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PubMed1976

Effect of acetone on production of aflatoxins and versicolorin pigments by resting cell cultures of Aspergillus parasiticus.

Resting cell cultures of Aspergillus parasiticus were grown in medium containing four different concentrations of glucose, with and without acetone. In addition, the effect of different equimolar concentrations of acetone, acetic acid, ethanol, and sodium acetate was compared at two glucose levels. Aflatoxin and versicolorin pigment production increased in resting cell medium containing increasing concentrations of glucose. In the presence of glucose high concentrations of acetone (1.0 and 0.25 M) inhibited secondary biosynthesis and low concentrations of acetone (0.1, 0.025 and 0.01 M) stimulated secondary biosynthesis of aflatoxins and versicolorin pigments.

Acetates↗
PubMed1986

The metabolism of acetone in the pregnant rat.

The administration of a single dose of acetone (100 mg/kg bw) to virgin and 21-day pregnant rats resulted in the appearance of relatively high concentrations of 1,2-propanediol, acetol and methylglyoxal in plasma and liver. In the fetuses no methylglyoxal was detectable. The acetone metabolism curves tend to indicate that the capacity for acetone disposal may be enhanced in the 48 hr-fasted pregnant rat, thus enabling the animal to re-use acetone metabolically, possibly for accelerated gluconeogenesis.

Acetone↗
PubMed1999

Identification of cerebral acetone by 1H-MRS in patients with epilepsy controlled by ketogenic diet.

Ketogenic diet (KD) is highly effective in controlling epileptic seizures in children. One of the mechanisms postulated, the accumulation of ketone bodies, acetoacetate (AcAc) and/or betahydroxybutyrate (beta-OHB) in the brain, would be detectable by non-invasive proton magnetic resonance spectroscopy (1H-MRS). 1H-MRS was performed in occipital cortical grey matter in 14 epileptics (E); ages 3.8-48.3 years), seven KD and seven without, and 16 healthy age-matched subjects. One E was examined before and after KD. A singlet resonance (sigma = 2.22 ppm), distinct from AcAc (sigma = 2.26 and 3.46 ppm), and identified as acetone was present in all spectra of children on KD (nine spectra in five children; concentration 0.7 +/- 0.2 mM). This resonance was absent from Control and E without diet. AcAc and beta-OHB, which were not detectable in KD brain, were found in urine or blood of all KD. Seizures were well controlled in all E in whom acetone was detected. Two of seven E, both adults, were seizure-free without detectable acetone. Cerebral acetone may contribute to seizure control in KD, but is unlikely to be the sole mechanism.

Acetone↗
PubMed1997

Biological monitoring of styrene exposure and possible interference of acetone co-exposure.

The object of this study is the evaluation of some of the toxicokinetic effects of exposure to low concentrations of styrene, and the possible influence of simultaneous exposure to acetone. To this end we studied 19 workmen simultaneously exposed to both solvents. During a week of 4-h work shifts, the workmen underwent daily personal environmental monitoring and the collection of urine samples, at both the beginning and the end of the work period, for the determination of mandelic acid (MA) and phenylglyoxylic acid (PGA). The presence of the solvents in the atmosphere was evaluated using passive personal monitoring and gas chromatography. Average exposure to styrene and acetone were respectively 72.2 mg/m3 and 225.7 mg/m3. MA and PGA were quantified by high-performance liquid chromatography (HPLC). The daily urinary concentration averages, both at commencement and at the end of work shifts, of both the metabolites studied and of the sum of the two were in statistically significant linear correlation with the average daily styrene exposure. Concentrations of MA and PGA in urine samples collected at the start of the work shift averaged 61.5 mg/g creatinine and 45.2 mg/g creatinine respectively, representing 41% and 72% of those at the endo of the work shift which were 148.3 and 62.6 mg/g creatinine, respectively. With equal exposure to styrene, the average urinary concentrations of MA and PGA at both the beginning and end of the work shift increased significantly (P < 0.001) during the working week. Moreover, we found that with equal exposure to styrene, urinary excretion of MA, PGA and MA + PGA at the end of the shift was inversely correlated with the intensity of acetone exposure (r = 0.4659, 0.3410 and 0.542 respectively, P < 0.001). In conclusion, these results express slower urinary kinetics of styrene metabolites than is usually described in the literature, and favor a tendency to accumulate MA and PGA in the organism as a consequence of the retardation of urinary excretion kinetics. Acetone apparently represents one of the determining factors in this interference.

Acetone↗
PubMed1986

Effect of acetone precipitation on the clinical prediction of respiratory distress syndrome when utilizing amniotic fluid lecithin/sphingomyelin ratios.

Amniotic fluid lecithin-to-sphingomyelin ratios are widely used to predict fetal lung maturity. The inclusion of acetone precipitation in the determination of the lecithin/sphingomyelin ratio has been widely accepted as a necessary step for enhancing predictivity. The lecithin/sphingomyelin ratio of 181 amniotic fluid samples was analyzed with and without acetone precipitation. Sensitivity, specificity, and predictive values were compared. Although there was a significant difference in the numeric value (p less than 0.001) between the two methods, the clinical prediction of the respiratory distress syndrome was not significantly enhanced by acetone precipitation. We conclude that acetone precipitation fails to improve the prediction of fetal lung maturity by lecithin/sphingomyelin ratio analysis.

Acetone↗
PubMed1986

Determination of the concentration and specific activity of acetone in biological fluids.

The concentration of acetone dissolved in liver perfusion medium was determined by injection of the sample into a gas chromatograph equipped with a Carbopack/Carbowax-packed glass column. Interference from labile acetoacetate which readily decomposes to acetone was eliminated by treating the samples with NaBH4 prior to the analysis. Acetone was detected and quantified as 2-propanol. Separation of labeled 2-propanol in the sample by high-performance liquid chromatography allowed the determination of its specific activity. These methods make possible the convenient and rapid determination of acetone concentration and specific activity in biological samples.

1-Propanol↗
PubMed1988

Accumulation of phenols and catechols in isolated mouse hepatocytes in starvation or after pretreatment with acetone.

Conditions leading to the accumulation of unconjugated phenols and catechols were investigated in mouse livers. The formation of unconjugated hydroxylated products of added p-nitrophenol and aniline was investigated in isolated hepatocytes prepared from 48 hr fasted or fed mice or from fed mice after acetone pretreatment. 4-Nitrocatechol and p-aminophenol--the hydroxylated products of p-nitrophenol and aniline--were accumulated in cells prepared from fasting animals, while in cells prepared from fed mice these unconjugated derivatives were not detectable. The accumulation of 4-nitrocatechol and p-aminophenol was also shown in isolated hepatocytes prepared from acetone pretreated fed mice. Inhibition of glucuronidation by N6,O2-dibutyryl cAMP or by D-galactosamine increased the accumulation of 4-nitrocatechol upon addition of p-nitrophenol in cells prepared from fasted mice. Both 48 hr starvation and acetone pretreatment enhanced the activity of microsomal p-nitrophenol and aniline hydroxylase by 300% and 600%, respectively, whereas p-nitrophenol conjugation in isolated hepatocytes as well as in hepatocyte homogenates was decreased by about 80% after 48 hr starvation. Acetone pretreatment did not alter the rate of p-nitrophenol conjugation measured in liver homogenates. It is suggested that a shift from conjugation toward hydroxylation in starvation gives rise to the formation of hazardous metabolites.

Acetone↗
PubMed1980

Differential effects of acetone or Aroclor 1254 pretreatment on the microsomal activation of dimethylnitrosamine to a mutagen.

Pretreatment of mice with acetone enhances the microsomal N-demethylation of dimethylnitrosamine (DMN) at low substrate concentrations (< 5 mM), while pretreatment with Aroclor 1254 represses this activity at low, but enhances it at high (> 35 mM) DMN concentrations. To relate the activity of DMN demethylase with the mutagenicity of DMN, liver microsomes were isolated aseptically from mice 18 h after acetone (3 ml/kg, ip), 5 days after Aroclor 1254 treatment (500 mg/kg, ip), or after treatment with the appropriate injection vehicles, and incubated with S. typhimurium (TA 1535), NADPH and DMN (1, 3 or 70 mM) for 5 to 60 min. After a 48-h incubation on minimal media, revertants per plate were determined. Microsomes from acetone pretreated mice bioactivated DMN to a mutagen at significantly higher (p < 0.001) levels when incubations were performed at 1 mM DMN. Aroclor-1254 microsomes exhibited a decreased ability to convert DMN to a mutagen at both 1 and 3 mM DMN (p < 0.05) and a significantly higher (p < 0.05) ability at 70 mM DMN. These data and published reports suggest multiple microsomal enzymes for DMN bioactivation and that acetone may enhance the enzyme that operates at environmentally important levels of DMN.

Acetone↗
PubMed1987

Metabolism and deposition of propanol and acetone vapors in the upper respiratory tract of the hamster.

While it is thought that local metabolism may enhance nasal deposition of inspired vapors, there have been no studies designed to quantitate this effect. In the current study, deposition of 1-propanol (a metabolized vapor) and acetone (a nonmetabolized vapor) was studied in the surgically isolated upper respiratory tract (URT) of the anesthetized Syrian hamster. The effect of inspiratory flow rate on URT deposition of acetone could be described by a ventilation-perfusion (V-P) model with a nasal perfusion rate of 0.046 ml/min. Theoretical considerations predict that at enzyme saturation, deposition efficiency will be dependent upon the inspired concentration and the URT metabolism rates can be estimated from the concentration-dependence data. A concentration dependence on propanol deposition efficiency was observed at a flow rate of 200 ml/min, but not at 38 or 71 ml/min. At a flow rate of 200 ml/min, an apparent URT metabolism rate of 3.8 micrograms/min (95% confidence limits 0.5-7.1 micrograms/min) was estimated. In vitro studies on nasal tissue homogenates provided metabolism rates of approximately 2 micrograms/min, values which did not differ significantly from, and therefore, were in reasonable agreement with, the estimates from the deposition studies. After correction for the effect of metabolism, URT propanol deposition could be described by the V-P model with a nasal perfusion rate of 0.050 ml/min. This value did not differ significantly from that observed in the acetone studies. Thus, deposition of both propanol and acetone in the URT of the Syrian hamster could be described by the V-P model.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Propanol↗
PubMed1989

Pharmacological and metabolic interactions between ethanol and methyl n-butyl ketone, methyl isobutyl ketone, methyl ethyl ketone, or acetone in mice.

Methyl n-butyl ketone (MnBK), methyl isobutyl ketone (MIBK), methyl ethyl ketone (MEK), and acetone are widely used industrial solvents to which certain groups of workers are exposed. Pharmacological and metabolic interactions between these solvents and ethanol were explored in male CD-1 mice. The effects of these solvents on the duration of ethanol-induced loss of righting reflex and on ethanol elimination in mice were studied. The solvents were dissolved in corn oil and injected intraperitoneally 30 min before ethanol 4 g/kg ip. The four solvents prolonged significantly the duration of ethanol-induced loss of righting reflex when given in the following doses (mmol/kg): MnBK, 3.75 and 5; MIBK, 5; MEK, 5 and 10, acetone, 20 and 40. This prolongation was dose related and increased as the dose of the solvent was increased. The concentrations of ethanol in blood or brain on return of the righting reflex were similar in solvent-treated and control animals, with the exception of the group of mice treated with 40 mmol/kg acetone in which the ethanol concentrations were significantly lower than in control animals. The mean elimination rate of ethanol was markedly reduced in mice treated with MnBK 5 mmol/kg, MEK 15 mmol/kg, and acetone 40 mmol/kg. All four solvents reduced the activity of mouse liver alcohol dehydrogenase in vitro. It is concluded that enhancement of the ethanol-induced loss of righting reflex by these solvents in mice is well correlated to reduced elimination rate of ethanol.

Acetone↗
PubMed1983

Acetone-induced potentiation of trihalomethane toxicity in male rats.

The acute hepato- and nephrotoxic potentials of two trihalomethane water contaminants, bromodichloromethane (BrCHCl2) and dibromochloromethane (Br2CHCl), were determined in male Sprague-Dawley rats. Br2CHCl possessed a greater hepatotoxic and lethal potential than BrCHCl2. However, both Br2CHCl and BrCHCl2 were weak hepatotoxicants as compared to a related trihalomethane, CHCl3. Br2CHCl and BrCHCl2 did not produce liver injury until near-lethal dosages were administered. Neither trihalomethane appeared to produce appreciable kidney injury during the 24-h challenge period. Pretreatment of rats with acetone (15 mmol/kg, p.o.) markedly potentiated the hepatotoxic response to BrCHCl2 and Br2CHCl. The potentiated response observed with acetone plus BrCHCl2 or Br2CHCl was equal to or greater than that observed with acetone plus an approximately equimolar dosage of CHCl3. That is, acetone appeared to convert these weak hepatotoxicants into strong hepatotoxicants.

Acetone↗
PubMed1989

Acetone compared to other ketones in modifying the hepatotoxicity of inhaled 1,2-dichlorobenzene in rats and mice.

The ability of acetone and 3 other ketone vapours to influence the hepatotoxicity of inhaled 1,2-dichlorobenzene (DCB) was examined in rats and mice. Methylethylketone, methylisobutylketone or cyclohexanone increased liver cytochrome P-450 content and glutathione-S-transferase (GST) activity, but did not affect serum glutamate dehydrogenase (GLDH) activity in rats. Pre-exposure to these ketones enhanced DCB-induced increase in serum GLDH activity (8-63-fold), while the increases in cytochrome P-450 content (33-86%) and GST activity (42-64%) were identical to those resulting from exposure to ketones alone. Each of the 3 levels of exposure to acetone elicited cytochrome P-450 and GST responses comparable with those caused by the other ketones. In spite of that, acetone pre-exposure potentiated (4785 ppm), reduced (10670 ppm) or suppressed (14790 ppm) DCB-induced liver toxicity. In mice, the 3 ketones mentioned above interacted with DCB on centrolobular liver glucose-6-phosphatase (G-6-Pase) while acetone pre-exposure elicited an interactive G-6-Pase response in the mediolobular area alone, suggesting topographic change.

Acetone↗
PubMed2004

Stability of toluene and reduction of acetone to 2-propanol in homogenates of the human liver, brain and lungs.

The homogenates of the livers, lungs and brains collected from five different cadavers were placed in the desiccator filled with vapours of rubber glue solvents and the concentrations of toluene, acetone and 2-propanol were determined during the 28-day storage at +25, +4 and -20 degrees C. It was demonstrated that only freezing of the material stabilised the initial concentration of these three xenobiotics while cooling to +4 degrees C resulted in limited conversion of acetone to 2-propanol and additionally reduced the biodegradation of toluene in the brain homogenates. Moreover, it was showed that at +25 degrees C the loss of acetone was almost equimolarly balanced by the 2-propanol increase, which allowed to estimate the initial concentration of acetone with the mean error of about 10%.

2-Propanol↗
PubMed2006

Olanzapine-induced hyperglycemic ketoacidosis and corresponding acetone concentrations post-mortem: a forensic interpretation.

Olanzapine has been shown to cause or have a contributory role in the development of hyperglycemia and diabetes mellitus. Without careful monitoring for the development of these conditions and control of the resulting adverse effects, patients receiving olanzapine may be at risk of developing fatal ketoacidosis. A review of post-mortem toxicological reports has revealed an increase in the incidence of post-mortem findings of acetone in decedents who were taking olanzapine over the past decade. A review of the current literature and a comprehensive review of case histories and toxicological findings were conducted at the Centre of Forensic Sciences (Toronto, Ontario). Olanzapine concentrations ranging from <62.5 to 858 ng/mL and acetone concentrations as high as 95 mg/dL were detected concurrently. Due to the unstable nature of olanzapine, in several instances quantitation was not possible despite elevated responses during qualitative screening procedures. Five cases suggesting olanzapine-induced ketoacidosis were identified based on the case history and toxicological findings. These data have been compiled and examined with respect to acetone concentrations following olanzapine use and the forensic relevance of post-mortem olanzapine and acetone concentrations are discussed.

Acetone↗
PubMed1991

High-performance liquid chromatographic determination of acetone in blood and urine in the clinical diagnostic laboratory.

A method for the determination of acetone in plasma or urine by high-performance liquid chromatography (HPLC) was developed. Plasma specimens are deproteinized with acetonitrile (1:1, v/v) 2,4-dinitrophenylhydrazine (DNPH) is added to the supernatant or to filtered urine samples, similarly treated with acetonitrile (2:1, v/v) to prevent crystallization of the synthesized phenylhydrazone. An aliquot (20 microliters) of the reaction mixture was subjected to HPLC at ambient temperature using a reversed-phase Pecosphere 3 x 3 C18 column with acetonitrile-water (45:55, v/v) as eluent at a flow-rate of 1 ml/min and detection at 365 nm. Hydroxyacetone and acetoacetate phenylhydrazone derivatives do not interfere. The identification of acetone by its retention time was confirmed by comparison with a laboratory-synthesized acetone DNPH derivative. The concentration of acetone, eluted within 3 min, was determined by the peak-height method. The detection limit was 0.034 mmol/l; the relative standard deviations were less than 5% within run (n = 20) and less than 10% between run (n = 20).

Acetone↗
PubMed2000

A screening level examination of the potential risks of acetone in aquatic and terrestrial environments using multi-media modeling.

Approximately half of the approximately 40 million tonnes per annum (t/a) of acetone released worldwide arises via natural processes. The remaining releases of acetone are the focus of this assessment and arise either as a photo-degradation by-product of other organic compounds (approximately 20 million t/a) or by entering the environment from manufacturing and end uses (59,000 t/a). Multi-media modeling was used to estimate regional concentrations of acetone in air, water, soil and sediment that may occur based on these anthropogenic releases to the environment. US toxics release inventory data were used to calculate local surface water concentrations. The distributions of all regional and local concentrations in all media were below applicable predicted no effect concentrations (PNECs). Calculated regional and local concentrations of acetone, originating from all anthropogenic sources, appear unlikely to cause adverse risks to the environment.

Acetone↗
PubMed2001

Effect of Phenyl-P/HEMA acetone primer on wet bonding to EDTA-conditioned dentin.

OBJECTIVES: The purpose of this study was to examine the effect of 2-methacryloyloxyethyl phenyl phosphoric acid (Phenyl-P)/2-hydroxyethyl methacrylate (HEMA) acetone-based primer on moist dentin surfaces that were preconditioned with ethylenediaminetetraacetate (EDTA) to remove the smear layer. METHODS: Bovine dentin were prepared with 180-grit paper, conditioned with 0.5M EDTA (pH 7.4) for 60s followed by water rinsing and then blot drying. Each surface was then primed with Phenyl-P/30 wt% HEMA in acetone for 10s followed by blot drying. A light-cured bonding agent was then applied, cured and trimmed to give dumbbell-shaped specimens. The Phenyl-P concentration ranged from 1 to 20 wt%. During the bonding procedure, no compressed air was used. After storage in water at 37 degrees C for one day, tensile bond strengths were measured and analyzed using one-way ANOVA. Dentin discs treated under the same conditions were observed under a scanning electron microscope (SEM). RESULTS: When the concentration of Phenyl-P was 12 wt%, the highest mean tensile bond strength was obtained (27 MPa). It was significantly higher than that of the 3, 5, 15 or 20 wt% groups (9-11 MPa) (p<0.05). The samples of 1 wt% group were all broken during trimming the dumbbell-shaped specimens. SEM observations showed a 1 microm-thick layer of hybridized dentin after polished cross-sections were chemically challenged with 6N HCl for 30s and then 1% NaOCl for 60 min. SIGNIFICANCE: The experimental Phenyl-P/HEMA acetone primer is effective in bonding resin to EDTA-conditioned dentin. Acetone as a solvent for Phenyl-P/HEMA primer has the clinical advantage of not requiring an air-stream to evaporate the solvent. The experimental bonding procedure can minimize the skin irritation by HEMA.

Acetone↗
PubMed2002

Comparing the performance of various advanced oxidation processes for treatment of acetone contaminated water.

Removal of low levels of organic pollutants can be quite challenging to many water treatment processes. Ketones, such as acetone, are often found in groundwaters and wastewaters at levels too low for supporting a bioreactor, yet since acetone is so soluble, it does not adsorb onto activated carbon very well, nor does it volatilize from water influent using air stripping. This study was undertaken to evaluate three advanced oxidation processes for their comparative ability to remove acetone from aqueous media. Optimization of the oxidation processes was attempted via adjustments of oxidizer inputs. The results indicated that all of the AOPs tested showed promise for removing acetone from water; however, ozonated systems undergoing UV photolysis achieved the highest rate and extent of treatment observed.

Acetone↗