of alkane production during aldehyde metabolism.

Aldehyde Dehydrogenase↗
PubMed1983

Lipid peroxidation in the newborn rat: influence of fasting and hyperoxia on ethane and pentane in expired air.

The rate of lipid peroxidation, as determined by expired air pentane and ethane measurements, was assessed in suckled or fasted newborn rats exposed to air or hyperoxia (FIO2 greater than 0.95). Pentane and ethane production in suckled newborn rats did not significantly change with exposure to hyperoxia after birth. Pentane production averaged over a 3-day exposure period was 2.8 pmol/100 g/min in hyperoxia versus 2.5 pmol/100 g/min in air. However, significant increases in ethane production occurred in fasted newborn rats over the first 18 h of life (less than 2.5 pmol/100 g/min increasing to greater than 6 pmol/100 g/min), which were not observed in suckled animals. Although hyperoxia did not cause an increase in pentane or ethane production above air-exposed controls, nutritional deprivation in newborn rats appeared to accelerate lipid peroxidation events and resulted in high mortality in newborn rats exposed to hyperoxia.

Animals↗
PubMed1991

Utility of breath ethane as a noninvasive biomarker of vitamin E status in children.

The purpose of our study was to determine if the ethane content of expired air could be a useful index of vitamin E status in children. Eight children with vitamin E deficiency secondary to chronic severe liver disease were studied: six of these children were treated with parenteral vitamin E (2-5 mg/kg/dose every 4-7 d). Measures of vitamin E status pre- and posttherapy were: serum vitamin E, 2 +/- 1 versus 7 +/- 1 micrograms/mL (p less than 0.001); serum vitamin E:total lipids, 0.3 +/- 0.1 versus 1.0 +/- 0.1 mg/g (p less than 0.001); and erythrocyte peroxide hemolysis test, 80 +/- 10 versus 6 +/- 12% (p less than 0.001). Fasting breath ethane in the patients pre- and posttherapy was 78 +/- 10 versus 31 +/- 11 pmol/kg/min (p less than 0.001). Breath ethane correlated negatively with serum vitamin E (p less than 0.042) and serum E:total lipids (p less than 0.004) and positively with the erythrocyte peroxide hemolysis test (p less than 0.003). Values for treated patients did not differ from those for fasted sibling controls (34 +/- 12 pmol/kg/min), postprandial sibling controls (31 +/- 12 pmol/kg/min), and healthy children sampled randomly, in the nonfasted state (21 +/- 14 pmol/kg/min). Breath ethane production in one patient (up to 168 pmol/kg/min) did not normalize after treatment of vitamin E deficiency until her selenium deficiency was corrected as well. We conclude that this noninvasive test can be useful as a screen for vitamin E deficiency in children and for ascertaining response to therapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMedDate not supplied

Chlorophyll photobleaching and ethane production in dichlorophenyldimethylurea- (DCMU) or paraquat-treated Euglena gracilis cells.

Light dependent (35 Klux) chlorophyll bleaching in autotrophically grown Euglena gracilis cells at slightly acidic pH (6.5-5.4) is stimulated by the photosystem II blockers DCMU and DBMIB (both 10(-5) M) as well as by the autooxidizable photosystem I electron acceptor, paraquat (10(-3) M). Chlorophyll photobleaching is accompanied by the formation of thiobarbituric acid -- sensitive material ("malondialdehyde") and ethane. Both chlorophyll photobleaching and light dependent ethane formation are partially prevented by higher concentrations (10(-4) M) of the autooxidizable photosystem II electron acceptor DBMIB or by sodium bicarbonate (25 mM). In vitro studies with cell free extracts (homogenates) from E. gracilis suggest that alpha-linolenic acid oxidation by excited (reaction center II) chlorophyll represents the driving force for both ethane formation and chlorophyll bleaching. Ethane formation thus appears to be a sensitive and non-destructive "in vivo" marker for both restricted energy dissipation in photosystem II and, conditions yielding reactive oxygen species at the reducing side of photosystem I.

Chlorophyll↗
PubMed2004

Reduction of halogenated ethanes by green rust.

Green rusts, mixed Fe(II)/Fe(III) hydroxide minerals present in many suboxic environments, have been shown to reduce a number of organic and inorganic contaminants. The reduction of halogenated ethanes was examined in aqueous suspensions of green rust, both alone and with the addition of Ag(I) (AgGR) and Cu(II) (CuGR). Hexachloroethane (HCA), pentachloroethane (PCA), 1,1,1,2-tetrachloroethane (1,1,1,2-TeCA), 1,1,2,2-tetrachloroethane (1,1,2,2-TeCA), 1,1,1-trichloroethane (1,1,1-TCA), 1,1,2-trichloroethane (1,1,2-TCA), 1,1-dichloroethane (1,1-DCA), and 1,2-dibromoethane were reduced in the presence of green rust alone, AgGR, or CuGR; only 1,2-dichloroethane and chloroethane were nonreactive. The reduction was generally more rapid for more highly substituted ethanes than for ethanes having fewer halogen groups (HCA > PCA > 1,1,1,2-TeCA > 1,1,1-TCA > 1,1,2,2-TeCA > 1,1,2-TCA > 1,1-DCA), and isomers with the more asymmetric distributions of halogen groups were more rapidly reduced than the isomer with greater symmetry (e.g., 1,1,1-TCA > 1,1,2-TCA). The addition of Ag(I) or Cu(II) to green rust suspensions resulted in a substantial increase in the rate of halogenated ethane reduction as well as significant differences in the product distributions with respect to green rust alone.

Ethane↗
PubMed1992

Are ethane and pentane evolution and thiobarbituric acid reactivity specific for lipid peroxidation in erythrocyte membranes?

Peroxidation of human erythrocyte membranes was followed in vitro with head space analysis of ethane and pentane and a thiobarbituric acid assay in a standardized system liberating free oxygen radicals. Simultaneously, the decrease of the membrane palmitic, linoleic, arachidonic and docosahexaenoic acid was monitored. The recoveries of the peroxidation products of the red cell ghost preparations were compared with those obtained by peroxidation of pure fatty acids. Experiments using purified fatty acids revealed that ethane was preferentially produced from docosahexaenoic and linolenic, and pentane from linoleic and arachidonic acids. Thiobarbituric acid-reactive material (TBAR) was produced from each unsaturated fatty acid tested, but the amount was dependent on the number of carbon chain double bonds. During peroxidation of the erythrocyte ghosts, 72% of ethane and 51% pentane were produced during the first 12 h of incubation, whereas TBAR was produced at a constant rate throughout the 36-h test period. Hydrocarbon and TBAR production were similarly inhibited by desferoxamine (at p less than 0.005 and p less than 0.0001, respectively). The total recoveries of ethane, pentane and TBAR exceeded the amount expected by 7.8-, 1.4- and 5.5-fold, respectively. It was concluded that measurement of pentane is a reliable method to monitor lipid peroxidation during oxidative damage of the erythrocyte membrane.

Erythrocyte Membrane↗
PubMed1980

Acute adriamycin treatment of rats does not increase ethane expiration.

Adriamycin (20 and 45 mg/kg) was injected i.p. to rats and the amount of ethane expired, which indicates lipid peroxidation in vivo, was determined. None of the doses applied resulted in significant increased ethane expiration of the animals as measured immediately, on the second or on the third day after treatment. Only with 45 mg adriamycin/kg a small increase of ethane formation could be observed on the second day after treatment. But some rats died during the experimental period. The treatment with 65 mg adriamycin/kg i.p. was lethal within 24 h, although an increased ethane production was not measurable. Our data suggest that lipid peroxidation is probably not occurring during metabolism of adriamycin in the rat, and that it is not responsible for the acute toxicity observed after adriamycin treatment.

Animals↗
PubMed1995

Ethane exhalation and vitamin E/ubiquinol status as markers of lipid peroxidation in ferrocene iron-loaded rats.

Organ damage caused by iron overload has been mostly attributed to iron-induced peroxidation of membrane lipids. Using the ferrocene iron-loaded rat model, we studied ethane exhalation as a direct marker of in vivo lipid peroxidation, as well as concentrations of alpha-tocopherol and ubiquinol 9/10 in liver and plasma as indirect markers of this process. The feeding of a diet enriched with 0.5% TMH-ferrocene up to 31 weeks resulted in a large increase in liver iron concentration to about 25 mg/g wet weight (w wt). At lower, predominantly hepatocellular liver siderosis, the breath ethane exhalation was dependent on dietary vitamin E (VitE) supplements (onset of ethane exhalation at liver-Fe > 2 mg/g w wt on vitE-restricted diet; > 5 mg Fe per gram on VitE-replete diet). At severe liver siderosis, breath ethane exhalation reached a maximum of approximately 8 nmol/kg/hr independent of VitE supplementation. Plasma as well as hepatic alpha-tocopherol decreased with progressive iron loading. In addition, a significant depletion in hepatic ubiquinol 9 and 10 was noted.

Animals↗
PubMed1986

Enhanced formation of ethane and n-pentane by rat hepatocytes in the presence of dimethyl sulfoxide.

Incubation of rat hepatocytes with 14 mM dimethyl sulfoxide (DMSO) produced an increase in the formation of ethane, measured by capillary column gas chromatography, to 18.0 pmoles/hr/10(7) cells from 11.2 pmoles/hr/1-(7) cells from 5.6 pmoles/hr/10(7) cells in control hepatocytes. This was about one-third the stimulation of ethane and n-pentane formation produced by incubation of hepatocytes with 13 mM carbon tetrachloride. DMSO-stimulated ethane and n-pentane formation was inhibited up to 63% by 0.1 microM alpha-tocopherol and up to 89% by N2. Formation of dimethylsulfide from DMSO by hepatocytes was the same in air and N2. DMSO increased methane production by hepatocytes to 31.3 pmoles/hr/10(7) cells from 6.9 pmoles/hr/10(7) cells in control hepatocytes. Although DMSO apparently stimulated lipid peroxidation by hepatocytes, as measured by ethane and n-pentane formation, there was no increase in the formation of thiobarbituric acid reactive material. DMSO was not toxic to hepatocytes, measured by release of cytosolic lactate dehydrogenase, over a 2-hr incubation. Possible mechanisms for the increase in alkane formation by DMSO are discussed.

Animals↗