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PubMed1988

Effects of short duration exposures to acetone and methyl ethyl ketone.

Workers are commonly exposed to mixtures or combinations of chemical agents, and these mixtures often consist of solvents. One group of solvents that has been extensively studied for its neurotoxic properties has been the ketones. However, previous research has focused on neuropathies produced by extended exposures and not on the simple pharmacokinetics or the reversible central nervous system (CNS) effects from short-duration exposures. In this research, 137 volunteers were recruited and tested for neurobehavioral performance changes and biochemical indicators during and after a short-duration (4-h) exposure to either acetone at 250 ppm, methyl ethyl ketone (MEK) at 200 ppm, acetone at 125 ppm with MEK at 100 ppm, or a chemical-placebo. Ethanol (95%, 0.84 ml/kg) was used as a positive control. Testing took place in an environmental chamber with four test stations. The computer-controlled test regimen took 10 h, and several measures were collected: (1) biochemical measurements of venous blood and alveolar breath; (2) psychomotor tests of choice reaction time, visual vigilance, dual task (auditory tone discrimination and tracking), and memory scanning; (3) one sensorimotor (postural sway) test; and (4) one psychological (Profile of Mood States [POMS]) test. Blood and breath concentrations during and after exposure did not demonstrate any interaction between the two solvents, nor were statistically significant sex differences present during uptake or elimination. The 250-ppm acetone exposure produced small but statistically significant differences from controls in two measures of the auditory tone discrimination task, and on the anger-hostility scale (males only) of the POMS test. The other chemical exposure conditions, MEK at 200 ppm and combination MEK with acetone, produced no consistent statistically significant results, which suggests there was no potentiation of the acetone effects with the co-exposure to MEK or vice versa under these test conditions. Ethanol at 0.07-0.08% blood alcohol concentration (BAC) caused significant decrements on both the auditory tone and tracking tests in the dual task.

Acetone↗
PubMed1991

Deposition of acetone vapor in the upper respiratory tract of the B6C3F1 mouse.

Deposition of inspired acetone vapor in the surgically isolated upper respiratory tract (URT) of the anesthetized B6C3F1 mouse was measured under unidirectional constant velocity flow conditions for comparison with our previous studies on the rat, hamster and guinea-pig. Acetone metabolism in mouse nasal mucosal homogenates was examined in vitro. Acetone was metabolized by nasal homogenates via an NADPH-dependent pathway with a Vmax of 12 micrograms/min/whole nose and an apparent Km of 72 micrograms/ml. The enzyme responsible was not identified; however, metabolism was inhibited by pyrazole but not inhibited by metyrapone or incubation under nitrogen. URT deposition efficiency was measured at flow rates of 21, 33 or 70 ml/min and averaged 25, 20 and 14%, respectively; the efficiencies at each flow rate were significantly different (P less than 0.01). Deposition was measured at inspired concentrations ranging from 1,500-20,000 micrograms/liter. Deposition efficiencies were similar at all concentrations; the lack of saturation suggests this vapor was not metabolized when inspired. Kinetic analysis of the deposition data revealed that metabolism rates of inspired acetone were only a small fraction of that measured in vitro, suggesting that in vitro data could not be directly extrapolated to the in vivo setting. Deposition efficiency of acetone in the URT of the mouse was similar to that previously observed in the URT of the F344 rat, but was less efficient than that in the Sprague-Dawley rat and more efficient than that in the hamster or guinea-pig.

Acetone↗
PubMed1998

Modulation of peroxisomal and microsomal fatty acid oxidation by acetone. A comparative study between liver and kidney.

The effect of acetone consumption on some microsomal and peroxisomal activities was studied in rat kidney and these results were compared with data from former investigations in liver. Acetone increased the microsomal lauric acid hydroxylation, the aminopyrine N-demethylation catalyzed by cytochrome P450 and the microsomal UDP-glucuronyltransferase activity. Also, acetone increased the peroxisomal beta-oxidation of palmitoyl CoA and catalase activities in kidney. These studies suggest that acetone is a common inducer of the microsomal and peroxisomal fatty acid oxidation, as previously shown in both starved and ethanol treated rats. Our results support the hypothesis that microsomal fatty acid omega-hydroxylation results in the generation of substrates being supplied for peroxisomal beta-oxidation. We propose that the final purpose of these linked fatty acid oxidations could be the catabolism of fatty acids or the generation of a substrate for the synthesis of glucose from fatty acids. This pathway would be triggered by acetone treatment in a similar way in liver and kidney.

Acetone↗
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↗
PubMed1999

High yield synthesis of [11C]-acetone through selective quenching of methyl lithium.

Carbon-11 labeled acetone is a useful radiosynthetic precursor. Previously, strict control of no-carrier-added stoichiometry was required to prepare it from reaction of CO2 and methyl lithium. However, excess methyl lithium may be selectively quenched to avoid reaction with nascent acetone to give tert-butanol. We report a simple pKa-based strategy to sequentially and selectively quench MeLi and acetone to give yields of up to 100% acetone even in the presence of a large excess of MeLi. The method gives good yields of acetone under conditions that previously precluded its synthesis.

Acetone↗
PubMed2006

Density functional theory (DFT) calculations of the infrared absorption spectra of acetaminophen complexes formed with ethanol and acetone species.

We have investigated the infrared (IR) vibrational spectra of acetaminophen (N(4-hydroxyphenyl) acetamide or paracetamol) complexes formed with ethanol and acetone in relation to the nature of the specific intermolecular interactions involved in the stabilization of the complexes. The structures and binding energies of the complexes have been determined using Hartree-Fock (HF) and DFT-B3PW91 procedures and different Pople's basis sets as well. The main results are presented and discussed by considering the hydroxyl (OH), amino (NH), and carbonyl (CO) chemical groups of acetaminophen interacting with the acetone or ethanol molecules either separately or in conjunction in the complex formation. The frequency shifts and IR intensity variations associated with the internal modes of acetaminophen (namely nu(OH), nu(NH), and nu(CO)) as well as the most pertinent vibrational probes of ethanol (nu(OH)) and acetone (symmetric nu(CO) and nu(CCC) stretching modes) interacting with acetaminophen have been analyzed. The predicted spectral changes have been critically discussed in comparison with IR absorption measurements of acetaminophen dissolved as a solute in ethanol or acetone CO2 expanded solutions. It is argued that the exchange-correlation contribution taken into account in DFT calculations is likely significant in determining the main IR spectral features of acetaminophen complexes formed with acetone or involving hydrogen-bonded as with ethanol.

Acetaminophen↗
PubMed1996

Influence of polyethylene glycol and acetone on the in vitro biotransformation of tamoxifen and alprazolam by human liver microsomes.

The use of in vitro hepatic microsomal models as a method of studying the biotransformation of xenobiotics can be complicated by the insolubility of a lipophilic substrate. Addition of solvent to an in vitro system is an approach used to increase solubility of such substrates, but solvents may interact with the microsomal enzymes and cause changes in the kinetic parameters. This study focused on the solvents polyethylene glycol-400 (PEG) and acetone and their influence on the human microsomal in vitro biotransformation of the antineoplastic agent tamoxifen (TAM). The antianxiety agent alprazolam (ALP), a verified P450 3A substrate, was also studied. TAM is a nonpolar drug that is metabolized to two oxidative metabolites, N-desmethyltamoxifen (DMT) and 4-hydroxytamoxifen (4-OH-TAM), by cytochrome P450 isoforms. DMT is formed primarily by 3A isoforms, and the pathway(s) responsible for 4-OH-TAM formation are unknown. Biotransformation of ALP is mediated by P450 3A isoforms, which form alpha-hydroxyalprazolam (alpha-OH-ALP) and 4-hydroxyalprazolam (4-OH-ALP). Both PEG and acetone at 5% of the total microsomal incubation volume were found to solubilize TAM in the in vitro system. However, both solvents had an effect on the P450 mediated metabolism of ALP and TAM. For ALP, PEG was a noncompetitive inhibitor of alpha-OH-ALP (mean Ki = 2.06%) and 4-OH-ALP (mean Ki = 2.37%) formation. Acetone stimulated the production of alpha-OH-ALP, but had no apparent influence on 4-OH-ALP formation. The solvent's influence on TAM metabolism varied. PEG decreased the amount of DMT formed by the microsomes as compared to the system containing no solvent (control); however, 4-OH-TAM formation in the presence of PEG was 146-226% of controls. Samples containing acetone produced smaller quantities of both DMT (39-63%) and 4-OH-TAM (45-69%) as compared to controls. Since PEG and acetone increased the solubility of TAM in the incubation buffer but inhibited or accelerated enzymatic reactions compared to buffer alone, actual solubility in buffer was not a determinant of the rate of TAM metabolism. TAM appeared to be taken up into the microsomal fraction, making it available for biotransformation by the P450 isoforms. Although solvents may increase the solubility of nonpolar agents in aqueous systems, careful evaluation of the effects of solvent on metabolite formation, as compared to buffer controls, is needed in order to properly evaluate an in vitro metabolic model.

Acetone↗
PubMed1990

Spectrophotometric determination of acetone using vanillin.

A sensitive method is described for the spectrophotometric determination of acetone in water. Acetone reacts with vanillin in alkaline medium forming a yellow-orange dye with an absorption maximum at 430 nm. Beer's law is obeyed in the range from 0.5 to 5 p.p.m. of acetone in water. Molar absorptivity and Sandell's sensitivity were found to be 11.0 x 10(3) +/- 100 l mol-1 cm-1 and 0.005 micrograms cm-2, respectively. The important parameters for complete colour development were optimised and the method was used for the determination of acetone in biological samples. The method was also applied successfully to the determination of acetone in air after absorption in sodium hydrogen sulphite solution.

Acetone↗
PubMed1987

Gluconeogenesis from acetone in diabetic rats.

Previous investigations have demonstrated that acetone is a true, if minor precursor of glucose in vivo. In diabetic rats 1.30% of the carbon atoms of circulating glucose arises from acetone, whereas 0.67% does in normal 3-day fasted animals. Calculated from these fractions and the turnover rate of glucose, 48 micrograms/kg. min acetone-carbon is converted to glucose-carbon in diabetic and 16 micrograms/kg. min in normal rats. In both groups of rats the labelling of plasma lactate was stronger than that of glucose. In view of these results we conclude that: the transfer of C-atoms from acetone to glucose increases in diabetes; acetone remains a minor source of glucose even in ketonemic diabetic rats.

Acetone↗
PubMed2007

Density functional investigation of the interaction of acetone with small gold clusters.

The structural evolution of Au(n) (n=2, 3, 5, 7, 9, and 13) clusters and the adsorption of organic molecules such as acetone, acetaldehyde, and diethyl ketone on these clusters are studied using a density functional method. The detailed study of the adsorption of acetone on the Au(n) clusters reveals two main points. (1) The acetone molecule interacts with one gold atom of the gold clusters via the carbonyl oxygen. (2) This interaction is mediated through back donation mainly from the spd-hybridized orbitals of the interacting gold atom to the oxygen atom of the acetone molecule. In addition, a hydrogen bond is observed between a hydrogen atom of the methyl group and another gold atom (not involved in the bonding with carbonyl oxygen). Interestingly, the authors notice that the geometries of Au(9) and Au(13) undergo a significant flattening due to the adsorption of an acetone molecule. They have also investigated the role of the alkyl chain attached to the carbonyl group in the adsorption process by analyzing the interaction of Au(13) with acetaldehyde and diethyl ketone.

Acetone↗
PubMed2003

Subchronic inhalation exposure to acetone vapor and scheduled controlled operant performance in male rats.

Groups of adult male rats (10/group) were used to assess whether subchronic inhalation exposure to 0, 1000, 2000, or 4000 ppm of acetone vapor altered schedule-controlled operant performance. Rats were exposed to acetone vapor for 6 h/day, 5 days/wk, for a 13-wk period. Extensive training prior to the exposure series established a stable baseline of lever-pressing on a multiple fixed-ratio-fixed-interval (FR 20-FI 120 s) schedule of food presentation. Operant sessions occurred prior to each daily exposure to avoid confounding the detection of enduring behavioral effects with transient acute effects. FI response rate, FI index of curvature, and FR running rate of response were not affected during or after the 13-wk exposure series. FR post-reinforcement pause duration for the control group increased during the course of the study more than that of the 2000 ppm and 4000 ppm groups, which changed only slightly relative to pretreatment baseline. Based on the performance of historical controls that had FR pause durations similar to those of acetone-treated groups, the differences in FR pause duration were probably due to drift of the concurrent control group and were not related to acetone treatment. Prolonged exposure to up to 4000 ppm acetone vapor does not appear to have enduring effects on nervous system functions that mediate the performance of a complex, learned task.

Acetone↗
PubMed1982

Isopropanol and acetone potentiation of carbon tetrachloride-induced hepatotoxicity: single versus repetitive pretreatments in rats.

Acute oral pretreatment of rats with isopropanol or acetone results in a dose-related potentiation of CCl4 hepatotoxicity. Minimally effective doses (MED) and noneffective doses (NED) of both agents were estimated to be 0.25 and 0.10 ml/kg, respectively. Six MED given twice a day over 3 d caused a greater potentiation than a single MED, but not as much as that produced by the total dose given singly. Six NED given over 3 d did not potentiate CCl4, whereas the total dose did when given singly. A threshold for isopropanol and acetone appears to exist in the rat. A total dose of 1.5 ml/kg acetone was administered by four different treatment regimens (bolus, divided doses, infusion) over 3 d. Potentiation of CCl4 hepatotoxicity was then correlated with blood pharmacokinetic parameters: area under the concentration-time curve and peak blood concentration. An excellent correlation was found between the degree of potentiation observed and the peak blood concentration attained, but no correlation was found with area under the curve. Results of iv acetone infusions (over 3 d) with higher doses support the hypothesis that a threshold concentration of acetone is critical in the potentiation of CCl4 hepatotoxicity in the rat.

1-Propanol↗
PubMed1981

Ethanol- or acetone-pretreatment of mice strongly enhances the bacterial mutagenicity of dimethylnitrosamine in assays mediated by liver subcellular fraction, but not in host-mediated assays.

The activation of dimethylnitrosamine (DMN) to a bacterial mutagen in liver subcellular fraction and in intrasanguinous host-mediated assays was studied, in particular the effect of pretreatment of the animals with ethanol or acetone. Salmonella typhimurium TA 92 was much more sensitive to DMN mutagenicity than TA 100 and TA 1535 or Escherichia coli WP2uvrA and was used for the main part of the study. Noteworthy, in part already known, features of the in vitro activation are the relatively low pH optimum (pH 6-6.4), the non-linear dose-mutagenic response-relationship and the relatively high doses of DMN required for activation with control preparations. Pretreatment of mice with ethanol or acetone greatly reduced the minimal mutagenically effective concentration of DMN in the in vitro assay. Pretreatment with Aroclor 1254, an inducer frequently used in mutagenicity research, showed little effect when used alone, but reduced the potentiation by acetone. The results of the host-mediated assays substantially differed from those of the in vitro activation assays (a) in the relatively low dose of DMN required for mutagenicity to occur and (b) in the lack of potentiation by acetone-or ethanol-pretreatment. Acetone even led to a marginal decrease in mutagenicity. As a possible explantation for this apparent discrepancy were assume that with the in vitro system the activity of the dilute metabolizing system is limiting for the activation of DMN and induction therefore will increase the mutagenicity, whereas in vivo DMN is quantitatively metabolized in both induced and non-induced animals. The results show that caution has to be taken in the interpretation from in vitro results to the in vivo situation. In particular our in vivo experiments do not support the hypothesis that the induction by ethanol of an activating system with a low Km (which would strongly activate traces of DMN ingested with many foods) is one of the reasons for the increased risk of liver tumors in alcoholics.

Acetone↗
PubMedDate not supplied

Elimination half-life of acetone in humans: case reports and review of the literature.

Two instances of finding abnormally high concentrations of acetone in urine (0.10 g/dL and 0.052 g/dL) without any measurable amounts of ethanol (<0.005 g/dL) or isopropanol (<0.005 g/dL) prompted a survey of the elimination kinetics of isopropanol and its metabolite acetone in humans. In a hospital patient who had ingested denatured alcohol, the elimination half-life (t(1/2)) of acetone during detoxification was 27 h and not 3-5 h as reported by other workers. Several other literature reports of individuals who had ingested isopropanol as well as controlled studies after administration of moderate amounts of acetone and/or isopropanol support the notion of a long elimination half-life of 17-27 h for acetone compared with a t(1/2) of 1-3 h for isopropanol.

2-Propanol↗
PubMedDate not supplied

Response of breath-alcohol analyzers to acetone.

Quantitative evidential breath-alcohol analyzers and screening testers in each of the five current categories of analytical principle were examined for response to dynamically-generated acetone vapor concentrations of 3, 100, 150, 350, and 600 micrograms/210 Liters. Nine of the 13 instruments tested were unaffected by acetone at any of these concentrations; three solid-state (Taguchi) sensing devices and one device employing single-wavelength infrared spectrometry displayed responses to acetone at the two highest tested concentrations. In view of a breath-acetone literature survey for ambulatory subjects and other considerations, response of the tested devices to acetone is not considered to be a significant problem in breath-alcohol analysis for traffic law enforcement purposes.

Acetone↗
PubMed2001

Effects of acetone, methanol, or paraformaldehyde on cellular structure, visualized by reflection contrast microscopy and transmission and scanning electron microscopy.

The authors recently showed variable subcellular immunoreactivity of the Bcl-2 and Bax proteins after fixation of cell monolayers with acetone, methanol, or paraformaldehyde (PF) followed by methanol (PF/methanol). Here, the authors demonstrate by reflection contrast microscopy and transmission electron microscopy that acetone or methanol fixation result in complete loss of integrity of intracellular structures in contrast with PF or glutaraldehyde fixation. Scanning electron microscopy revealed poor preservation of plasma membrane integrity after fixation in acetone or methanol. Fixation with PF before methanol reduced damage to intracellular and plasma membranes. In addition, Western blot analysis demonstrated loss of Bcl-2 and Bax protein during acetone or methanol fixation, whereas PF fixation before methanol permeabilization markedly reduced this loss. For studies on the intracellular localization of soluble or unknown types of antigen, the authors discourage the use of acetone and methanol as single fixatives.

Acetone↗
PubMed2006

Quantification of breath carbon disulphide and acetone following a single dose of disulfiram (Antabuse) using selected ion flow tube mass spectrometry (SIFT-MS).

Selected ion flow tube mass spectrometry (SIFT-MS) has been used to measure simultaneously the concentrations of both carbon disulphide and acetone in exhaled breath following the ingestion of a single dose of disulfiram (Antabuse). Carbon disulphide is a product of the metabolism of disulfiram and is excreted mainly through the lungs. Acetone is a product of normal metabolism and appears in the breath of all individuals. These breath analyses were performed in single exhalations and the results were available in real time. The levels of breath acetone and carbon disulphide were compared with levels obtained from a control subject who had not ingested disulfiram. Breath carbon disulphide was seen to increase from 15 p.p.b. to 618 p.p.b. over a 28-hour period, in the single individual tested, following ingestion of disulfiram, while acetone levels increased from 300 p.p.b. (normal) to over 4000 p.p.b. (greatly elevated). No such increases were seen in the breath of the control subject over the same period. An obvious positive correlation between breath carbon disulphide and acetone concentrations following disulfiram ingestion is seen and discussed.

Acetone↗
PubMed1995

14CO2 exchange with acetoacetate catalyzed by dialyzed cell-free extracts of the bacterial strain BunN grown with acetone and nitrate.

The nitrate-reducing bacterial strain BunN is able to grow with acetone and nitrate under anoxic conditions. Dialyzed crude cell-free extracts of acetone-plus-nitrate-grown cells of strain BunN catalyzed the exchange of 14CO2 into acetoacetate in an ADP-dependent reaction. The rates of exchange catalyzed by extracts of acetate-grown or 3-hydroxybutyrate-grown cells were only 13% of that catalyzed by extracts of acetone-grown cells. The activity was enzymic since it was destroyed by boiling and was proportional to the amount of added extract. The optimal acetoacetate concentration was 100 mM and the apparent Km was 11.1 mM. The pH optimum was 6.5, the exchange was not dependent on the addition of biotin, and the activity was not inhibited by avidin. The exchange activity was not stimulated (less than two fold) by a variety of metal ions or by a range of possible cofactors. Under optimal conditions (100 mM acetoacetate, 5 mM ADP, 10 mM NaHCO3, pH 6.5, under N2), the exchange activity was 2.7 nmol.min-1.mg protein-1; 2% of the in vivo carboxylation activity of acetone-plus-nitrate-grown cultures. It is suggested that the exchange reaction is a partial reaction catalyzed by the enzyme (or enzyme complex) that carboxylates acetone, and that the methods developed in this study provide a means with which to investigate this reaction further.

Acetoacetates↗