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PubMed1994

Fermentative degradation of acetone by an enrichment culture in membrane-separated culture devices and in cell suspensions.

A mixed culture, WoAct, growing on acetone, consisted of two dominant morphotypes: a rod-shaped acetone-fermenting bacterium producing acetate, and an acetate-utilizing Methanosaeta species. Dense cell suspensions, largely free of the aceticlastic methanogen and supplemented with bromoethanesulfonate, were able to degrade acetone and grow in small volumes in membrane-separated culture devices in which the acetate produced could diffuse into a large volume of medium. Acetone degradation and growth halted when the acetate concentration reached about 10 to 12 mM. Cell suspensions were able to degrade acetone in the absence of active methanogenesis, but the addition of 10 mM acetate inhibited acetone metabolism. Addition of an active culture of Methanosaeta sp. greatly stimulated the rate of acetone degradation. The results show that acetate removal in the mixed culture is not a prerequisite for growth and acetone degradation by the acetone-fermenting bacterium.

Acetates↗
PubMed1997

Reclamation of acetone in plastination laboratories: a simple and inexpensive method.

Since the introduction of the plastination process by von Hagens [Anat Rec 194/2: 247-256, 1979], the cost of acetone used for the dehydration step has been considered an important factor in the cost of plastination. We have developed a three-step method that permits the reuse of acetone. The first step simply consists of storing the contaminated acetone in the freezer and separating the congealed fat by filtration. The second step is vacuum distillation of the acetone and can be conducted with the freezer and vacuum pump (found in any plastination laboratory) with just a few additions. It produces 95-97% pure acetone. The last step uses a desiccant to take away the residual water from the distilled acetone and brings the purity to 99.5%. With this method, we have reduced the amount of acetone to be purchased to a minimum and completely eliminated the cost of discarding used acetone. In addition vaporized acetone released during the impregnation step of plastination is recaptured.

Acetone↗
PubMed2004

Phenotypic and genetic influences on test-day measures of acetone concentration in milk.

The objectives of this study were to estimate heritability of acetone concentration in milk, based on monthly samples of milk obtained as part of a routine milk testing program, and to evaluate the feasibility of using such data in a genetic evaluation program for selection against ketosis incidence. Milk samples were collected from January to December of 1999 in herds enrolled in the Ontario Dairy Herd Improvement Association, and acetone concentration was measured using an inline chemical procedure. The original data included more than 50,000 records. Because ketosis is generally a problem during early lactation, only the single test with the fewest days in milk was retained. In addition, data were retained only for cows with pedigree information. The final data set included 10,375 records. Among these data, only 6.56% had detectable levels of acetone. Acetone data were log-transformed prior to statistical analysis. Simple ANOVA indicated that herd, parity number, days in milk, and month of test had significant effects on acetone concentration. Acetone levels increased with lactation number and were higher in early lactation. Three approaches were applied for genetic analysis. First, REML was used with a simple linear animal model. Then, a separate procedure used data augmentation and Gibbs Sampling to obtain continuously distributed underlying values for records with zero acetone concentration, and these data were analyzed with both an animal and sire model. Heritability of acetone concentration was less than 1% for all 3 analyses. Herd effects accounted for about 5% of the phenotypic variance. Low estimates of heritability were due either to low actual levels of genetic variance or inability to detect all of the genetic variance present, due to infrequent recording during the early part of the lactation. Genetic evaluation based on recording of acetone concentration on a monthly basis seems of little use as a selection tool to decrease incidence of ketosis.

Acetone↗
PubMed1993

Bacterial degradation of acetone in an outdoor model stream.

Diurnal variations of the acetone concentration in an outdoor model stream were measured with and without a nitrate supplement to determine if the nitrate supplement would stimulate bacterial degradation of the acetone. Acetone loss coefficients were computed from the diurnal data using a fitting procedure based on a Lagrangian particle model. The coefficients indicated that bacterial degradation of the acetone was occurring in the downstream part of the stream during the nitrate addition. However, the acetone concentrations stabilized at values considerably above the limit of detection for acetone determination, in contrast to laboratory respirometer studies where the acetone concentration decreased rapidly to less than the detection limit, once bacterial acclimation to the acetone had occurred. One possible explanation for the difference in behavior was the limited 6-hour residence time of the acetone in the model stream.

Journal Article↗
PubMed2005

Breath acetone predicts plasma ketone bodies in children with epilepsy on a ketogenic diet.

OBJECTIVE: The high-fat ketogenic diet has long been used to treat refractory childhood seizures, but whether there is a relation between the degree of ketosis and effectiveness of seizure control remains unclear. Frequent measurements of plasma ketones are difficult in children so the goal was to determine the utility of breath acetone as a marker of systemic ketosis and seizure control in children given the ketogenic diet because of seizures refractory to medication. METHODS: In experiment I, breath acetone and plasma ketones were assessed every 2 h during an 8-h test day in seven children. In experiment II, a preliminary assessment of the possible relation between breath acetone and seizure frequency was made over 14 d in five children and one adolescent on the ketogenic diet. RESULTS: Breath acetone was positively and curvilinearly related to plasma acetone (r2 = 0.99, P < 0.0001), plasma acetoacetate (r2 = 0.89, P < 0.0001), and plasma beta-hydroxybutyrate (r2 = 0.94, P < 0.0001). No significant relation was found between breath acetone and seizure frequency or change in seizure frequency. CONCLUSIONS: Breath acetone is indicative of systemic ketosis while on the ketogenic diet. However, owing to the wide range of seizure types and plasma acetone, more subjects will be needed to determine whether there is a clear link between breath acetone and seizure frequency or decreased seizure frequency while on the high-fat ketogenic diet.

Adolescent↗
PubMed2001

Switch-over in photochemical reaction mechanism from hydrogen abstraction to exciplex-induced quenching: interaction of triplet-excited versus singlet-excited acetone versus cumyloxyl radicals with amines.

The fluorescence and phosphorescence quenching of acetone by 13 aliphatic amines has been investigated. The bimolecular rate constants lie in the range of 10(8)-10(9) M(-1) s(-1) for singlet-excited acetone and 10(6)-10(8) M(-1) s(-1) for the triplet case. The rate data indicate that a direct hydrogen abstraction process dominates for triplet acetone, while a charge-transfer mechanism, namely, exciplex-induced quenching, becomes important for singlet-excited acetone. Pronounced stereoelectronic effects toward H abstraction, e.g., for 1,4-diazabicyclo[2.2.2]octane (DABCO), and significant steric hindrance effects, e.g., for N,N-diisopropyl-3-pentylamine, are observed. A negative activation energy (E(a) = -0.9 +/- 0.2 kcal mol(-1) for triethylamine and DABCO) and the absence of a significant solvent effect on the fluorescence quenching of acetone are indicative of the involvement of exciplexes. Full electron transfer can be ruled out on the basis of the low reduction potential of acetone, which was found to lie below -3.0 V versus SCE. The participation of H abstraction for triplet acetone is corroborated by the respective quenching rate constants, which resemble the reaction rate constants for cumyloxyl radicals. The latter were measured for all 13 amines and showed also a dependence on the electron donor properties of the amines. It is suggested that the H abstraction proceeds directly and not through an exciplex or ion pair. Further, abstraction from N-H bonds in addition to alpha C-H bonds has been corroborated as a significant pathway for excited acetone. Product studies and quantum yields for photoreduction of singlet- and triplet-excited acetone by triethylamine (8% for S(1) versus 24% for T(1)) are in line with the suggested mechanisms of quenching through an exciplex and photoreduction through direct H abstraction.

Journal Article↗
PubMed2000

Relative roles of CYP2E1 and CYP1A2 in mouse uroporphyria caused by acetone.

Porphyria cutanea tarda is a liver disease characterized by excess production of uroporphyrin. We previously reported that acetone, an inducer of CYP2E1, enhances hepatic uroporphyrin accumulation in mice treated with iron dextran (Fe) and 5-aminolevulinic acid (ALA). Cyp2e1(-/-) mice treated with Fe and ALA were used to investigate whether CYP2E1 is required for the acetone effect. Hepatic uroporphyrin accumulation was stimulated by acetone in Cyp2e1(-/-) mice to the same extent as in wild-type mice. In the absence of acetone, uroporphyrin accumulated in Cyp2e1(-/-) mice treated with Fe and ALA, but less than in wildtype mice. However, in Cypla2(-/-) mice, uroporphyrin accumulation caused by Fe and ALA, with or without acetone, was completely prevented. Acetone was not an inducer of hepatic CYP1A2 in the wild-type mice. Although acetone is an inducer of CYP2E1, CYP1A2 appears to have the essential role in acetone-enhancement of uroporphyria.

Acetone↗
PubMed1998

Assay of low deuterium enrichment of water by isotopic exchange with [U-13C3]acetone and gas chromatography-mass spectrometry.

A sensitive assay of the 2H-enrichment of water based on the isotopic exchange between the hydrogens of water and of acetone in alkaline medium is described and validated. For low 2H-enrichments (0.008 to 0.5%), the sample is spiked with [U-13C3]acetone and NaOH. After exchange, 2H-enriched [U-13C3]acetone is extracted with chloroform and assayed by gas chromatography-mass spectrometry. With some instruments, ion-molecule reactions, resulting in increased baseline enrichment, are minimized by lowering the electron ionization energy from the usual 70 to 10 eV. The 2H-enrichment of water is amplified nearly sixfold in the M4/M3 ratio of [U-13C3]acetone. For high 2H-enrichments (0.25 to 100%), the use of unlabeled acetone suffices. After exchange, the mass isotopomer distribution of acetone is analyzed, yielding the 2H-enrichment of water. The assay with [U-13C3]acetone allows measuring the 2H-enrichment of water even in biological samples containing acetone. This technique is more rapid and economical than the classical isotope ratio mass spectrometric assay of the enrichment of hydrogen gas derived from the reduction of water.

Acetone↗
PubMed1981

Inhalation pharmacokinetics based on gas uptake studies. II. Pharmacokinetics of acetone in rats.

Inhalation pharmacokinetics of acetone in rats was studied using gas uptake techniques. Under conditions of negligible metabolism (saturation of metabolizing enzymes) the coefficient of distribution Keq between organism and gas phase was 220 which confirmed that acetone is mainly (but not exclusively) distributed within the body water compartment. The metabolic elimination of acetone from the animals followed strict Michaelis-Menten saturation kinetics; the km corresponded to 160 ppm in the atmosphere, Vmax was 230 mumol x h(-1) x kg(-1). A shift in the distribution pattern of acetone under conditions of prevalent metabolism was theoretically predicted and experimentally proven; as the partial process of metabolic elimination was dose-dependent, this "depleted" the animal compartment from acetone in a dose-dependent fashion causing a shift in the "steady-state-constant", Kst. Part of the acetone which was metabolically eliminated (4.7%) appeared in the urine as formate within 7 days after ending a 48-h exposure to acetone; this excretion was linear with time. The data suggested existence of a formate pool in the organism from which formate was released with delay. Hence, limitations may be inferred as to the applicability of urinary formate excretion as a quantitative indicator for changing conditions of acetone exposure.

Acetone↗
PubMed2003

Ethanol and acetone stimulate the proliferation of HaCaT keratinocytes: the possible role of alcohol in exacerbating psoriasis.

Alcohol has been reported to be a risk factor in psoriasis mainly based on the observation that there is a higher prevalence of alcohol abuse in individuals with psoriasis. The mechanism by which alcohol affects this disease is still elusive. So far there are no reports describing the effects of metabolites relevant to alcohol metabolism on the growth of human keratinocytes. In the present study we examined the effects of ethanol and acetone, which exceeds its normal endogenous level in the blood of heavy drinkers, on the proliferation of HaCaT keratinocytes. HaCaT cells were incubated for 30 min in the presence of various concentrations of ethanol (2.14 m M-1.71 M) and acetone (1.7 mM-1.36 M). The numbers of viable and proliferating cells were determined at different times after ethanol and acetone treatment. The effects of ethanol and acetone on the mRNA levels of genes characteristic for proliferating keratinocytes such as alpha5 integrin, keratinocyte growth factor receptor and cyclin D1 were studied by reverse-transcriptase polymerase chain reaction. Both ethanol and acetone induced proliferation of HaCaT cells. The maximum increase in the number of viable cells and the maximum proliferative response was observed with 4.28 m M ethanol and 13.6 m M acetone. The alpha5 integrin, keratinocyte growth factor receptor and cyclin D1 mRNA levels were higher compared to the controls as early as 2 h after ethanol and 30 min after acetone treatment of the cells. The stimulatory effect of ethanol and acetone on human keratinocytes may be one of the reasons why psoriasis can be precipitated by alcohol misuse.

Acetone↗
PubMed1988

Increased microsomal interaction with iron and oxygen radical generation after chronic acetone treatment.

In vivo administration of acetone influences a variety of reactions catalyzed by rat liver microsomes. The effect of chronic treatment with acetone (1% acetone in the water for 10-12 days) on interaction with iron and subsequent oxygen radical generation by liver microsomes was evaluated. Microsomes from the acetone-treated rats displayed elevated rates of H2O2 generation, an increase in iron-dependent lipid peroxidation, and enhanced chemiluminescence upon the addition of t-butylhydroperoxide. The ferric EDTA-catalyzed production of formaldehyde from DMSO or of ethylene from 2-keto-4-thiomethylbutyrate was increased 2-fold after acetone treatment. This increase in hydroxyl radical generation was accompanied by a corresponding increase in NADPH utilization and was sensitive to inhibition by catalase and a competitive scavenger, ethanol, but not to superoxide dismutase. In vitro addition of acetone to microsomes had no effect on oxygen radical generation. Associated with the chronic acetone treatment was a 2-fold increase in the microsomal content of cytochrome P-450 and in the activity of NADPH-cytochrome-P-450 reductase. It appears that increased oxygen radical generation by microsomes after chronic acetone treatment reflects the increase in the major enzyme components which comprise the mixed-function oxidase system.

Acetone↗
PubMed1990

Effects of acetone administration on drug-metabolizing enzymes in mice: presence of a high-affinity diethylnitrosamine de-ethylase.

Treatment of CD1 mice with acetone raised activities of hepatic microsomal p-nitrophenol hydroxylase, ethoxycoumarin de-ethylase, acetone hydroxylase and diethylnitrosamine de-ethylase (DENd) several-fold. P-450IIE1-linked acetone hydroxylase showed the highest inducibility. In microsomes from acetone-pretreated mice the cytochrome b5 and P-450 content was nearly doubled and their electrophoretic profile showed induction of a protein of Mr 53,000, probably P-450IIE1. Liver phase II enzymes were not affected by acetone treatment. Kinetic analyses of DENd were performed in control or acetone-induced microsomes and Km and Vmax were determined. Two distinctly apparent Km values (0.56 and 20.3 mM) were observed for DENd of control microsomes and at least 3 apparent Km values (0.05, 0.51, 8.4 mM) were observed in acetone-induced microsomes. Thus, acetone administration to mice induces a high-affinity form of DENd which can be important in vivo at low diethylnitrosamine (DEN) exposure as this enzyme functions when DEN concentration is below 0.1 mM.

Acetone↗
PubMed2005

Relationship between skin acetone and blood beta-hydroxybutyrate concentrations in diabetes.

BACKGROUND: Acetone is emitted from the skin and acetone concentrations correlate with blood beta-hydroxybutyrate. METHODS: Skin acetone concentrations of 63 patients with diabetes and 32 control subjects were measured by cold trapping followed by gas chromatography. RESULTS: Skin acetone concentrations of patients with diabetes (188+/-17 ppb; mean+/-SE) were significantly higher than those of the control subjects (87+/-10 ppb, p<0.01). There was no significant difference in skin acetone concentrations among patients with diabetes with regard to mode of treatment. Skin acetone concentrations were correlated with blood beta-hydroxybutyrate (r=0.669, p<0.01), blood glucose (r=0.608, p<0.01), and HbA1c (r=0.292, p<0.05) in patients with diabetes. Skin acetone concentration was high (940 ppb) in a patient with diabetic ketoacidosis, and it fell to 80 ppb after insulin therapy. CONCLUSION: Measurement of skin acetone can be used as a screening test for ketoacidosis provided the analytical methods and tools become simpler. Moreover, it could become a marker of diabetic control and of ketone production in diabetes and other ketogenic conditions.

3-Hydroxybutyric Acid↗
PubMed2004

Rapid determination of acetone in human plasma by gas chromatography-mass spectrometry and solid-phase microextraction with on-fiber derivatization.

Acetone is an important volatile disease marker. Due to its nature of activity and volatility, it is a difficult task to measure the concentration of acetone in biological samples with accuracy. In this paper, we developed a novel method for determination of trace amount acetone in human plasma by solid-phase microextraction technique with on-fiber derivatization. In this method, the poly(dimethylsiloxane)/divinylbenzene (PDMS/DVB) fiber was used and O-2,3,4,5,6-(pentafluorobenzyl) hydroxylamine hydrochloride (PFBHA) was first loaded on the fiber. Acetone in plasma sample was agitated into headspace and extracted by solid-phase microextraction (SPME) fiber and subsequently derivatized with PFBHA on the fiber. Acetone oxime was analyzed by gas chromatography-mass spectrometry (GC-MS). Quantitative analysis of acetone in plasma was carried out by using external standard method. The SPME conditions (extraction temperature and time) and the method validation were studied. The present method was tested by determination of acetone in diabetes plasma and normal plasma. Acetone concentration in diabetes plasma was found to be higher than 1.8mM, while in normal plasma was lower than 0.017 mM. The results show that the present method is a potential tool for diagnosis of diabetes.

Acetone↗
PubMed2005

Removal kinetics of acetone and MIBK from a complex industrial wastewater by an acclimatized activated sludge.

Removal rates of acetone and methyl isobutyl ketone (MIBK) were determined singularly and in combination in batch experiments employing an acclimatized activated sludge from a pilot system treating an organic chemical manufacturer industrial wastewater, as well as during the course of operation of the pilot system. Both acetone and MIBK removals were described by first-order removal kinetics. Acetone, as a single substrate, was biodegraded at a rate of 1.7 day(-1). MIBK was biodegraded, during the single-substrate experiments, at an observed rate of 2.23 day(-1). Relative to the control (no spike) experiments, acetone removal was augmented by a factor of 3 during the acetone spike, with an observed biomass-specific removal rate of 0.0023 L/mg VSSday. MIBK removal during an MIBK spike was also enhanced by a factor of 2, and the greatest biomass-specific removal rate of MIBK was observed during the acetone spike of 0.0019 L/mg VSSday. The observed rates were approximately 3 orders of magnitude greater than the observed rates in the pilot scale system. MIBK exerted a synergistic effect on the acetone-removal rate while acetone exerted an inhibitory impact on the MIBK-removal rate.

Acetone↗
PubMed1988

Ethanol-, fasting-, and acetone-inducible cytochromes P-450 in rat liver: regulation and characteristics of enzymes belonging to the IIB and IIE gene subfamilies.

Two major forms of hepatic microsomal cytochrome P-450 were purified from starved and acetone-treated rats. On the basis of amino acid sequence analysis, they were identified as P-450j and P-450b. Ethanol or acetone treatment of rats caused a 9-fold increase in the amount of P-450j in liver microsomes accompanied by similar increases in the rate of NADPH-dependent metabolism of carbon tetrachloride, acetone, and benzene. Immunological experiments indicated that P-450j constitutes the major catalyst of the microsomal metabolism of the latter agents and contributes by about 50% to microsomal P-450-dependent ethanol oxidation under the conditions used. The P-450j-dependent catalytic activities had a high rate of turnover. In contrast, this was not the case for the immunodetectable P-450j, indicating the occurrence of inactive forms of this protein in microsomes. Starvation or ethanol or acetone treatment caused 10-30-fold increases in the amount of both mRNA and apoprotein of P-450b,e compared to control. Run-on experiments and the concomitant increases of the P-450b,e gene products at the mRNA and protein levels indicated the appearance of mainly a transcriptional activation by acetone, ethanol, or starvation. Fasting exerted, in addition, a pronounced synergistic effect on acetone-dependent induction of P-450b,e mRNA (3-fold), apo-P-450b,e (4.3-fold), P-450j mRNA (2-fold), and apo-P-450j (2-fold). No increase of mRNA coding for P-450j, compared to control, was seen after acetone or ethanol treatment alone. The results indicate that effects of ethanol, acetone, and/or starvation on drug and xenobiotic metabolism are caused by the induction of P-450 forms belonging to at least two gene subfamilies.

Acetone↗
PubMedDate not supplied

Enhanced glucose to fructose conversion in acetone with xylose isomerase stabilized by crystallization and cross-linking.

The effects of acetone and ethanol on glucose to fructose conversion catalyzed by soluble and cross-linked crystalline (CLXIC) xylose isomerase were studied. Relative to pure buffer solvent, the fructose production rate was more than doubled in 50% acetone. The same kind of increase in the isomerization rate was not seen with ethanol. Increase both in acetone and in ethanol concentration in the reaction solvent enhanced the production of fructose. At 50 degrees C in pure buffer solvent the reaction mixture contained 49% fructose in equilibrium and in 90% acetone the fructose equilibrium content was 64%. Furthermore, CLXIC was relatively stable in the presence of high concentration of acetone: 70-80% of activity was left after incubation for 24 h at 50 degrees C in buffer solutions (pH 7.2) containing 10-90% acetone. In buffer containing 50% ethanol only 2% of the initial activity of CLXIC was retained after 24 h at 50 degrees C. Soluble xylose isomerase was considerably less stable than CLXIC in both acetone- and ethanol-containing solutions. These results show that the addition of acetone enhances the production of fructose from glucose by enhancing the reaction rate and shifting the equilibrium toward fructose. However, xylose isomerase must be in the form of cross-linked crystals for maximal activity and stability.

Acetone↗
PubMed1997

[Survival after poisoning due to intake of ten-times lethal dose of acetone].

HISTORY AND ADMISSION FINDINGS: A 42-year-old man was found unconscious, having swallowed 800 ml of an unknown liquid with suicidal intent. On admission, when his breath smelled strongly of acetone, he was intubated and ventilated, and several gastric lavages were performed. INVESTIGATION: The serum acetone concentration was 2000 mg/l, that in urine 2300 mg/l. The residue of the liquid in the bottle from which he had drunk was pure acetone. DIAGNOSIS, TREATMENT AND COURSE: Acetone poisoning having been established he was carefully hyperventilated, haemofiltration was performed over 16 hours and forced diuresis with high fluid intake was undertaken. His condition quickly improved and he was extubated after 14 hours. There was no subsequent evidence of organ damage. Repeated measurements of acetone in blood and urine indicated its elimination with a half-life of 11 hours. Literature search revealed that this was the second highest concentration of acetone in blood and urine followed by survival. CONCLUSION: This case demonstrates that, after acute acetone poisoning with an amount ten times the lethal dose, intensive care and rapid elimination of acetone can achieve sequelae-free survival.

Acetone↗