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PubMed1989

The effects of prenatal tertiary butanol administration in CBA/J and C57BL/6J mice.

Pregnant mice of the CBA/J and C57BL/6J strains were given either tertiary butanol (10.5 mmoles/kg, p.o.) or an equivalent volume of tap water twice daily from day 6 through day 18 of gestation. Examination on day 18 revealed significantly more resorptions per litter in the t-butanol-treated animals but no interstrain difference. Tertiary butanol did not significantly affect the body weight of the survivors nor produce significant abnormalities in either strain. Subsequent blood concentration profiles in female C57BL/6J mice indicated that the treatment regimen produced blood levels equivalent to teratogenic ethanol treatment. Mice receiving 3 days of t-butanol treatment did not eliminate the drug more rapidly than control animals, indicating that tolerance was not a factor in the treatment regimen. Since t-butanol shares membrane disordering effects with ethanol but is not metabolized by the same pathway, a role for acetaldehyde or the process of ethanol metabolism is suggested in ethanol teratogenicity.

Abnormalities, Drug-Induced↗
PubMed1994

2-Butanol metabolism by rat hepatic and pulmonary cytochromes P450.

Three microsomal enzyme inducers, ethanol, phenobarbital (PB), and beta-naphthoflavone (beta NF), were compared for their effects on butanol oxidase activity in rat hepatic and pulmonary microsomes. Four concentrations of 2-butanol (1.0, 5.0, 10, and 33 mM) were used to determine if the effects of induction on 2-butanol metabolism were substrate concentration dependent. Ethanol induced at all substrate concentrations in the liver while PB induced at only the high substrate concentrations (5.0, 10, and 33 mM). beta NF did not induce at any substrate concentration. 2-Butanol oxidation in the lung was not induced by any of the treatments. Thus, both ethanol and phenobarbital induce hepatic enzymes capable of 2-butanol oxidation, and the isozyme(s) induced by the latter has a somewhat lesser affinity for this alcohol.

Alcohol Oxidoreductases↗
PubMed1996

Gas chromatographic procedures for determination of ethanol in postmortem blood using t-butanol and methyl ethyl ketone as internal standards.

Three gas chromatographic procedures for the determination of ethanol in postmortem blood using alternative internal standards to n-propanol are presented: a direct injection procedure using t-butanol, and two headspace methods using t-butanol and methyl ethyl ketone. t-Butanol and methyl ethyl ketone were well resolved from ethanol, acetone, methanol and other commonly observed putrefactive volatiles using direct injection or headspace analysis. CVs for the direct injection method were below 5% for ethanol and below 10% for the other volatiles. The lower limits of detection (LOD) were 25-50 mg/L. The CVs for the headspace methods were below 5% for ethanol and below 6% for the other volatiles. The LODs were 10 mg/L using either t-butanol or methyl ethyl ketone as internal standards. The use of t-butanol or methyl ethyl ketone as alternatives to n-propanol avoids the possibility of error in the quantitation of ethanol due to the presence of n-propanol and allows for the identification of other volatiles that may aid in distinguishing antemortem ingestion from postmortem production of ethanol.

Butanols↗
PubMedDate not supplied

Effects of ethanol and tertiary butanol on blood glucose levels and body temperature of rats.

The mechanisms of ethanol's hyperglycemic and hypothermic effects were investigated by comparing the effects of ethanol with those of tertiary butanol. Tertiary butanol is an intoxicant like ethanol, but unlike ethanol it is only minimally metabolized. Consequently, tertiary butanol does not produce appreciable amounts of active metabolites or energy. Tertiary butanol exerts its neural effects primarily by directly altering the physico-chemical properties of nerve cell membranes. It was found that ethanol and tertiary butanol produce hyperglycemic and hypothermic effects whose magnitude and time course are nearly identical. These data suggest that the hyperglycemic and hypothermic effects of ethanol represent a primary physico-chemical effect on nerve cell membranes and are not secondary to its energy content or metabolites.

Animals↗
PubMed1978

Microbiological production of acetone-butanol by Clostridium acetobutylicum.

Trials succeeded in raising the efficiencies of the fermentation medium, used in the fermentative production of acetone-butanol by Clostridium acetobutylicum. Egyptian black strap molasses (50.0% sugars) was suitable as carbon source in the fermentation medium, and (NH4)2SO4 was utilized with great success as inorganic nitrogen source. 140.0 g/l black strap molasses (about 7.0% sugars) and 3.0 g/l (NH4)2SO4 were the optimum concentrations for obtaining good yields of acetone and butanol. Molasses and (NH4)2SO4 were preferred because they are cheaper than the other carbon and organic nitrogen sources, used in the fermentative production of acetone-butanol. The percentage increase of the total solvents produced in the fermentation (production medium) was increased by 64.0. The slop (by-product of the acetone-butanol fermentation after distillation) was re-used in the fermentation medium as organic nitrogen source and supported the microorganisms for a good production of acetone and butanol, while when stillage was used in the production medium, the total solvents output was less than that produced in the medium containing slop.

Acetone↗
PubMed1992

Titration calorimetric and differential scanning calorimetric studies of the interactions of n-butanol with several phases of dipalmitoylphosphatidylcholine.

The interactions of n-butanol with dipalmitoylphosphatidylcholine (DPPC) were studied using titration calorimetry and differential scanning calorimetry (DSC). DSC results indicated that n-butanol induces the interdigitated phase in DPPC above 10 mg/mL butanol. A new application of titration calorimetry for measuring partition coefficients of nonsaturating solutes into lipids was developed. The partition coefficients and the heat of binding of n-butanol into DPPC were measured for the L beta', P beta', L alpha, and L beta I phases of DPPC. The partition coefficients were temperature dependent and ranged from 70 to 110 for the L beta I phase, from 170 to 183 for the L alpha phase, and similar to that for the L beta I phase in the P beta' phase. The binding to the L beta' phase could not be detected, giving an upper limit for this partition coefficient of 23. The enthalpies for binding to the L beta I and L alpha phases were 1.0 and 1.5 kcal/mol, respectively. The van't Hoff enthalpy was in good agreement with the calorimetric enthalpy for the partitioning into the L alpha phase; however, it was greater than the calorimetric enthalpy for the L beta I phase, suggesting that the interaction of n-butanol with this phase is cooperative in some way.

1,2-Dipalmitoylphosphatidylcholine↗
PubMed1997

The effect of n-butanol on Triton X-114 phase partitioning.

n-Butanol interferes with the fractionation of amphiphilic and hydrophilic molecules during the Triton X-114 phase separation procedure. The indicators oil red (hydrophobic) and p-nitrophenol (hydrophilic) were useful for predicting the effectiveness of the Triton X-114 partition method. For n-butanol extracts containing oil red, 5'-nucleotidase, or alkaline phosphatase, the hydrophobic molecules and Triton X-114 were retained in the aqueous phase during incubations at 30 degrees C. The n-butanol interference was concentration-dependent and was reduced by lowering the final n-butanol concentration of the sample to 1.5% (v/v) or less. The results demonstrate how buffer-diluted n-butanol extracts of 5'-nucleotidase and alkaline phosphatase can be successfully employed for subsequent Triton X-114 fractionation of the enzymes.

1-Butanol↗
PubMedDate not supplied

Time course of sensory eye irritation in humans exposed to N-butanol and 1-octene.

In this study, we investigated the time course effect of sensory eye irritation in 16 subjects exposed (i.e., eye only) to n-butanol and 1-octene. Half the subjects were exposed to n-butanol, and the remaining subjects were exposed to 1-octene. Each subject was studied on 5 different days; during each day each subject was exposed in three runs (i.e., run 1, run 2, and run 3) to a constant concentration of either n-butanol or 1-octene. We performed run 1 and run 3, both of which lasted 15 min each, to evaluate persistence in "sensitization." We performed run 2, which lasted 60 min, to study the time course of sensory irritation. Ratings of ocular irritation intensity were obtained continuously during all three runs. The exposure concentrations for n-butanol were 0 mg/m3, 300 mg/m3, 900 mg/m3, and 3 000 mg/m3, and the exposure concentrations for 1-octene were 0 mg/m3, 6 000 mg/m3, 10 400 mg/m3, and 18 000 mg/m3. During run 2, we observed a slight increase in perceived eye irritation intensity for the lower concentrations of 1-octene and for all exposure concentrations of n-butanol. However, the threshold for irritation was clearly exceeded for only the 1-octene 10 400-mg/m3 and 18 000-mg/m3 exposures. During these two exposures, the response increased 10-fold following 20-40 min of exposure during run 2, after which the response remained constant. We investigated the existence of persistence in "sensitization" by comparing intensity of responses between run 1 and run 3. Persistence in "sensitization" was apparent for only the 1-octene exposure.

1-Butanol↗
PubMed1989

Effect of 2-butanol and 2-butanone on rat hepatic ultrastructure and drug metabolizing enzyme activity.

The effect of a single oral dose of 2-butanol (2.2 ml/kg) or 2-butanone (1.87 ml/kg) on hepatic ultrastructure and drug-metabolizing enzyme activity was studied in the rat. A 135-197% increase in acetanilide hydroxylase activity was found in rats sacrificed 12-40 h after dosing with 2-butanol or 2-butanone. A 40-h pretreatment with 2-butanone produced a 155% increase in aminopyrine N-demethylase activity. NADPH-cytochrome c reductase activity and the concentrations of cytochromes P-450 and b5 were largely unaltered 2-40 h after dosing with either agent. Electron microscopic examination of hepatocytes from rats sacrificed 16 h after 2-butanol or 2-butanone revealed a marginal increase in the prevalence of smooth endoplasmic reticulum. However, by 40 h, there was a marked proliferation of the smooth endoplasmic reticulum and reduction in rough endoplasmic reticulum in response to both agents. The most marked potentiation of CCl4 hepatotoxicity occurred when rats were pretreated with 2-butanol or 2-butanone 16 h before CCl4 administration. The coincidental finding of maximal CCl4-induced hepatic injury and elevation of microsomal xenobiotic activity within the same time frame following 2-butanol or 2-butanone supports the hypothesis that aliphatic alcohols and ketones potentiate CCl4 hepatotoxicity by enhancing biotransformation of the halocarbon to cytotoxic metabolites.

Aminopyrine N-Demethylase↗
PubMed1982

The in vivo metabolism of tertiary butanol by adult rats.

The metabolism of tertiary butanol has been considered to be limited to direct conjugation of the hydroxyl group. Therefore, the alcohol has been used to differentiate between the direct effects of ethanol and those caused by metabolism or metabolic products of ethanol. The in vitro oxidation of tertiary butanol has been reported, and in this report we describe the in vivo oxidation of tertiary butanol. Radiolabeled and stable isotope-labeled acetone was recovered from animals treated with corresponding labeled t-butanol. 14CO2 was also recovered from animals treated with [14C]t-butanol.

Acetone↗
PubMed1985

Regulation and butanol inhibition of D-xylose and D-glucose uptake in Clostridium acetobutylicum.

Clostridium acetobutylicum exhibited diauxie growth in the presence of mixtures of glucose and xylose. Both glucose- and xylose-grown cells had a glucose uptake activity. On the other hand, growth on xylose was associated with the induction of a xylose permease activity, which was repressed by glucose in xylose-induced cells. The rate of sugar uptake with increasing sugar concentrations showed saturation kinetics with an apparent Km of 1.25 X 10(-5) M for glucose and 5 X 10(-3) M for xylose. Concomitant with the production of solvents, the activities of the glucose and xylose transport systems decreased. Among the main products of fermentation, butanol was shown to be a potent inhibitor of the growth of the organism and of the rate of sugar uptake as well as of sugar incorporation into cell materials. These inhibitory effects of butanol were more pronounced in xylose-grown cells than in glucose-grown cells. Butanol completely inhibited growth at a concentration of 14 g/liter for cultures growing on glucose and 8 g/liter for cultures growing on xylose. Concentrations of 7 and 10.5 g/liter of butanol caused a 50% inhibition of the xylose and glucose incorporations into cell materials. These inhibitory levels of butanol were found in typical glucose or xylose fermentation.

Biological Transport↗
PubMed1997

The genes for butanol and acetone formation in Clostridium acetobutylicum ATCC 824 reside on a large plasmid whose loss leads to degeneration of the strain.

Degeneration is the process whereby Clostridium acetobutylicum ATCC 824 loses the capacity to produce acetone and butanol after repeated vegetative transfers or in continuous culture. Two degenerate mutants (M5 and DG1) of C. acetobutylicum ATCC 824 do not contain the four genes (ctfA, ctfB, adc, and aad) for acetone and butanol formation. Strain ATCC 824 contains a 210-kb plasmid (pSOL1) which is absent in M5 and DG1. pSOL1 carries the four acetone and butanol formation genes. A restriction map of pSOL1 was constructed by using ApaI, SmaI, SstII, and NarI digestions. M5 and DG1 could be complemented for acetone and butanol formation by expressing the corresponding genes (ctfA, ctfB, and adc for acetone; aad for butanol) on the plasmid. Degeneration of this strain thus appears to be the result of pSOL1 loss.

Acetone↗
PubMed1978

The A, M, N, and P1 blood group substances in butanol extracts of human erythrocytes.

Aqueous phase and butanol phase extracts of group A1, O, M, N, P1 and P2 human erythrocytes perpared by extraction of red cell stromata with n-butanol were examined for the presence of blood group substances in inhibition of agglutination experiments using antisera and test cells of human origin. Group A substance was recovered in both aqueous phase and butanol phase extracts, M and N substance in aqueous phase extracts only, and P1 substance only in butanol phase extracts. Use of high concentrations of extract resulted in detection of P1 activity in aqueous phase extracts and of N specific inhibition in the aqueous phase extracts of group M erythrocytes. Distilled water appeared to be superior to digitonin and hypotonic phosphate buffer solutions for preparation of stromata for the recovery of group A and M substances in the butanol extracts but not for group N and P1 substances.

ABO Blood-Group System↗
PubMed1975

Freeze-drying from tertiary butanol in the preparation of endocardium for scanning electron microscopy.

The scanning electron microscope appearances and shrinkage of blocks of canine endocardium prepared by freeze-drying directly, by freeze-drying after replacing tissue water with tertiary butanol (2-methyl propan-2-ol) and by critical point drying were compared. All three methods demonstrated endothelial cells which showed nuclear prominences, microvilli and intercellular boundaries. The microvilli varied in size and number from dog to dog but were generally less well defined in specimens freeze-dried from water. Shrinkage due to t-butanol dehydration was significantly less than that which occurred in ethanol in the critical point drying method. Overall the reduction in surface area was significantly less in specimens freeze-dried directly at -65 C (6.8%) than in those dried from t-butanol at -20 C (15.4%) and those prepared bly critical point drying (22.1%). However the amount of shrinkage observed in t-butanol treated tissue was not significantly different from that which was critical point dried. It was not possible to distinguish between comparable samples prepared by these two methods on the basis of their scanning electron microscopic appearances. Thus the relative simplicity and convenience of the t-butanol method, together with its saving of time, its use of standard freeze-drying equipment and the avoidance of ice-crystal artefact justify its consideration as an alternative method of preparing wet biological tissue for scanning electron microscopy.

Animals↗
PubMed1990

[Utilization of butanols by disease-associated Mycobacterium avium and Mycobacterium intracellulare classified by DNA probe test and relationship with their ability to grow at 45 degrees C].

Utilization of n-butanol and iso-butanol by Mycobacterium avium and M. intracellulare classified by DNA probe test (20 strains each) was studied. The majority (14 strains) of M. avium could grow at 45 degrees C, but none of M. intracellulare grew at the same temperature. All M. avium and the majority of M. intracellulare (80%) utilized n-butanol but failed to utilize iso-butanol. Therefore, the utilization test of butanols is inadequate for classification of these species.

Butanols↗
PubMed1980

Effect of n-butanol on Na+, K+-ATPase.

The effect of n-butanol on the activity of Na+, K+-ATPase has been found different at different temperatures. Below the phase-transition temperature, n-butanol has a stimulating effect provided the concentration is not higher than 0.3 M. But if the activity is determined above the phase-transition temperature, n-butanol has an inhibitory effect. The p-nitrophenyl phosphatase activity has been found to be inhibited by n-butanol even at comparatively low temperatures. This is in accord with the finding that the Arrhenius plot for p-nitrophenyl phosphatase did not show any break. It is suggested that at lower temperatures the conformational change involved in the transport of Na+, K+ ions may be the rate-limiting factor in the overall reaction, and n-butanol may be used as a probe for perturbation of the membrane to elucidate the mechanism of Na+, K+-ATPase.

4-Nitrophenylphosphatase↗
PubMed1981

Immunobiological properties of 1-butanol-extracted cell surface antigens.

Extracts of viable 3-methylcholanthrene-induced murine sarcoma cells (MCA-F and MCA-2A) prepared using single-phase (2.5%) 1-butanol significantly retarded the outgrowth of the homotypic, but not the heterotypic, tumor of syngeneic C3H/HeJ mice. Butanol extracts specifically evoked a delayed hypersensitivity response in tumor-immune syngeneic mice, but not in alloimmune DBA/2J mice. Crude butanol extracts of MCA-F cells did not contain alloantigenic activity, as shown by their inability to block H-2 or Ia-specific antibodies in a complement-dependent cytotoxicity assay. Absorption of these same allospecific reagents with untreated or with butanol-extracted cells indicated that H-2 antigens remain associated with the cell surface during extraction. Thus, butanol appears to release tumor antigens, but not alloantigens, from the cell surface.

Animals↗
PubMed1999

Extractive acetone-butanol-ethanol fermentation using methylated crude palm oil as extractant in batch culture of Clostridium saccharoperbutylacetonicum N1-4 (ATCC 13564).

The possibility of employing methylated crude palm oil (CPOE) as an extraction solvent to reduce end-product inhibition and to enhance solvent productivity in acetone-butanol-ethanol (ABE) fermentation was evaluated using oleyl alcohol as the standard butanol extractant. Fermentation was carried out at an initial glucose concentration of 90 g/l. CPOE did not inhibit the growth of the fermentative organism. Without solvent extraction, butanol production ceased after 30 h at a concentration of 15.4 g/l limiting cell growth to 3.98 g/l and glucose consumption to 62%. Applying CPOE as the extraction solvent, about 47% of the total butanol produced was extracted, glucose consumption was increased to 83% and relatively high glucose consumption rates and solvent productivities were obtained. Butanol production increased to 20.9 g/l; total ABE solvents and yield also increased from 21.2 g/l and 38% (in conventional fermentation) to 29.8 g/l and 40.4%, respectively.

Journal Article↗