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PubMed1994

Bacterial oxidation of propane.

The bacterial metabolism of propane and the pathway(s) involved are poorly understood, as the relative importance of terminal versus subterminal oxidation of propane, via propan-1-ol and propan-2-ol, respectively, is still unclear. In the case of bacteria, the ability to oxidize propane appears to be confined mainly to the Gram-positive Corynebacterium - Nocardia - Mycobacterium - Rhodococcus complex. Studies on propane oxidation have been hampered by a lack of firm enzymological data; for example, to date there are no reports of a purified propane oxygenase system. However, oxygenase activity has been confirmed by the production of propan-1-ol and/or propan-2-ol, and more recently by the co-oxidation of propene to 1,2-epoxypropane in cell extracts of propane-grown cells. Here, we review the use of genetic, biochemical and immunological techniques to assess the role(s) of terminal and subterminal oxidation in the metabolism of propane by Rhodococcus rhodochrous PNKb1 and present a general overview of the topic.

Alcohol Oxidoreductases↗
PubMed1984

In vitro cultivation of Mycobacterium X from Mycobacterium leprae infected tissues in propane-tetradecane medium (a preliminary communication).

Host grown Mycobacterium leprae and cultures of Mycobacterium X, cultivated from M. leprae infected armadillo and human specimens, were inoculated into propane and propane-tetradecane media. The media contained in one litre distilled water KH2PO4, 7 g; Na2HPO4, 0.5 g; (NH4)2SO4, 2 g; MgSO4, 0.1 g; ferric ammonium citrate, 20 mg and yeast extract (Difco), 0.1 g. Twenty ml media, distributed into each of 50 ml screw cap tubes, were inoculated with the bacilli and bubbled aseptically for 10 s with 99% purity propane gas. Tetradecane-propane media were prepared by adding 0.1 ml tetradecane to each of the tubes containing 20 ml propane medium. When incubated at 32 degrees C a logarithmic growth rate was counted in the propane-tetradecane media following a one to two week latency period. The time of division was estimated at seven days. In the propane-tetradecane medium, growth occurred at the interface of the tetradecane oil and water as a thin veil developing into a 1 to 3 mm thick emulsion in two to three months. No growth occurred in the propane medium and growth was extremely slow in the tetradecane medium. When added to the tetradecane medium, propane considerably shortened the latency period and the generation time, resulting in increased bacterial yield. Bacilli were strongly acid-fast; the culture did not grow on Löwenstein-Jensen or in Dubos media, but produced the localized disease typical of M. leprae in the foot pads of mice.

Alkanes↗
PubMed1994

Mutagenic activity of halogenated propanes and propenes: effect of bromine and chlorine positioning.

A series of halogenated propanes and propenes were studied for mutagenic effects in Salmonella typhimurium TA100 in the absence or presence of NADPH plus liver microsomes from phenobarbital-induced rats as an exogenous metabolism system. The cytotoxic and mutagenic effects of the halogenated propane 1,2-dibromo-3-chloropropane (DBCP) has previously been studied in our laboratories. These studies showed that metabolic activation of DBCP was required to exert its detrimental effects. All of the trihalogenated propane analogues were mutagenic when the microsomal activation system was included. The highest mutagenic activity was obtained with 1,2,3-tribromopropane, with approximately 50-fold higher activity than the least mutagenic trihalogenated propane, 1,2,3-trichloropropane. The order of mutagenicity was as follows: 1,2,3-tribromopropane > or = 1,2-dibromo- 3-chloropropane > 1,3-dibromo-2-chloropropane > or = 1,3-dichloro-2-bromopropane >> 1-bromo-2,3-dichloropropane > 1,2,3-trichloropropane. Compared to DBCP, the dihalogenated propanes were substantially less mutagenic. Only 1,2-dibromopropane was mutagenic and its mutagenic potential was approximately 1/30 of that of DBCP. In contrast to DBCP, 1,2-dibromopropane showed similar mutagenic activity with and without the addition of an activation system. The halogenated propenes 2,3-dibromopropene and 2-bromo-3-chloropropene were mutagenic to the bacteria both in the absence and presence of the activation system, whereas 2,3-dichloropropene did not show any mutagenic effect. The large differences in mutagenic potential between the various halogenated propanes and propenes are proposed to be due to the formation of different possible proximate and ultimate mutagenic metabolites resulting from the microsomal metabolism of the various halogenated propanes and propenes, and to differences in the rate of formation of the metabolites. Pathways are proposed for the formation of genotoxic metabolites of di- and trihalogenated propanes and dihalogenated propenes.

Alkenes↗
PubMed2005

Formation of M2+(O2)(C3H8) species in alkaline-earth-exchanged Y zeolite during propane selective oxidation.

The adsorption of oxygen and d2-propane (CH3CD2CH3) on a series of alkaline-earth-exchanged Y zeolite at room temperature was studied with in situ infrared spectroscopy. Surprisingly at room temperature, oxygen adsorption led to the formation of supercage M2+(O2) species. Further, at low propane coverage, propane was found to adsorb linearly on Mg2+ cations, but a ring-adsorption structure was observed for propane adsorbing on Ca2+, Sr2+, and Ba2+ cations. It is demonstrated that O2 and propane can simultaneously attach to one active center (M2+) to form a M2+(O2)(C3H8) species, which is proposed to be the precursor in thermal propane selective oxidation. Selectivity to acetone in the propane oxidation reaction decreases with increasing temperature and cation size due to the formation of 2-propanol and carboxylate ions. An extended reaction scheme for the selective oxidation of propane over alkaline earth exchanged Y zeolites is proposed.

Journal Article↗
PubMed1983

Purification and properties of a NAD-linked 1,2-propanediol dehydrogenase from propane-grown Pseudomonas fluorescens NRRL B-1244.

NAD-dependent 1,2-propanediol dehydrogenase (EC 1.1.1.4) activity was detected in cell-free crude extracts of various propane-grown bacteria. The enzyme activity was much lower in 1-propanol-grown cells than in propane-grown cells of Pseudomonas fluorescens NRRL B-1244, indicating that the enzyme may be inducible by metabolites of propane subterminal oxidation. 1,2-Propanediol dehydrogenase was purified from propane-grown Ps. fluorescens NRRL B-1244. The purified enzyme fraction shows a single-protein band upon acrylamide gel electrophoresis and has a molecular weight of 760,000. It consists of 10 subunits of identical molecular weight (77,600). It oxidizes diols that possess either two adjacent hydroxy groups, or a hydroxy group with an adjacent carbonyl group. Primary and secondary alcohols are not oxidized. The pH and temperature optima for 1,2-propanediol dehydrogenase are 8.5 and 20-25 degrees C, respectively. The activation energy calculated is 5.76 kcal/mol. 1,2-Propanediol dehydrogenase does not catalyze the reduction of acetol or acetoin in the presence of NADH (reverse reaction). The Km values at 25 degrees C, pH 7.0, buffer solution for 1,2-propan1,2-propanediol dehydrogenase are 8.5 and 20-25 degrees C, respectively. The activation energy calculated is 5.76 kcal/mol. 1,2-Propanediol dehydrogenase does not catalyze the reduction of acetol or acetoin in the presence of NADH (reverse reaction). The Km values at 25 degrees C, pH 7.0, buffer solution for 1,2-propan1,2-propanediol dehydrogenase are 8.5 and 20-25 degrees C, respectively. The activation energy calculated is 5.76 kcal/mol. 1,2-Propanediol dehydrogenase does not catalyze the reduction of acetol or acetoin in the presence of NADH (reverse reaction). The Km values at 25 degrees C, pH 7.0, buffer solution for 1,2-propanediol and NAD are 2 X 10(-2) and 9 X 10(-5) M, respectively. The 1,2-propanediol dehydrogenase activity was inhibited by strong thiol reagents, but not by metal-chelating agents. The amino acid composition of the purified enzyme was determined. Antisera prepared against purified 1,2-propanediol dehydrogenase from propane-grown Ps. fluorescens NRRL B-1244 formed homologous precipitin bands with isofunctional enzymes derived from propane-grown Arthrobacter sp. NRRL B-11315, Nocardia paraffinica ATCC 21198, and Mycobacterium sp. P2y, but not from propane-grown Pseudomonas multivorans ATCC 17616 and Brevibacterium sp. ATCC 14649, or 1-propanol-grown Ps. fluorescens NRRL B-1244. Isofunctional enzymes derived from methane-grown methylotrophs also showed different immunological and catalytic properties.

Amino Acids↗
PubMed1991

Oxidative denitrification of 2-nitropropane and propane-2-nitronate by mouse liver microsomes: lack of correlation with hepatocytotoxic potential.

2-Nitropropane (2-NP) is an industrial chemical with hepatotoxic and genotoxic properties. It exists in chemical equilibrium with propane-2-nitronate, which is much more genotoxic than 2-NP. In this work the link between toxicity and metabolism of 2-NP and its nitronate was investigated. To that end 2-NP or propane-2-nitronate were incubated with murine hepatic microsomes at concentrations of up to 10 mM, and generation of nitrite was measured as product of metabolic oxidation of the two species. Under the acidic reaction conditions of the colorimetric nitrite assay propane-2-nitronate decomposed chemically to nitrite. Therefore an ion-pair HPLC assay at neutral pH was developed which enabled determination of nitrite formed from the nitronate. The rate of metabolic nitrite generation from propane-2-nitronate was 5-10-fold that obtained with 2-NP. Metabolism of either species to nitrite was dependent on the presence in the incubate of viable microsomes and of NADPH, and it was inhibited in the presence of carbon monoxide or the cytochrome P-450 inhibitor SKF525A. Acetone could also be measured as a metabolite of 2-NP. Optical difference spectra were recorded in mixtures of propane-2-nitronate with liver microsomes from phenobarbital-pretreated rats. The spectral dissociation constant was found to be 30 mM, which compares with 10 mM reported for 2-NP. 2-NP and propane 2-nitronate were incubated with mouse hepatocytes in suspension and cytotoxicity was determined by measurement of leakage of cellular lactate dehydrogenase into the medium. Both species were hardly toxic, as concentrations of 20 mM were required to elicit significant damage to the cells. The results demonstrate that propane-2-nitronate, like 2-NP, undergoes microsomal oxidative denitrification, probably catalysed by cytochrome P-450. Metabolism of both species occurs at markedly different rates, but the difference in metabolism is not reflected by a difference in hepatocytotoxic potential.

Animals↗
PubMed2002

Ruthenium-catalyzed transfer hydrogenation of imines by propan-2-ol in benzene.

Transfer hydrogenation of a variety of different imines to the corresponding amines by propan-2-ol in benzene catalyzed by [Ru2(CO)4(mu-H)(C4Ph4COHOCC4Ph4)] (1) has been studied. The reaction is highly efficient with turnover frequencies of over 800 per hour, and the product amines were obtained in excellent yields. A remarkable concentration dependence of propan-2-ol was observed when the reaction was run in benzene as cosolvent. An optimum was obtained at 24 equivalents of propan-2-ol to imine, and further increase of the propan-2-ol led to a dramatic decrease in rate. Also the use of polar cosolvents with 24 equivalents of propan-2-ol gave a low rate. It was found that ketimines react faster than aldimines and that electron-donating substituents on the imine increase the rate of the catalytic transfer hydrogenation. Electron-withdrawing substituents decreased the rate. An isomerization was observed with imines having an alpha-hydrogen at the N-alkyl substituent, which is in accordance with a mechanism involving a ruthenium-amine intermediate. It was demonstrated that the ruthenium-amine complex from alpha-methylbenzylamine, corresponding to the postulated intermediate, can replace 1 as catalyst in the transfer hydrogenation of imines. A primary deuterium isotope effect of kCH/CD = 2.7 +/- 0.25 was observed when 2-deuterio-propan-2-ol was used in place of propan-2-ol in the transfer hydrogenation of N-phenyl-(1-phenylethylidene)amine.

2-Propanol↗
PubMed1990

Propane-1,2-diol as a potential component of a vitrification solution for corneas.

Any method of cryopreservation of the cornea must maintain integrity of the corneal endothelium, a monolayer of cells on the inner surface of the cornea that controls corneal hydration and keeps the cornea thin and transparent. During freezing, the formation of ice damages the endothelium, and vitrification has been suggested as a means of achieving ice-free cryopreservation of the cornea. To achieve vitrification at practicable cooling rates, tissues must be equilibrated with high concentrations of cryoprotectants. In this study, the effects of propane-1,2-diol on the structure and function of rabbit corneal endothelium were studied. Corneas were exposed to concentrations of propane-1,2-diol ranging from 10 to 30% v/v in a Hepes-buffered Ringer's solution containing glutathione, adenosine, 5 mmol/liter sodium bicarbonate, and 6% w/v bovine serum albumin. Endothelial function was assessed by monitoring corneal thickness during perfusion of the endothelial surface at 34 degrees C for 6 hr. Exposure to 10-15% v/v propane-1,2-diol was well tolerated for 20 min at 4 degrees C when the cryoprotectant was removed in steps or by sucrose dilution. However, exposure to 25% v/v propane-1,2-diol for 20 min at 0 or -5 degrees C was consistently tolerated only when 2.5% w/v chondroitin sulfate was included in the vehicle solution. Exposure to 30% v/v propane-1,2-diol was harmful at -5 and -10 degrees C. The endothelial damage following exposure to 30% v/v propane-1,2-diol was probably the result of a toxic effect rather than osmotic stress. Although 25% v/v propane-1,2-diol does not vitrify at cooling rates that are practicable for corneas, it could at this concentration form a major component of a vitrification solution comprising a mixture of cryoprotectants.

Animals↗
PubMed1996

Effect of propanal and diacetyl on quantity of remaining double bonds of chemically cured BisGMA/TEGDMA resins.

The aim of the present study was to determine the effect of propanal and diacetyl addition on the quantity of remaining double bonds of chemically cured dental resins. Propanal (propionaldehyde) or diacetyl (2,3-butanedione) was added to monomer mixtures, which were then made chemically curable. The monomer mixtures were varied with respect to content of propanal or diacetyl. Addition of propanal or diacetyl to chemically curable resins resulted in a decrease in the quantity of remaining double bonds from 19.6% to 1.9% and from 19.6% to 11.4%, respectively. A negative correlation of statistical significance was found between content of propanal and quantity of remaining double bonds, while the relationship between content of diacetyl and quantity of remaining double bonds was found not to be linear. Propanal was equally effective in reducing the quantity of remaining double bonds in chemically cured and in the light cured resins studied previously. As regards diacetyl, a more pronounced effect on quantity of remaining double bonds was noted for light cured resins as compared with chemically cured resins. The most likely common reaction mechanism of propanal and diacetyl seemed to be that of chain transfer reactions. Furthermore, analysis of the data indicated a possible additional photoinitiating function of diacetyl.

Aldehydes↗
PubMed1991

Investigation of the chemical basis of nitroalkane toxicity: tautomerism and decomposition of propane 1- and 2-nitronate under physiological conditions.

Unlike primary nitroalkanes, such as 1-nitropropane, the secondary nitroalkane 2-nitropropane is geno- and hepatotoxic. Nitroalkanes exist in equilibrium with alkane nitronates. In order to investigate the relationship between nitroalkane toxicity and generation and stability of nitronates, propane 1- or 2-nitronate (4-6 mM) were incubated in buffer (pH 3.8 -7.4) in the absence or presence of cysteine. Equilibrium formation and degradation were studied by 1H-NMR spectroscopy and ion pair HPLC chromatography. Propane 1-nitronate generated 1-nitropropane rapidly and almost quantitatively. In the case of propane 2-nitronate equilibrium at pH 7.4 was reached within 8 h, when 48% of initial nitronate had tautomerised to 2-nitropropane. The pKa of the reaction 2-nitropropane less than--greater than propane 2-nitronate measured by HPLC was 7.63. Equilibrium formation, hydrolysis and reduction of nitronates were pH-dependent and, in the case of propane 2-nitronate, yielded mainly acetone, nitrite and acetone oxime, apart from 2-nitropropane. Hydrolysis of propane 2-nitronate (4 mM) to nitrite was modulated by cysteine (4 mM) and p-methoxyphenol (0.4 mM). At pH 7.4 they increased nitrite generation by 300 and 28%, respectively, at pH 4.8 they decreased nitrite formation by 91 and 82%, respectively, probably by scavenging radical intermediates. Differences between nitroalkanes in terms of content of nitronate tautomer at equilibrium are probably an important chemical determinant of their toxic potential.

Animals↗
PubMedDate not supplied

Effect of bromine and chlorine positioning in the induction of renal and testicular toxicity by halogenated propanes.

A series of halogenated propanes were studied for renal and testicular necrogenic effects in the rat and correlated to their ability to induce in vivo renal and testicular DNA damage and in vitro testicular DNA damage. 1,2-Dibromo-3-chloropropane (DBCP) and 1,2,3-tribromopropane were most potent in causing organ damage in both kidney and testes. Extensive necrosis was evident at 85 mumol/kg in kidney and at 170 mumol/kg in testis. The dibromomonochlorinated analogue 1,3-dibromo-2-chloropropane was less organ toxic than DBCP and 1,2,3-tribromopropane, but induced more organ damage than the dichloromonobrominated analogues 1-bromo-2,3-dichloropropane and 1,3-dichloro-2-bromopropane. Dihalogenated propanes were even less necrogenic. These observed differences in toxic potency between the halogenated propanes could not be explained by relative differences in tissue concentrations. The ability of the halogenated propanes to induce DNA damage in vivo correlated well with their ability to induce organ damage. However, DNA damage occurred at lower doses and at a shorter period of exposure than organ necrosis. This indicates that DNA damage might be an initial event in the development of organ necrosis by halogenated propanes in general. Further, testicular DNA damage induced by the halogenated propanes in vivo correlated well with the DNA damage observed in isolated testicular cells in vitro, showing that toxicity was due to in situ activation. The numbers, positions, and the types of halogen substituents appear to be important determinants in causing DNA damage and necrogenic effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2006

Novel acetone metabolism in a propane-utilizing bacterium, Gordonia sp. strain TY-5.

In the propane-utilizing bacterium Gordonia sp. strain TY-5, propane was shown to be oxidized to 2-propanol and then further oxidized to acetone. In this study, the subsequent metabolism of acetone was studied. Acetone-induced proteins were found in extracts of cells induced by acetone, and a gene cluster designated acmAB was cloned on the basis of the N-terminal amino acid sequences of acetone-induced proteins. The acmA and acmB genes encode a Baeyer-Villiger monooxygenase (BVMO) and esterase, respectively. The BVMO encoded by acmA was purified from acetone-induced cells of Gordonia sp. strain TY-5 and characterized. The BVMO exhibited NADPH-dependent oxidation activity for linear ketones (C3 to C10) and cyclic ketones (C4 to C8). Escherichia coli expressing the acmA gene oxidized acetone to methyl acetate, and E. coli expressing the acmB gene hydrolyzed methyl acetate. Northern blot analyses revealed that polycistronic transcription of the acmAB gene cluster was induced by propane, 2-propanol, and acetone. These results indicate that the acmAB gene products play an important role in the metabolism of acetone derived from propane oxidation and clarify the propane metabolism pathway of strain TY-5 (propane --> 2-propanol --> acetone --> methyl acetate --> acetic acid + methanol). This paper provides the first evidence for BVMO-dependent acetone metabolism.

Acetone↗
PubMed1975

The effects of an antimetastatic agent, (plus or minus)-1,2-bis(3,5-dioxopiperazin-1-yl)propane (ICRF 159), on platelet behavior.

Some agents that inhibit platelet aggregation, e.g., aspirin and dipyridamole, ahve been reported to prevent metastasis formation. To see whether inhibition of platelet aggregation could account for the antimetastatic action of (plus or minus)-1,2- bis(3,5-dioxopiperazin-1-yl)propane, this compound was investigated in vivo for any effects on platelet behavior and thrombogenesis. (plus or minus)-1,2-Bis(3,5-dioxopiperazin-1-yl)propane inhibited the formation of platelet thrombi in blood vessels on the surface of the rat brain and in the hamster cheek pouch. 1,2-Bis(dioxo-4-methylpiperazin-1-yl)ethane, a closely related analog of (plus or minus)-1,2-bis(3,5-dioxopiperazin-1-yl)propane, but without antimetastatic action, inhibited thrombus formation in vivo as effectively as (plus or minus)-1,2-bis(3,5-dioxopiperazin-1-yl)propane. It seems unlikely therefore that the antimetastatic action of (plus or minus)-1,2-bis(3,5-dioxopiperazine-l-yl)propane derives from its effects on thrombogenesis. Neither platelet numbers nor the ionized plasma calcium concentrations were changed after (plus or minus)-1,2-bis(3,5-dioxopiperazin-l-yl)propane administration.

Animals↗
PubMed1991

Corneal tolerance of vitrifiable concentrations of propane-1,2-diol.

The merit of corneal cryopreservation by vitrification as opposed to conventional freezing is the avoidance of ice damage which is believed to disrupt the integrity of the corneal endothelium resulting in loss of corneal transparency. The cornea must be equilibrated with high concentrations of cryoprotectant in order to achieve vitrification at practicable cooling rates. In an earlier study, corneas were exposed to 3.4 mol/liter propane-1,2-diol (Rich and Armitage (1990) Cryobiology 27, 42-54). The present study exposed rabbit corneas to concentrations of propane-1,2-diol between 3.4 and 5.4 mol/liter in a Hepes-buffered Ringer's solution containing glutathione, adenosine, 5 mmol/liter sodium bicarbonate, 6% (w/v) bovine serum albumin, and 2.5% (w/v) dextran sulfate. Dextran sulfate was as effective as chondroitin sulfate at improving endothelial tolerance of 3.4 mol/liter propane-1,2-diol. This beneficial effect may be linked to the polyanionic nature of these molecules. Corneas exposed to 5.4 mol/liter propane-1,2-diol were cooled in liquid nitrogen vapor at a temperature of -140 degrees C for 2 h. Warming was achieved by direct transfer to a dilution solution at -10 degrees C. Endothelial function was assessed by monitoring corneal thickness during perfusion of the endothelial surface at 34 degrees C for 6 h. Endothelial structure was observed by specular microscopy during the perfusion and by scanning electron microscopy after perfusion. Corneas tolerated exposure to 3.4 mol/liter propane-1,2-diol for 20 min at 0 degrees C and to 4.1 mol/liter for 10 min at -10 degrees C. Exposure to 4.8 and 5.4 mol/liter for 10 min at -10 degrees C caused endothelial damage, although a degree of endothelial function was retained. Function following exposure to 5.4 mol/liter was improved by reducing the temperature of exposure to -15 degrees C. Corneas cooled after exposure to 5.4 mol/liter propane-1,2-diol for 10 min at -15 degrees C apparently vitrified, but devitrified on warming. The corneas swelled to such an extent during perfusion that the endothelium could not be viewed by specular microscopy, subsequent scanning electron microscopy showed a severely disrupted endothelium.

Animals↗
PubMed1984

New type of oxygenase involved in the metabolism of propane and isobutane.

Nocardia paraffinicum (Rhodococcus rhodochrous), a hydrocarbon-degrading microorganism, was used in a study of propane and isobutane metabolism. The bacterium was able to utilize propane or isobutane as a sole source of carbon, and oxygen was found to be essential for its metabolism. Gas chromatographic analysis showed that n-propanol was the major compound recovered from the metabolism of propane by resting cells, although trace amounts of isopropanol and acetone were detected. When a mixture of propane and isobutane was used, drastic inhibition (72 to 88%) of hydrocarbon utilization by resting cells occurred. The ratio of hydrocarbon to oxygen consumed was found to be approximately 2:1 during the metabolism of propane or isobutane by resting cells when these substrates were provided individually to the organism. Gas chromatographic-mass spectrometric analysis of products formed from O(2) confirmed that the initial oxidative step in the metabolism of these substrates involved molecular oxygen. The proportion of the alcohol containing O was the same as that of O(2) in the gas mixture. Only a negligible amount of O was detected in the alcohol when H(2)O was incorporated into the system. The observed 2:1 ratio of hydrocarbon to oxygen consumption suggests that the oxygenase in N. paraffinicum, unlike the conventional mono- or dioxygenases, requires two hydrocarbon-binding sites for each of the oxygen-binding sites and is therefore an intermolecular dioxygenase. The newly described oxygenase, which catalyzes the reaction of two molecules of propane with one molecule of oxygen to yield two molecules of a C(3) alcohol, is proposed as the initial oxidation step of the hydrocarbon substrate.

Journal Article↗
PubMed1987

Role of Carbon Dioxide in Catabolism of Propane by "Nocardia paraffinicum" (Rhodococcus rhodochrous).

The catabolism of propane by "Nocardia paraffinicum" (Rhodococcus rhodochrous) has been shown to involve CO(2) fixation after its oxidation to propionic acid. "N. paraffinicum" failed to grow on either propane or 1-propanol in the absence of CO(2). The rate of propane utilization was directly related to the initial CO(2) concentration, and Warburg respirometry suggested that CO(2) was required for the catabolism of 1-propanol, propionaldehyde, and propionate but not for 2-propanol. These data also suggested that the predominant pathway for the utilization of propane by "N. paraffinicum" was through 1-propanol. The use of [2-C]propane and CO(2) confirmed the catabolism of propane and the fixation of CO(2). Through the use of these isotopes and the pyruvate carboxylase inhibitor sodium arsenite, the labeled 2,4-dinitrophenylhydrazine derivative of pyruvate was trapped and isolated via thin-layer chromatography. The trapping of [C]pyruvate in this manner was considered to be indicative of the presence of the methylmalonyl coenzyme A pathway for CO(2) fixation.

Journal Article↗
PubMed1995

Evaluation of urinary mercury excretion after administration of 2,3-dimercapto-1-propane sulfonic acid to occupationally exposed men.

The purpose of this study was to determine the clinical efficacy of 2,3-dimercapto-1-propane sulfonic acid, Na salt, on the urinary excretion of mercury as well as its possible adverse effects. Ten men with occupational mercury exposure (urinary level of 50 micrograms/g creatinine or more) were assigned to receive 2,3-dimercapto-1-propane sulfonic acid p.o. (DIMAVAL capsules, 100 mg) 300 mg/d for five days. Informed written consent was obtained from each subject. Hematology analyses, blood, chemistry, and urinalysis were obtained at the start of the study, at the end of the 2,3-dimercapto-1-propane sulfonic acid treatment and 72 hours after the administration of the final dose of 2,3-dimercapto-1-propane sulfonic acid. Twenty-four-hour urine mercury levels were closely monitored throughout therapy. All data and measurements before and during drug doses were evaluated by analyses of variance. In all subjects mean urine mercury was significantly increased (p < .05) after pre-2,3-dimercapto-1-propane sulfonic acid treatment. One subject had a moderate hypersensitivity reaction (rash) to 2,3-dimercapto-1-propane sulfonic acid but no other toxic effects were observed.

Adult↗
PubMed2000

[Propane abuse. Extreme dose increase due to development of tolerance].

In spite of its serious sequelae, volatile substance abuse (VSA) attracts very little public attention in Germany. Our case report describes an adult male who inhaled propane for recreational purposes. Initially, he achieved short-lived euphoria and hallucinations. He compensated for the developing tolerance by increasing the dosage, finally consuming 5 litres of fluid propane daily. Getting such quantities was facilitated by his occupational access to propane. Since he abused the propane in an apartment house, he also exposed third parties to the danger of explosion. Clinical examination revealed disturbances in orientation, restricted perceptivity and concentration, reduced mnemonic performance, and psychomotor agitation. All these symptoms diminished during a 6-month follow-up. The relationship of his organic mental disorder to the abuse of propane was not clear, since he had also abused alcohol.

Administration, Inhalation↗