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PubMedDate not supplied

Abnormal exhaled ethane concentrations in scleroderma.

Scleroderma (systemic sclerosis) is a chronic multisystem autoimmune disease in which oxidative stress is suspected to play a role in the pathophysiology. Therefore, it was postulated that patients with scleroderma would have abnormally high breath ethane concentrations, which is a volatile product of free-radical-mediated lipid peroxidation, compared with a group of controls. There was a significant difference (p<0.05) between the mean exhaled ethane concentration of 5.27 pmol ml(-1) CO(2) (SEM=0.76) in the scleroderma patients (n=36) versus the mean exhaled concentration of 2.72 pmol ml(-1) CO(2) (SEM=0.71) in a group of healthy controls (n=21). Within the scleroderma group, those subjects taking a calcium channel blocker had lower ethane concentrations compared with patients who were not taking these drugs (p=0.05). There was a significant inverse association between lung diffusion capacity for carbon monoxide (per cent of predicted) and ethane concentration (b=-2.8, p=0.026, CI=-5.2 to -0.35). These data support the presence of increased oxidative stress among patients with scleroderma that is detected by measuring breath ethane concentrations.

Breath Tests↗
PubMed1977

Lipid peroxidation in vivo during vitamin E and selenium deficiency in the rat as monitored by ethane evolution.

Ethane evolution was monitored from vitamin E and selenium (Se)-deficient rats to determine if lipid peroxidation occurs in vivo when these rats develop fatal organ lesions. Weanling rats were fed a vitamin E and Se-deficient, or supplemented, diet for 40 to 90 days. Each was then prefasted for 4 hours and fasting was continued for 24 to 40 hours while ethane was collected. Approximately 50% of the doubly-deficient rats died as a result of fasting. Pathological signs included hematuria, lung hemorrhage, and liver necrosis. Ethane evolution increased exponentially 10 to 20 hours before death and then declined 2 hours before death. Rats that survived (at least 5 days after ethane collection) evolved 7.4+/-1.3 nmoles ethane/100 g body weight/24 hours compared to 100+/-6 for rats that died. Supplementation of the basal diet with vitamin E (200 IU/kg), Se (0.2 ppm, as Na2SeO3), or both, completely prevented mortality and reduced ethane evolution values to 0.4+/-0.2, 3.1+/-0.4, or 0.2+/-0.2, respectively. These experiments indicate that lipid peroxidation occurs in vivo as a result of vitamin E and Se deficiency, and the peroxidation process greatly accelerates during the terminal phase of the fatal disease.

Animals↗
PubMed1974

Ethane evolution: a new index of lipid peroxidation.

Homogenates of mouse liver and brain at 37 degrees C spontaneously formed lipid peroxides and simultaneously evolved ethane. alpha-Tocopherol, a lipid antioxidant, blocked ethane formation. When mice were injected with carbon tetrachloride (a liquid prooxidant for liver), the animals produced ethane. Ethane evolution in vivo was stimulated by prior administration of phenobarbital and it was diminished by prior injection of alpha-tocopherol. These data suggest that ethane production may be a useful index of lipid peroxidation in tissue homogenates and in intact animals.

Aldehydes↗
PubMed1976

Oxidation of ethane by an Acremonium species.

Ethane oxidation was studied in ethane-grown resting cells (mycelia) of an Acremonium sp. and in cell-free preparations of such mycelia. From resting cell experiments evidence was found for a pathway of ethane oxidation via ethanol, acetaldehyde, and acetic acid. In vitro studies indicated that ethane-oxidizing activity in such mycelia occurred predominantly in the microsomal fraction of crude homogenates. Microsomal preparations were inactive in the absence of added coenzyme. Marked stimulation of activity was obtained in such preparations with reduced nicotinamide adenine dinucleotide phosphate and to a much lesser degree with nicotinamide adenine dinucleotide phosphate. Ethane oxidation was inhibited by sodium azide and carbon monoxide.

Alcohol Oxidoreductases↗
PubMed1986

Ethane production as a measure of lipid peroxidation after renal ischemia.

After renal ischemia, oxygen free radicals are formed and produce tissue injury, in large part, through peroxidation of polyunsaturated fatty acids. We used an in vivo method to monitor lipid peroxidation after renal ischemia, the measurement of ethane in expired gas, to determine the time course of lipid peroxidation and the effect of several agents to limit lipid peroxidation after renal ischemia. In anesthetized rats there was no significant increase in ethane production during 60 min of renal ischemia. During the first 10 min of renal reperfusion, there was a prompt increase in ethane production from 2.9 +/- 1.3 to 6.3 +/- 1.9 pmol/min (P less than 0.05). Ethane production was significantly increased during the first 50 min of reperfusion and then rapidly tapered to base-line levels. Preischemic administration of allopurinol to prevent superoxide radical generation or the superoxide radical scavenger superoxide dismutase prevented the increase in ethane production during postischemic reperfusion. These studies confirm that there is increase lipid peroxidation following renal ischemia that can be prevented by agents which limit the formation or accumulation of oxygen free radicals. This in vivo method for measuring lipid peroxidation could also be employed to study the effects of ischemia on lipid peroxidation in other organs, as well as to monitor lipid peroxidation in other forms of injury.

Allopurinol↗
PubMed2003

Online recording of ethane traces in human breath via infrared laser spectroscopy.

A method is described for rapidly measuring the ethane concentration in exhaled human breath. Ethane is considered a volatile marker for lipid peroxidation. The breath samples are analyzed in real time during single exhalations by means of infrared cavity leak-out spectroscopy. This is an ultrasensitive laser-based method for the analysis of trace gases on the sub-parts per billion level. We demonstrate that this technique is capable of online quantifying of ethane traces in exhaled human breath down to 500 parts per trillion with a time resolution of better than 800 ms. This study includes what we believe to be the first measured expirograms for trace fractions of ethane. The expirograms were recorded after a controlled inhalation exposure to 1 part per million of ethane. The normalized slope of the alveolar plateau was determined, which shows a linear increase over the first breathing cycles and ends in a mean value between 0.21 and 0.39 liter-1. The washout process was observed for a time period of 30 min and was modelled by a threefold exponential decay function, with decay times ranging from 12 to 24, 341 to 481, and 370 to 1770 s. Our analyzer provides a promising noninvasive tool for online monitoring of the oxidative stress status.

Adult↗
PubMed1990

Ethane production in copper-deficient rats.

Evidence is accumulating which indicates that copper-deficient animals are prone to oxidative damage. To investigate this possibility further, we measured the production of breath ethane, a hydrocarbon by-product of lipid peroxidation, in copper-deficient rats. Male, weanling Sprague-Dawley rats were fed either a purified diet which was deficient in copper (CuD) or the same diet made sufficient with 5 ppm of copper (CuS). After 33 to 34 days the rats were placed individually in gastight metabolic cages through which ethane-free air or 100% O2 was passed. Expired ethane was absorbed onto cold, activated charcoal, liberated by heating, and measured by gas chromatography. Ethane production rates (pmoles/min/100 g +/- SD) were 3.3 +/- 0.8 (CuS-air), 4.3 +/- 1.4 (CuD-air), 8.3 +/- 2.5 (CuS-O2), and 12.2 +/- 4.3 (CuD-O2). Repeated measures analysis of variance indicated that both copper deficiency (P less than 0.01) and breathing 100% O2 (P less than 0.0001) enhanced ethane production, with no interaction between treatments. This finding complements previous evidence that increased lipid peroxidation occurs in copper-deficient rats.

Animals↗
PubMedDate not supplied

Ethene (ethylene) and ethane exhalation in Ni[II]-treated rats, using an improved rebreathing apparatus.

To assess the effects of NiCl2 on lipid peroxidation, exhalation rates of ethene (ethylene) and ethane were measured in Fischer-344 rats, using modifications of a recently published rebreathing apparatus and gas chromatographic assay. Technical improvements included more efficient removal of H2O vapor, NH3, and CO2, use of economical, readily available components, convenient standardization procedure, and no necessity for a charcoal concentrator accessory for the gas chromatograph. The detection limit was one pmol ethene or ethane per five mL air sample; the within-run precision (CV) of analysis was 2.1 percent at an ethane concentration of 16 pmol per five mL sample. A minimum of eight hours post-injection was necessary for exhalation rates of ethene or ethane to become significantly increased in NiCl2-treated rats. Ethene exhalation rate was increased 2.0- to 3.5-fold at 13 to 16 and 20 to 23 hours after NiCl2 injection (0.50 or 0.75 mmol per kg, body wt, sc). Ethane exhalation rate was increased 1.5- to 1.6-fold at the lower dosage, but was not significantly increased at the higher dosage of NiCl2. This study corroborates previous reports that lipid peroxidation is enhanced in target tissues (liver, kidney, lung) of NiCl2-treated rats.

Animals↗
PubMed1989

Characterization of new bacterial transformation products of 1,1,1-trichloro-2,2-bis-(4-chlorophenyl) ethane (DDT) by gas chromatography/mass spectrometry.

The microbial transformation of DDT, DDD and DDE was studied in Gram-negative strain B-206 and a number of phenolic metabolites were identified as the trimethylsilyl derivatives in the bacterial extracts by gas chromatography/mass spectrometry. The major metabolites of DDT were DDD, DDE, DDMU, 1,1,1-trichloro-2-(2-hydroxy-4-chlorophenyl)-2-(4'-chlorophenyl) ethane, 1,1,1-trichloro-2-(2-hydroxy-4-chlorophenyl)-2-(4'-hydroxyphenyl) ethane, and 1,1,1-trichloro-2,2-bis-(2-hydroxy-4-chlorophenyl) ethane. Conversely, DDD was mainly degraded into DDE, 1,1-dichloro-2-(2-hydroxy-4-chlorophenyl)-2-(4'-chlorophenyl) ethane and 1,1-dichloro-2-(2-hydroxy-4-chlorophenyl)-2-(4'-hydroxyphenyl) ethane. Finally, DDE was transformed into DDMU, 1,1-dichloro-2-(2-hydroxy-4-chlorophenyl)-2-(4'-chlorophenyl) ethylene, 1,1-dichloro-2-(2-hydroxy-4-chlorophenyl)-2-(4'hydroxyphenyl) ethylene and 1-chloro-2-(2-hydroxy-4-chlorophenyl)-2-(4'-chlorophenyl) ethylene. The phenolic metabolites exhibited [M - TMSCl]+., [M - HCl - TMSCl]+. and/or [M - HCl - TMSCl - Me]+ fragment ions which reflect the presence of an ortho hydroxyl group in these molecules. Other mass spectral features used to determine their structure are presented and a metabolic scheme accounting for their formation is proposed.

Bacteria↗
PubMed1987

Ultrastructural analysis of the effect of ethane dimethanesulphonate on the testis of the rat, guinea pig, hamster and mouse.

The morphological response of the testis of rats, guinea pigs. Syrian hamsters and mice to treatment with the cytotoxin ethane dimethanesulphonate was examined using light and electron microscopy. One to two days after a single administration of ethane dimethanesulphonate to adult rats, guinea pigs, and hamsters, the Leydig cells showed marked ultrastructural alterations suggestive of degeneration and cell death. The former alterations included karyopyknosis, cytoplasmic vesiculation and accumulation of lipid inclusions and large lipofuscin bodies. Fragments of necrotic Leydig cells were often engulfed by the interstitial tissue macrophages. The morphology of the seminiferous epithelium of these three species was unchanged from the morphology observed in vehicle-injected control animals. In contrast, multiple injections of ethane dimethane-sulphonate given to mice produced no ultrastructural alternation to Leydig cells yet the seminiferous epithelium exhibited disruption of spermatogenesis. Although the Leydig cells of the mouse appear resistant to ethane dimethanesulphonate, this agent exerts a selective cytotoxic action upon leydig cells of the rat, guinea pig and hamster thus identifying ethane dimethanesulphonate as a useful chemical for future endocrine and physiological studies of testicular function in three common laboratory species.

Acrylates↗
PubMed2005

Copper(II) complexes of a series of polypyridine ligands possessing a 1,2-bis(2-pyridyl)ethane common moiety: incorporation and hydrolysis of phosphate esters.

Two tetradentate ligands 1,2-bis[2-((dimethylamino)methyl)-6-pyridyl]ethane (L1) and 1,2-bis[2-(N-piperidinomethyl)-6-pyridyl]ethane (L2) and a hexadentate ligand 1,2-bis(2-((methyl(pyridylmethyl)amino)methyl)-6-pyridyl)ethane (L3) were prepared as part of a series of new polypyridine ligands possessing a 1,2-bis(2-pyridyl)ethane common moiety. L1 and L2 form mononuclear Cu(II) complexes [Cu(L)(Cl)](ClO4) [L = L1 (1) and L2 (2)], respectively. L3 forms a dinuclear Cu(II) complex [Cu2(L3)((PhO)2PO2)2](ClO4)2 (3) or a hexanuclear Cu(II) complex [Cu6(L3)3((PhO)PO3)4](ClO4)4 (4) in the presence of (PhO)2PO2- monoanion or (PhO)PO3(2-) dianion, respectively. The structures of 1-4 were determined by X-ray analysis. The structures in solution were investigated by means of FAB and CSI MS spectrometers. The structural flexibility of the common 1,2-bis(2-pyridyl)ethane moiety and of the pendant groups allows complexes 1-4 to adapt to the various structures. Each Cu ion in 1 and 2 adopts a square pyramidal geometry with one Cl ion and two pendant groups (L1 and L2) binding in a bis-bidentate chelate mode. There is no steric repulsion between the pendant groups, so that the ligands specifically stabilize the mononuclear structures. L3 binds two Cu(II) ions with two pendant groups in tridentate chelate modes and, with the incorporation of phosphate esters, various dinuclear units are formed in 3 and 4. In 4, a dinuclear unit of [Cu2(L3)]4+ links two dinuclear units of [Cu2(L3)(PhOPO3)2] with four (mu3)-1,3-PhOPO3(2-) bridges. The hydrolytic activity of 2 and a dicopper(II) complex of L3 was examined with tris(p-nitrophenyl) phosphate (TNP) as a substrate.

Journal Article↗
PubMed2006

Unusual infrared spectrum of ethane adsorbed by gallium oxide.

The present study reports an unusual diffuse reflection Fourier transform (DRIFT) spectrum of ethane adsorbed by gallium oxide. One of the stretching C-H bands in this spectrum with a maximum at 2753 cm(-1) is more than by 100 cm(-1) shifted toward lower frequencies in comparison with gaseous ethane. In addition, the relative intensity of this band is unusually high. This indicates a very strong polarizability of the corresponding chemical bonds resulting from perturbation of ethane by the low coordinated Ga(3+) cations. The assignment of this band to the very strongly perturbed initially fully symmetric nu(1) C-H stretching vibration is confirmed by a DFT modeling of ethane adsorption by the simplest Ga(2)O(3) cluster. The obtained results also indicate heterolytic dissociative adsorption and dehydrogenation of ethane by Ga(3+) Lewis sites at elevated temperature. This is evidenced by the appearance of new IR bands from zinc alkyl fragments and acidic protons followed by decomposition of resulting zinc ethyl species. In parallel, the most intense IR band at lower frequency from the most strongly polarized C-H chemical bond decreased in intensity. The obtained results indicate that these vibrations are involved in subsequent heterolytic dissociative adsorption. The obtained results demonstrate that, similar to the shifts of C-H stretching vibrations to the low-frequency, intensities of IR C-H stretching bands can be also used as an index of chemical activation of adsorbed paraffins via their polarization by the low-coordinated cations.

Journal Article↗
PubMed2001

Hyperconjugation not steric repulsion leads to the staggered structure of ethane.

Many molecules can rotate internally around one or more of their bonds so that during a full 360 degrees rotation, they will change between unstable and relatively stable conformations. Ethane is the textbook example of a molecule exhibiting such behaviour: as one of its two methyl (CH3) groups rotates once around the central carbon-carbon bond, the molecule will alternate three times between an unstable eclipsed conformation and the preferred staggered conformation. This structural preference is usually attributed to steric effects; that is, while ethane rotates towards an eclipsed structure, the electrons in C-H bonds on the different C atoms are drawing closer to each other and therefore experience increased repulsion, introducing a rotation barrier that destabilizes the eclipsed structure. Stabilization of the staggered structure through rotation-induced weakening of the central C-C bond and hyperconjugation has been considered to be involved, but evaluation of the contributions of these effects to ethane's internal rotation barrier and conformational preference remains difficult. Here we report a series of ethane structure optimizations, where successive removal of different interactions indicates that ethane's staggered conformation is the result of preferential stabilization through hyperconjugation. Removal of hyperconjugation interactions yields the eclipsed structure as the preferred conformation, whereas repulsive forces, either present or absent, have no influence on the preference for a staggered conformation.

Journal Article↗
PubMed2000

The effect of raloxifene on the uterine weight response in immature mice exposed to 17beta-estradiol, 1,1,1-trichloro-2, 2-bis(p-chlorophenyl)ethane, and methoxychlor.

OBJECTIVE: The purpose of this study was to determine the effects of raloxifene on the uterine responses to both estradiol and the environmental estrogens 1,1,1-trichloro-2, 2-bis(p-chlorophenyl)ethane and methoxychlor in immature mice. STUDY DESIGN: Immature female mice received the following compounds alone or in combination: sesame oil (control), 17beta-estradiol 1 mg/kg body weight, tamoxifen 1 mg/kg body weight, raloxifene 5 mg/kg body weight, 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane 10 mg/kg body weight, and methoxychlor 10 mg/kg body weight. The animals were treated subcutaneously once a day for 5 consecutive days with the compound or compounds of interest in 0.1 mL sesame oil. Approximately 24 hours after the final treatment the animals were killed and the uteri were excised, stripped of remaining fat and mesentery, and weighed. Groups were analyzed with analysis of variance. RESULTS: Estradiol increased the mean (+/-SE) weight from 20 +/- 6.4 mg (as measured in the control group) to 77 +/- 6.2 mg. Tamoxifen increased uterine weight to 60 +/- 6.2 mg; however, raloxifene had no effect on uterine weight. Both 1,1,1-trichloro-2, 2-bis(p-chlorophenyl)ethane and methoxychlor increased uterine weight significantly, to 82 +/- 2.4 mg and 35 +/- 6.0 mg respectively. When raloxifene was coadministered with 17beta-estradiol it did not block the increase in uterine weight; however, when raloxifene was coadministered with 1,1,1-trichloro-2, 2-bis(p-chlorophenyl)ethane or methoxychlor, it completely blocked the uterine weight gain induced by either xenoestrogen. CONCLUSION: Raloxifene blocked the xenoestrogens 1,1,1-trichloro-2, 2-bis(p-chlorophenyl)ethane and methoxychlor but did not block 17beta-estradiol in the mouse model described. These results suggest that the xenoestrogens exert their estrogenic activities through a different site on the estrogen receptor or through a different mechanism than 17beta-estradiol.

Animals↗
PubMed1977

Isolation and Identification of the Precursor of Ethane in Phaseolus vulgaris L.

Ethane production by homogenates of Phaseolus vulgaris L. cv. Harvester was studied. The precursor of ethane was identified as linolenic acid. The liberation of ethane was optimum at pH 4.2 and was highest from homogenates of leaves and apical buds. When roots were homogenized in linolenic acid solution, ethane and ethylene production were stimulated. In corn root homogenates, ethylene biosynthesis was stimulated nearly 8-fold by linolenic acid. The enzyme responsible for ethane production from oat root homogenates was soluble and had a high molecular weight.

Journal Article↗
PubMed1979

Emission of ethylene and ethane by leaf tissue exposed to injurious concentrations of sulfur dioxide or bisulfite ion.

Leaf tissues injured with SO(2) gas or bisulfite ion in solution emit ethylene and ethane. The amounts of these gases produced by the tissues depend on the degree of exposure to SO(2) or bisulfite. The amount of ethylene produced in response to SO(2) fumigation correlates positively with SO(2) exposure (0 to 5.5 microliters per liter for 16 hours), SO(2) absorbed, and the amount of visible injury sustained by the leaf tissues. Ethane production is correlated positively with the injury resulting from treatment with bisulfite ion. The rate of emission of ethane from leaf discs of cucurbit cultivars as a result of exposure to bisulfite solutions is in agreement with the order and the degree of their resistance to injury by SO(2). Thus, exposure to bisulfite and the subsequent release of ethane can be used to determine the relative resistance of different species and cultivars to SO(2) gas.A rapid, simple, objective assay for SO(2) resistance based on ethane emission is described. This assay should preferentially detect SO(2) resistance which does not depend on stomatal behavior. The screening of several other cucurbits with this assay showed a 24-fold difference between the most and the least sensitive plants tested.

Journal Article↗
PubMed1981

Microbial formation of ethane in anoxic estuarine sediments.

Estuarine sediment slurries produced methane and traces of ethane when incubated under hydrogen. Formation of methane occurred over a broad temperature range with an optimum above 65 degrees C. Ethane formation had a temperature optimum at 40 degrees C. Formation of these two gases was inhibited by air, autoclaving, incubation at 4 and 80 degrees C, and by the methanogenic inhibitor, 2-bromoethanesulfonic acid. Ethane production was stimulated by addition of ethylthioethanesulfonic acid, and production from ethylthioethanesulfonic acid was blocked by 2-bromoethanesulfonic acid. A highly purified enrichment culture of a methanogenic bacterium obtained from sediments produced traces of ethane from ethylthioethanesulfonic acid. These results indicate that the small quantities of ethane found in anaerobic sediments can be formed by certain methanogenic bacteria.

Journal Article↗
PubMed1987

In vivo ethane production in vitamin E-deficient rats with DMH-induced colon cancer.

The effect of both a vitamin E-deficient and a high polyunsaturated fat (PUFA) diet was tested on rats injected with the colon carcinogen 1,2-dimethylhydrazine (DMH). In vivo lipid peroxidation was monitored by measuring exhaled ethane from the animals. Higher mean weights were found in animals fed high PUFA and vitamin E-sufficient diets. There was no difference in ethane exhalation between DMH-treated and control animals regardless of diet. Mean ethane exhalation was highest in animals fed either vitamin E-deficient or high PUFA diets. There was no difference in tumor formation between the vitamin E-deficient and the vitamin E-sufficient groups. The high PUFA groups had more tumors than the low PUFA groups. Diet was shown to be the major factor affecting ethane exhalation. There was no evidence that vitamin E-deficiency promoted DMH-induced tumors or that DMH caused increased lipid peroxidation.

1,2-Dimethylhydrazine↗