Increase In Ethane Production Research Articles

Ethane-Based Enhanced Oil Recovery: An Innovative and Profitable Enhanced-Oil-Recovery Opportunity for a Low-Price Environment

Summary This paper summarizes the current state of the ethane industry in the United States (US) and explores the opportunity for using ethane for enhanced oil recovery (EOR). We show both simulation data and field examples to demonstrate that ethane is an excellent EOR injectant. After decades of research and field application, the use of carbon dioxide (CO2) as an EOR injectant has proved to be very successful. However, there are limited supplies of low-cost CO2 available, and there are also significant drawbacks, especially corrosion, involving its use. The rich gases and volatile oils developed by horizontal drilling and fracturing in the shale reservoirs have brought about an enormous increase in ethane production. Ethane prices have dropped substantially. In the US, ethane is no longer priced as a petrochemical feedstock, but is priced as a fuel. Also, substantial quantities of ethane are currently being flared. Ethane-based EOR can supplement the very successful CO2-based EOR industry in the US. There simply is not enough low-cost CO2 available to undertake all the potential gas EOR projects in the US. The current abundance of low-cost ethane presents a significant opportunity to add new gas EOR projects. The ethane-based EOR opportunity can be summarized as follows: CO2-based EOR works well, and is well-understood. Ethane has more solubility in oil, lower minimum miscibility pressures (MMPs), and better solvent efficiency than CO2. Ethane is operationally simpler than CO2 for EOR. Ethane is now inexpensive, and will likely stay inexpensive. Ethane-based EOR has become a viable option in the Lower 48 (lower 48 states in US). Large volumes of low-cost ethane are available. Recent additions to the growing ethane infrastructure now deliver ethane to locations where ethane-based EOR targets are plentiful.

Effect of oxygen concentration on production of ethane and thiobarbituric acid‐reactive substances by peroxidizing lung and liver homogenates and formation of ethanol by peroxidizing docosahexaenoic acid preparations under hyperoxic conditions

The oxygen dependence of ethane formation was investigated in rat lung and liver homogenates, incubated in sealed flasks, in which the peroxidation was stimulated by the addition of ferrous ions. For both tissues, the production of ethane was maximal under a 20% oxygenated gas phase, while hyperoxic conditions led to a decreased ethane in the gas phase. The formation of thiobarbituric acid-reactive substances (TBA-RS), another marker of the lipid peroxidation process, in the homogenates of lung and liver was strongly stimulated at 100% compared to 20% oxygen. Experiments were also carried out on iron-stimulated peroxidation of pure docosahexaenoic acid preparations, which under air led to a large production of ethane. As for tissue homogenates, the TBA-RS content was increased in the presence of 100% oxygen. Those conditions, however, did not induce an increase in ethane production but led to the formation of ethanol. Therefore, the quenching of ethyl radical by molecular oxygen seems to be a very attractive hypothesis to explain the lack of increased ethane production in favor of ethanol when iron-induced lipid peroxidation was stimulated by oxygen.

Assessment of lipid peroxidation associated with lung damage induced by oxidative stress in vivo and in vitro studies

The lung thiobarbituric acid-reactive substances (TBA-RS) content and the amount of ethane exhaled, two potential markers of the lipid peroxidation process, were measured in rats following intratracheal administration of chemicals stimulating the production of free radicals, i.e. paraquat, phorbol myristate acetate and ferrous ions. Five hours after treatment, autopsy revealed gross pulmonary damage but the lung TBA-RS and the ethane exhalation were not different from control animals. On the contrary, a large increase in ethane production was observed 2 hr after intraperitoneal administration of the hepatotoxic carbon tetrachloride. In vitro, incubation of lung and liver homogenates from control rats with ferrous iron led to the development of a lipid peroxidation process in both tissues but the accumulation of TBA-RS and ethane was much lower with homogenates from lung as compared to liver tissue. Those results suggest that the lung may be more resistant than the liver to the initiation and/or propagation of a lipid peroxidation process. The possibility that others markers than ethane and TBA-RS are more appropriate to detect this process in the lung must also be considered. Key words: lung; liver; lipid peroxidation; in vivo; in vitro

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.

Genetic evidence for an Azotobacter vinelandii nitrogenase lacking molybdenum and vanadium.

We have constructed a strain of Azotobacter vinelandii which has deletions in the genes for both the molybdenum (Mo) and vanadium (V) nitrogenases. This strain fixed nitrogen in medium that did not contain Mo or V. Growth and nitrogenase activity were inhibited by Mo and V. In highly purified medium, growth was limited by iron. Addition of other metals (Co, Cr, Cu, Mn, Ni, Re, Ti, W, and Zn) did not stimulate growth. Like the V-nitrogenase, the nitrogenase synthesized by the double deletion strain reduced acetylene to both ethylene and ethane (C2H6/C2H4 ratio, 0.046). There was an approximately 10-fold increase in ethane production when Mo was added to the deletion strain grown in medium lacking Mo and V. This change in reactivity may be due to the incorporation of an Mo-containing cofactor into the nitrogenase synthesized by the double-deletion strain. A strain synthesizing the V-nitrogenase did not show a similar increase in ethane production. The growth characteristics of the double-deletion strain, together with the metal composition reported for a nitrogenase isolated from a tungstate-tolerant strain lacking genes for the molydenum enzyme grown in the absence of Mo and V (J. R. Chisnell, R. Premakumar, and P. E. Bishop, J. Bacteriol. 170:27-33, 1988) show that A. vinelandii can synthesize a nitrogenase which lacks both Mo and V. Reduction of dinitrogen by nitrogenase can therefore occur at a center lacking both these metals.

Comparative Toxicology of Ozone and t-Butyl Hydroperoxide on Isolated Rat Lung

Comparative studies were undertaken on the effects of ozone and t-butyl hydroperoxide (t-BuOOH) on alkane production, glutathione and lactate dehydrogenase (LDH) release from isolated rat lungs. Specifically, ethane and pentane production, as well as glutathione and LDH release were simultaneously determined at different time intervals from the isolated lung preparation in the absence and presence of toxic concentrations of ozone or t-BuOOH. When compared to control conditions, both toxic agents produced a marked decrease in the dry weight to wet weight ratios, reflecting the development of acute pulmonary edema. These toxic agents also caused a marked increase in the efflux of glutathione into the effluent. A much higher glutathione efflux into the effluent was observed during t-BuOOH perfusion in comparison to ozone exposure. In parallel with the enhancement of glutathione release a significant increase in ethane production was also observed during t-BuOOH perfusion. However, the production of either alkane by ozone inhalation was not significantly different from that in the control conditions. Unlike glutathione release, there was no marked increase of LDH release into the effluent following exposure to t-BuOOH or ozone. This suggests that the observed increase in glutathione release caused by t-BuOOH or ozone treatment was not associated with non-specific destruction of cell membrane integrity.

Ethylene and ethane production in response to salinity stress

Abstract Ethylene and ethane production in mung bean hypocotyl sections were evaluated as possible indicators of stress due to contact with four salts that are common in natural sites. Ethylene production decreased with increasing concentrations of applied NaCl and KCl. When CaCl2 was applied, the ethylene evolution was greater. However, when MgCl2 was applied, ethylene evolution remained high then decreased and at higher salt concentrations again showed an increase. NaCl (up to 0.1 kmol m−1) and KCl (up to 0.5 kmol m−3) caused a concentration‐dependent increase in ethane production. The ethane production with CaCl2 was the lowest among the salts tested and only a minute increase was noticed with the increase of concentration from 0.01 to 1 kmol m−3. Ethane production showed a distinct maximum at 0.2 kmol m−3 MgCl2. The introduction of 0.01 kmol m−3 CaCl2, as well as anaerobic conditions obtained by purging vials with N2, eliminated that high ethane production. Respiratory activity of the mung bean hypocotyl sections in MgCl2 concentrations from 0 to 0.5 kmol m−3 was correlated with ethane but not with ethylene production. The ethane/ethylene ratio showed three patterns for the four salts tested.

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.

Effect of pretreatment with cimetidine or phenobarbital on lipoperoxidation in carbon tetrachloride- and trichloroethylene-dosed rats

Lipid peroxidation (LP) in vivo as reflected by the exhalation of ethane and n-pentane and by thiobarbituric acid reactive substances (TBARS) in liver microsomes was studied in rats injected with carbon tetrachloride (CCl 4) and trichloroethylene (TCE), each at 2 dose levels. Interactions between these chlorinated solvents and cimetidine (CM), an inhibitor of cytochrome P-450-dependent monooxygenases, or phenobarbital (PB) the well known inducer of microsomal enzyme activities were also assessed. A non-hepatotoxic dose of CCl 4 did not cause a significant increase in ethane production except in PB-induced rats but did enhance n-pentane elimination, whereas an hepatotoxic dose increased the emission of both hydrocarbons. No interactions between CM and CCl 4 could be shown but, as expected, PB potentiated the effect of CCl 4. TCE administration led to a moderate dose-dependent elevation of n-pentane production but did not affect that of ethane and the effect of TCE was smaller in PB-induced than in CM- or non-pretreated rats. There was no difference in microsomal TBARS content in rats injected with the chlorinated hydrocarbons. The use of butylated hydroxytoluence (BHT) and ethylene diaminetetraacetic acid (EDTA) revealed that direct measurements of TBARS gave inadequate results due to substantial chemical LP in vitro during the whole procedure. With the “ethane-pentane test” it was established that: (i) CM cannot prevent CCl 4-induced LP; and (ii) TCE hepatotoxicity does not involve increased LP of membrane lipids.

Interaction of metals and carbon tetrachloride on lipid peroxidation and hepatotoxicity

Rats were administered ferrous sulfate, cadmium chloride, or sodium vanadate alone and in combination with carbon tetrachloride (CCl 4) to determine if lipid peroxidation is associated with the toxicity of the three metals and to determine if there is an interaction between these metals and CCl 4 in producing lipid peroxidation and hepatotoxicity. Expired ethane was used as an index of lipid peroxidation while serum alanine aminotransferase (ALT) and histopathology were used to assess liver damage. Lipid peroxidation did not appear to be associated with the hepatotoxicity of cadmium since no measurable increase in ethane production was observed when serum ALT concentrations were doubled relative to controls. Cadmium did not increase ethane when administered with CCl 4 and the increase in ALT was additive. Iron and vanadate produced small significant increases in ethane production but no increase in ALT and only minor histopathologic changes, yet potentiated lipid peroxidation and liver damage when administered with CCl 4. Thus, Cd did not produce lipid peroxidation and did not potentiate the lipid peroxidation and hepatotoxicity of CCl 4, while iron or vanadate which produced lipid peroxidation alone potentiated the lipid peroxidation and hepatotoxicity of CCl 4.

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.

Effects of vitamin E and selenium on copper-induced lipid peroxidation in vivo and on acute copper toxicity.

AbstractCopper sulfate injected intraperitoneally at a dose of 2 mg Cu/kg into vitamin E-and selenium-deficient rats caused a sixfold increase in the formation in vivo of the lipid peroxidation product ethane, and caused acute mortality in 4/5 rats. Selenium supplementation of the diet at 0.5 ppm Se largely prevented the increase in ethane production caused by copper injection and reduced mortality to 1/5 rats. Vitamin E supplementation of the diet at 200 IU/kg fully eliminated the increase in ethane production caused by copper injection, and completely prevented mortality. Vitamin E-deficient rats injected with copper sulfate at 5 mg Cu/kg produced over 10 times the ethane produced by rats injected with sodium sulfate or left uninjected. The ethylene produced by the rats injected with copper sulfate was 5% of the ethane produced, and did not differ significantly from the ethylene produced by the controls. Adding copper sulfate at 5 ppm Cu to a liver homogenate stimulated the production of ethane but not ...

Ethane production and liver necrosis in rats after administration of drugs and other chemicals

Lipid peroxidation and liver necrosis due to a number of drugs and chemicals were studied. The agents were administered to control, vitamin E-deficient, and selenium-deficient rats. Vitamin E deficiency was documented by a low serum tocopherol level (0.34 mg/100 ml) and selenium deficiency by a specific activity of the selenoenzyme glutathione peroxidase in 105,000 g liver supernatant which was approximately 1% of the control value. Glutathione S-transferase specific activity, measured with 1-chloro-2,4-dinitrobenzene as substrate, was doubled by selenium deficiency. Ethane production was measured as the index of in vivo lipid peroxidation. Hepatic necrosis was assessed histologically and by measuring serum glutamic-pyruvic transaminase. When no agents were administered, vitamin E-deficient rats produced more ethane than did control or selenium-deficient rats. Phenobarbital did not cause an increase in ethane production. CCl 4 (60 μl/100 g) and BrCCl 3 (5 μl/100 g) caused large ethane production and moderately severe liver necrosis. The vitamin E-deficient and selenium-deficient groups given BrCCl 3 produced more ethane than the controls but had no more severe hepatic necrosis than the controls. Thioacetamide (5 mmol/kg) and acetaminophen (3 g/kg) caused moderate to severe liver necrosis but only small ethane production. Vitamin E deficiency potentiated acetaminophen hepatotoxicity and selenium deficiency inhibited it. Iodipamide (1.5 mmol/kg) caused very large ethane production and death within hours in vitamin E-deficient rats. At a dose of 2 mmol/kg it caused severe liver necrosis in control rats but only small ethane production. This dose caused no liver necrosis in selenium-deficient rats. Acetylhydrazine (30 mg/kg) caused moderate ethane production in all groups but no liver necrosis. A single dose of ethanol (0.68 ml/100 g) led to small production of ethane in all groups. This study shows that many agents are capable of causing in vivo lipid peroxidation, but that lipid peroxidation does not always correlate with liver necrosis. Selenium deficiency is not a simple glutathione peroxidase deficiency state, as hepatic glutathione S-transferase is increased by it and it protects against acetaminophen and iodipamide hepatotoxicity.