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PubMed1997

Induction of cytochromes P450 1A, 2B and 2E in hamster tissues by acetone.

The inductive effects of acetone on cytochromes P450 1A, 2B and 2E in liver, kidney and lung were studied using hamsters administered acetone in drinking water. Acetone administration caused five-, two- and sixfold increases of the activities of aniline hydroxylase, ethoxyresorufin O-dealkylase and pentoxyresorufin O-dealkylase in liver microsomes; eight- and twofold increases of aniline hydroxylation and ethoxyresorufin O-dealkylation in kidney; and a twofold increase of aniline hydroxylation in lung, respectively. Immunoblot analyses of microsomal proteins using mouse monoclonal antibody 1-12-3 to rat P450 1A1 and rabbit antibody to human P450 2E1 revealed that acetone resulted in about three-, four- and twofold increases of proteins immunorelated to P450s 1A and 2E in hamster liver, kidney, and lung, respectively. Protein blot analysis using mouse monoclonal antibody 2-66-3 to rat P450 2B1 showed that acetone caused five- and twofold increases, respectively, of an immunoreactive protein in hamster liver and kidney but decreased the P450 2B protein by 48% in lung. RNA blot analyses using cDNA probes derived from mouse P450 1A1 and rat P450 2B1 cDNA clones demonstrated that acetone elicited two- and twelvefold increases of the mRNA levels of P450s 1A and 2B in hamster liver, respectively. Northern blot analyses using oligonucleotide probes derived from hamster P450 2E1 cDNA sequence detected two species of hybridizable mRNA in control liver. Acetone preferentially caused a threefold increase in the level of the larger-sized mRNA. Acetone produced little increase or no effect on mRNAs of cytochromes P450 1A, 2B and 2E in kidney and lung. The present study demonstrates that acetone induces the catalytic activity, protein and mRNA levels of P450s 1A, 2B and 2E in hamster liver, and causes various changes of the P450 levels in kidney and lung. Acetone induction of hamster P450s 1A, 2B and 2E might involve transcriptional and post-transcriptional mechanisms.

Acetone↗
PubMed1991

Toxicity studies of acetone administered in the drinking water of rodents.

Two- and thirteen-week toxicity studies were conducted using male and female F344/N rats and B6C3F1 mice. Animals were exposed to the following concentrations of acetone in their drinking water: two-week studies 0; 5000; 10,000; 20,000; 50,000; or 100,000 ppm acetone. Thirteen-week rat and female mouse studies 0; 2500; 5000; 10,000; 20,000; or 50,000 ppm acetone. Thirteen week male mice were exposed to 0; 1250; 2500; 5000; 10,000; or 20,000 ppm acetone. Depressed body weight gain was restricted to the 50,000 and 100,000 ppm exposure groups. Male and female mice exposed respectively to 20,000 or 50,000 ppm acetone for 2 weeks developed hepatocellular hypertrophy. This change was not apparent after 13 weeks of exposure although relative and absolute liver weight was increased in high dose female mice. Bone marrow hypoplasia was observed in 5/5 high dose (100,000 ppm) male rats during the 2-week studies. Treatment of male rats for 13 weeks resulted in a variety of mild and subtle hematological changes that often occurred at relatively low levels of exposure (5000 ppm) and resembled those seen during the clinical condition of megaloblastic anemia. Changes characteristic of hypogonadism (depressed sperm motility and cauda epididymal and epididymal weight and elevated incidence of abnormal sperm) were observed in male rats receiving 50,000 ppm acetone for 13 weeks. The incidence and severity of a kidney lesion that is morphologically similar to the spontaneously occurring nephropathy among aging F-344 rats were increased at 20,000 and 50,000 ppm acetone, respectively, in 13-week male rats. In summary, the effects of acetone were either subtle in nature or occurred during very high levels of exposure confirming acetone's low level of toxicity. The daily levels of acetone exposure were often several-fold greater than possibly encountered by humans during the accidental consumption of contaminated groundwater (250 ppm; 5 mg/day) and frequently exceeded maximum levels reported following acute toxic exposures (2,500 mg/kg).

Acetone↗
PubMed1991

Inhalation versus oral administration of acetone: effect of the vehicle on the potentiation of CCl4-induced liver injury.

Acetone potentiation of liver injury is greater when corn oil is given with acetone 18 h prior to a challenge with CCl4. This study aimed to further characterize the effects of the vehicle used to administer acetone on the severity of acetone-potentiated CCl4-induced liver injury. The more severe acetone-potentiated liver injury observed when corn oil was the vehicle does not seem to be due to greater liver acetone concentrations. When corn oil was used as the vehicle to administer acetone, liver and blood CCl4 concentrations were not significantly different from those where water was the vehicle. Therefore the relationship between blood or liver acetone concentration and plasma ALT activity for orally-administered acetone was modified by corn oil. Liver triglyceride concentration measured 18 h after a gavage of corn oil was significantly higher than that for the water-treated group. A direct effect of corn oil on liver, in particular a promotion of the propagation phase in the lipid peroxidation process induced by CCl4, is proposed to explain the increase in acetone-potentiated CCl4-induced liver injury.

Acetone↗
PubMed1979

Plasma acetone metabolism in the fasting human.

The metabolism of acetone was studied in lean and obese humans during starvation ketosis. Acetone concentrations in plasma, urine, and breath; and rates of endogenous production, elimination in breath and urine, and in vivo metabolism were determined. There was a direct relationship between plasma acetone turnover (20-77 mumol/m(2) per min) and concentration (0.19-1.68 mM). Breath and urinary excretion of acetone accounted for a 2-30% of the endogenous production rate, and in vivo metabolism accounted for the remainder. Plasma acetone oxidation accounted for congruent with60% of the production rate in 3-d fasted subjects and about 25% of the production rate in 21-d fasted subjects. About 1-2% of the total CO(2) production was derived from plasma acetone oxidation and was not related to the plasma concentration or production rate. Radioactivity from [(14)C]acetone was not detected in plasma free fatty acids, acetoacetate, beta-hydroxybutyrate, or other anionic compounds, but was present in plasma glucose, lipids, and proteins. If glucose synthesis from acetone is possible in humans, this process could account for 11% of the glucose production rate and 59% of the acetone production rate in 21-d fasted subjects. During maximum acetonemia, acetone production from acetoacetate could account for 37% of the anticipated acetoacetate production, which implies that a significant fraction of the latter compound does not undergo immediate terminal oxidation.

Acetone↗
PubMed2002

Epilepsy and the ketogenic diet: assessment of ketosis in children using breath acetone.

High-fat ketogenic diets increase ketones (acetoacetate, beta-hydroxybutyrate, and acetone) and are used to treat refractory seizures. Although ketosis is an integral aspect of these therapeutic regimens, the direct importance of ketosis to seizure control needs further investigation. An examination of this relationship requires a reliable, minimally invasive measure of ketosis that can be performed frequently. In the present study, we examined the use of breath acetone as a measure of ketosis in children with refractory seizures on a classic ketogenic diet. Results were compared with breath acetone levels in epilepsy and healthy controls. Children on the ketogenic diet had significantly higher fasting breath acetone compared with epilepsy or healthy controls (2530 +/- 600 nmol/L versus 19 +/- 9 nmol/L and 21 +/- 4 nmol/L, respectively; p < 0.05). One hour after consumption of a ketogenic breakfast meal, breath acetone increased significantly in epilepsy and healthy controls (p < 0.05), but not in children on a ketogenic diet. Children who were on the ketogenic diet for longer periods of time had a significantly lower fasting breath acetone (R(2) = 0.55, p = 0.014). In one child on the ketogenic diet, breath acetone was determined hourly over a 9-h period, both by gas chromatography and by a prototype hand-held breath acetone analyzer. Preliminary results using this hand-held breath acetone analyzer are encouraging. Breath acetone may be a useful tool in examining the relationship between ketosis and seizure control and enhancing our understanding of the mechanism of the ketogenic diet.

Acetone↗
PubMed2005

Photooxidation of acetone on TiO2(110): conversion to acetate via methyl radical ejection.

It is generally held that radicals form and participate in heterogeneous photocatalytic processes on oxide surfaces, although understanding the mechanistic origins and fates of such species is difficult. In this study, photodesorption and thermal desorption techniques show that acetone is converted into acetate on the surface of TiO2(110) in a two-step process that involves, first, a thermal reaction between acetone and coadsorbed oxygen to make a surface acetone-oxygen complex, followed second by a photocatalytic reaction that ejects a methyl radical from the surface and converts the acetone-oxygen complex into acetate. Designation of the photodesorption species to methyl radicals was confirmed using isotopically labeled acetone. The yield of photodesorbed methyl radicals correlates well with the amount of acetone depleted and with the yield of acetate left on the surface, both gauged using postirradiation temperature programmed desorption (TPD). The thermal reaction between adsorbed acetone and oxygen to form the acetone-oxygen complex exhibits an approximate activation barrier of about 10 kJ/mol. A prerequisite to this reaction is the presence of surface Ti3+ sites that enable O2 adsorption. Creation of these sites by vacuum reduction of the surface prior to acetone and oxygen coadsorption results in an initial spike in the acetone photooxidation rate, but replenishment of these sites by photolytic means (i.e., by trapping excited electrons at the surface) appears to be a slow step in a sustained reaction. Evidence in this study for the ejection of organic radicals from the surface during photooxidation catalysis on TiO2 provides support for mechanistic pathways that involve both adsorbed and nonadsorbed species.

Journal Article↗
PubMed2005

Molecular modeling of phase behavior and microstructure of acetone-chloroform-methanol binary mixtures.

Force fields based on a Lennard-Jones (LJ) 12-6 plus point charge functional form are developed for acetone and chloroform specifically to reproduce the minimum pressure azeotropy found experimentally in this system. Point charges are determined from a CHELPG population analysis performed on an acetone-chloroform dimer. The required electrostatic surface for this dimer is determined from ab initio calculations performed with MP2 theory and the 6-31g++(3df,3pd) basis set. LJ parameters are then optimized such that the liquid-vapor coexistence curve, critical parameters, and vapor pressures are well reproduced by simulation. Histogram-reweighting Monte Carlo simulations in the grand canonical ensemble are used to determine the phase diagrams for the binary mixtures acetone-chloroform, acetone-methanol, and chloroform-methanol. The force fields developed in this work reproduce the minimum pressure azeotrope in the acetone-chloroform mixture found in experiment. The predicted azeotropic composition of x(CHCl3) = 0.77 is in fair agreement with the experimental value of x(CHCl3)expt = 0.64. The new force fields were also found to provide improved predictions of the pressure-composition behavior of acetone-methanol and chloroform-methanol when compared to other force fields commonly used for vapor-liquid equilibria calculations. NPT simulations were conducted at 300 K and 1 bar for equimolar mixtures of acetone-chloroform, acetone-methanol, and methanol-chloroform. Analysis of the microstructure reveals significant hydrogen bonding occurring between acetone and chloroform. Limited interspecies hydrogen bonding was found in the acetone-methanol or chloroform-methanol mixtures.

Journal Article↗
PubMed2005

Acetone and water on TiO2(110): H/D exchange.

Isotopic H/D exchange between coadsorbed acetone and water on the TiO2(110) surface was examined using temperature programmed desorption (TPD) as a function of coverage and two surface pretreatments (O2 oxidation and mild vacuum reduction). Coadsorbed acetone and water interact repulsively on reduced TiO2(110) on the basis of results from the companion paper to this study, with water exerting a greater influence in destabilizing acetone and acetone having only a nominal influence on water. Despite the repulsive interaction between these coadsorbates, about 0.02 monolayers (ML) of a 1 ML d6-acetone on the reduced surface (vacuum annealed at 850 K to a surface oxygen vacancy population of 7%) exhibits H/D exchange with coadsorbed water, with the exchange occurring exclusively in the high-temperature region of the d6-acetone TPD spectrum at approximately 340 K. The effect was confirmed with combinations of d0-acetone and D2O. The extent of exchange decreased on the reduced surface for water coverages above approximately 0.3 ML due to the ability of water to displace coadsorbed acetone from first layer sites to the multilayer. In contrast, the extent of exchange increased by a factor of 3 when surface oxygen vacancies were pre-oxidized with O2 prior to coadsorption. In this case, there was no evidence for the negative influence of high water coverages on the extent of H/D exchange. Comparison of the TPD spectra from the exchange products (either d1- or d5-acetone depending on the coadsorption pairing) suggests that, in addition to the 340 K exchange process seen on the reduced surface, a second exchange process was observed on the oxidized surface at approximately 390 K. In both cases (oxidized and reduced), desorption of the H/D exchange products appeared to be reaction limited and to involve the influence of OH/OD groups (or water formed during recombinative desorption of OH/OD groups) instead of molecularly adsorbed water. The 340 K exchange process is assigned to reaction at step sites, and the 390 K exchange process is attributed to the influence of oxygen adatoms deposited during surface oxidation. The H/D exchange mechanism likely involves an enolate or propenol surface intermediate formed transiently during the desorption of oxygen-stabilized acetone molecules.

Journal Article↗
PubMed2003

Anticonvulsant properties of acetone, a brain ketone elevated by the ketogenic diet.

The ketogenic diet (KD), a treatment for drug-resistant epilepsy, elevates brain acetone. Acetone has been shown to suppress experimental seizures. Whether elevation of acetone is the basis of the anticonvulsant effects of the KD and whether acetone, like the KD, antagonizes many different types of seizures, however, is unknown. This study investigated the spectrum of the anticonvulsant effects of acetone in animal seizure models. Rats were injected with acetone intraperitoneally. Dose-response effects were measured in four different models: (1) the maximal electroshock test, which models human tonic-clonic seizures; (2) the subcutaneous pentylenetetrazole test, which models human typical absence seizures; (3) the amygdala kindling test, which models human complex partial seizures with secondary generalization; and (4) the AY-9944 test, which models chronic atypical absence seizures, a component of the Lennox-Gastaut syndrome. Acetone suppressed seizures in all of the models, with the following ED(50)'s (expressed in mmol/kg): maximal electroshock, 6.6; pentylenetetrazole, 9.7; generalized kindled seizures, 13.1; focal kindled seizures, 26.5; AY-9944, 4.0. Acetone appears to have a broad spectrum of anticonvulsant effects. These effects parallel the effects of the KD. Elevation of brain acetone therefore may account for the efficacy of the KD in intractable epilepsy.

Acetone↗
PubMed1982

Multiple drug metabolism: p-nitroanisole reversal of acetone enhanced aniline hydroxylation.

The unique effect of acetone on the p-hydroxylation of aniline was evaluated in microsomes prepared from control, phenobarbital- and 3-methylcholanthrene-pretreated animals. The existence of multiple forms of the hydroxylase was evaluated as an explanation of the acetone enhancement. Simultaneous metabolism of aniline in the presence of either p-nitroanisole (pNA) or ethylmorphine (EM) was evaluated to probe the participation of different mixed function oxidase systems. Aniline inhibited both N- and O-demethylation, while pNA and EM both inhibited p-hydroxylation of aniline. Acetone decreased the individual demethylation reactions, but enhanced aniline hydroxylation. In multiple drug reactions, acetone decreased N-demethylation and proportionately increased aniline p-hydroxylation. On the other hand, p-nitroanisole blocked the acetone enhancement of aniline metabolism. Kinetic evaluation of the acetone and p-nitroanisole effects on aniline metabolism indicated that each agent increased the apparent Km' by 4- to 5-fold for aniline in the hydroxylation reaction, but only acetone increased the Vmax'. From the Eadie-Scatchard analysis of the rates of aniline hydroxylation, acetone appeared to produce a biphasic increase in the hydroxylation above 0.75 mM aniline, even in the presence of pNA. Thus, multiple forms of the aniline p-hydroxylase are indicated by their altered activities in the presence of other drugs, and acetone seemed to specifically alter a species having a higher Km' for aniline.

Acetone↗
PubMed1988

Microsomal metabolism of acetonitrile to cyanide. Effects of acetone and other compounds.

Oral acetone exposure delays and potentiates acetonitrile toxicity in rats. Results of previous pharmacokinetic studies suggested that acetone exerted a biphasic effect on the metabolism of acetonitrile to cyanide; the presence of acetone in vivo appeared to inhibit the metabolism of acetonitrile to cyanide, whereas the disappearance of acetone from serum was followed by stimulation of acetonitrile metabolism. The current experiments were designed to characterize further the metabolism of acetonitrile to cyanide and the effects of acetone and other compounds upon this metabolism. Liver microsomes were isolated and pooled 24 hr after oral pretreatment of female Sprague-Dawley rats (180-250 g) with acetone (1960 mg/kg) or water. Microsomal metabolism of acetonitrile to cyanide was found to be oxygen and NADPH dependent, and heat-inactivated tissue was unable to catalyze the reaction. NADH antagonized the NADPH-dependent metabolism of acetonitrile. The metabolism of acetonitrile to cyanide was linear with protein concentrations of 0-8 mg per incubation. Following a characteristic lag period of 10 min, the reaction was linear from 15 to 30 min. This metabolism was inhibited by carbon monoxide, metyrapone and SKF 525-A. Acetone pretreatment (-24 hr) in vivo increased the apparent Vmax for acetonitrile metabolism without affecting the apparent Km. When added in vitro, acetone competitively inhibited the metabolism of acetonitrile, with a KI of 0.41 mM. Dimethyl sulfoxide (KI = 0.51 mM) and ethanol (KI = 0.11 mM) were also competitive inhibitors of acetonitrile metabolism, and aniline HCl (KI = 4.77 microM) appeared to be a mixed inhibitor. These data are consistent with the hypothesis that the metabolism of acetonitrile to cyanide is mediated by a specific acetone-inducible isozyme of cytochrome P-450.

Acetone↗
PubMed1990

Effect of acetone administration on renal, pulmonary and hepatic monooxygenase activities in hamster.

Administration of acetone in drinking water to Syrian Golden hamsters for 9-10 days altered microsomal P-450 dependent monooxygenase activities in the liver and the kidney but not in the lung. While hepatic microsomal NADPH-cytochrome c reductase was unaffected, cytochrome b5 and P-450 content increased (about 100%) in liver but not in kidney. Furthermore acetone treatment resulted in an increase of microsomal reverse type I binding with DMSO and in an increase in the P-450IIE1-linked renal and hepatic activities such as aniline hydroxylase (AnH) and p-nitrophenol hydroxylase (pNPH). The SDS-PAGE analysis confirmed the induction in acetone-treated microsomes of a hepatic protein with the M.W. of ethanol inducible P-450IIE1 of hamster. The acetone treatment however, unlike ethanol, induced other activities such as benzphetamine N-demethylase and ethoxycoumarin O-deethylase in liver and aminopyrine N-demethylase in kidney. No change of ethoxyresorufin O-deethylase and pentoxyresorufin O-depentylase was observed in either renal or hepatic microsomes. Addition of acetone in vitro had an inhibitory effect on pNPH by hepatic microsomes from control or acetone induced hamsters, while AnH was not affected. Interruption of acetone administration for 24 h resulted in a return of AnH and pNPH activities to essentially basal levels in the liver suggesting a rapid turnover of the hamster P-450IIE1 (ham P-450j). Our results indicate that, as found in rat, acetone is a good inducer of the P-450IIE1 (ham P-450j) in hamster in both the liver and kidney. However other P-450 forms, such as, probably, the renal and hepatic P-450IIB1, are also induced. Thus acetone-treated hamsters, which, in certain respects, show a qualitatively different induction pattern from that reported for ethanol, can be used as an useful animal model to study the toxicity of certain xenobiotics.

Acetone↗
PubMed2004

Determination of acetone in human breath by gas chromatography-mass spectrometry and solid-phase microextraction with on-fiber derivatization.

Analysis of breath acetone has been used as a diagnostic tool for diabetes. Due to its nature of volatility and activity, it is very difficult to accurately measure the concentration of acetone in human breath by gas chromatography-mass spectrometry (GC-MS). To overcome this problem, we developed a new method using GC-MS and solid-phase microextraction (SPME) with on-fiber derivatization to determine acetone in human breath. Breath gas from controls and diabetic patients was collected in 3-l Tedlar bags. O-2,3,4,5,6-(Pentafluorobenzyl) hydroxylamine hydrochloride (PFBHA) in solution was firstly adsorbed on the SPME fiber of 65 microm polydimethylsiloxane-divinylbenzene (PDMS-DVB), and then the fiber was further headspace exposed in exhaled gas in the Tedlar bag at 40 degrees C for 4 min. Finally, the formed acetone oxime on the fiber was desorbed and analyzed by GC-MS. Using external standard method, acetone in the human breath was quantitatively analyzed by measurement of its oxime. The method provided a low detection limit of 0.049 ppbv for acetone in breath, relative standard deviation (R.S.D.) value of 3.4%, excellent accuracy. In addition, the method required simple sample preparation and no organic solvent. Acetone in diabetic breath was found to be higher than 1.71 ppmv, while its concentration in normal breath was lower than 0.76 ppmv. The results show that GC-MS and SPME with on-fiber derivatization is a simple, rapid and sensitive and solvent-free method for determination of low concentration acetone in breath and analysis of breath acetone can be used as supplementary tool for diagnosis of diabetes.

Acetone↗
PubMed2004

Effects of the acetone content of single solution dentin bonding agents on the adhesive layer thickness and the microtensile bond strength.

OBJECTIVES: This study investigated the hypothesis that varying the acetone content of single solution dentin bonding agents may affect the adhesive layer thickness and microtensile bond strength (MTBS) of the bonded complex, and explored whether the adhesive layer thickness is a valid predictor for MTBS. METHODS: Experimental dentin bonding agents containing (27, 37, 47, 57, or 67) mass fraction% acetone were used to bond composite resin onto occlusal dentin surfaces of extracted human molars. The adhesive layer thickness was determined by digitized image analysis. MTBS was measured after 48 h. The fracture surfaces were observed using SEM. RESULTS: With increasing acetone content, MTBS varied from 38 MPa (67% acetone) to the highest MTBS of 64 MPa (37% acetone), while the adhesive layer thickness decreased linearly. Both dependent variables demonstrated moderate inverse correlation with the acetone content (p<0.0001), but were not correlated with each other (p>0.05). Ninety-four percent of the specimens showed fractures within the adhesive layer extending toward the interfaces with the hybrid layer or the composite resin. In the groups containing 57 and 67% acetone, cracks were observed at these interfaces. SIGNIFICANCE: Rather than the adhesive layer thickness, interfacial cracks in specimens with acetone-rich bonding agents may have caused lower MTBS. Within the scope of this investigation, lower acetone concentrations, as could be anticipated from solvent evaporation during clinical use of the bonding agent, did not seem to lower MTBS, but rather improved the integrity of the dentin/adhesive bond.

Acetone↗
PubMed1999

Acetone preservation: a practical technique for molecular analysis.

In attempts to establish a convenient and reliable method for field collection and archival preservation of insects and their endosymbiotic microorganisms for molecular analysis, acetone, ethanol, and other organic solvents were tested for DNA preservability of the pea aphid Acyrthosiphon pisum and its intracellular symbiotic bacterium Buchnera sp. After 6 months' storage, not only the band of high-molecular-size DNA but also the bands of rRNA were well preserved in acetone, ethanol, 2-propanol, diethyl ether and ethyl acetate. Polymerase chain reaction (PCR) assays confirmed that the DNA of both the insects and their symbionts was well preserved in these solvents. In contrast, methanol and chloroform showed poor DNA preservability. When water-containing series of acetone and ethanol were examined for DNA preservability, acetone was apparently more robust against water contamination than ethanol. Considering that most biological materials contain high amounts of water, acetone may be a more recommendable preservative for DNA analysis than ethanol which has been widely used for this purpose. The DNA of various insects could be preserved in acetone at room temperature in good condition for several years. In addition to the DNA of the host insects, the DNA of their endosymbionts, including Buchnera and other mycetocyte symbionts, Wolbachia, and gut bacteria, was amplified by PCR after several years of acetone storage. The RNA and protein of the pea aphid and its endosymbiont were also preserved for several years in acetone. After 2 years' storage in acetone, proteins of A. pisum could be analysed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblotting, and the endosymbiotic bacteria were successfully detected by immunohistochemistry and in situ hybridization on the tissue sections.

Acetone↗
PubMed2002

A novel method for removing residual acetone from gelatin microspheres.

PURPOSE: To develop a method for removing residual acetone from gelatin microspheres. METHODS: Free-flowing gelatin microspheres were either heated under vacuum or subjected to a stream of humidified air in a specially designed apparatus for removal of the residual acetone. To understand the removal mechanism, hygroscopic and thermal properties of the microspheres were examined. RESULTS: Heating the gelatin microspheres under vacuum did not reduce the acetone level below 2%, but the use of humidified air under fluidizing condition reduced the residual acetone in gelatin microspheres by an additional two orders of magnitude. The rate of acetone removal was a strong function of the relative humidity (RH) of the air stream; higher RH accelerated acetone removal. Other variables influencing the acetone removal rate are the mean particle diameter and the linear velocity of the humidified air. Under high relative humidities, significant amounts of moisture were absorbed into gelatin microspheres, reducing their glass transition temperature below 25 degrees C. CONCLUSION: The residual acetone in gelatin microspheres can be efficiently removed when exposed to air of high RH. Mechanisms of water-dependent acetone removal are proposed.

Acetone↗
PubMed1989

High affinity diethylnitrosamine-deethylase in liver microsomes from acetone-induced rats.

The effects of acetone treatment on microsomal cytochrome P-450-dependent mono-oxygenases of the rat liver have been investigated to elucidate the role of this system in the metabolism of diethylnitrosamine (DEN). Acetone markedly enhanced the hepatic P-450 content and the activities of p-nitrophenol hydroxylase, acetone hydroxylase, ethoxycoumarin deethylase and DEN deethylase (DENd), whereas activities of pentoxy-resorufin O-deethylase and ethoxy-resorufin O-deethylase were not affected. Two distinct apparent Km values (0.43 and 9.1 mM), dependent on the substrate concentration, were observed for the DENd of acetone-induced microsomes. Only one Km value (8.4 mM) was observed for the DENd of control microsomes. In control microsomes at a DEN concentration of 1 mM, the N-deethylation of DEN was undetectable whereas in acetone-induced microsomes the N-deethylation rate was approximately 2.3 nmol/mg protein per min. The results suggest that acetone-induced microsomes of rat liver contain a high affinity form of DEN-deethylase which should be the P-450j isozyme (known to catalyze the oxidation of dimethylnitrosamine at low Km). P-450j is strongly enhanced by acetone treatment as indicated by the increase of the specific acetone hydroxylase. The treatment also enhanced the metabolism of DEN at substrate concentrations higher than 1 mM, suggesting that other P-450(s) catalyse DEN-deethylation although with lower substrate affinity. The low Km form of DENd is a P-450-dependent mono-oxygenase. It requires NADPH and O2, is inhibited by CO, but not by mannitol, superoxide dismutase, catalase or desferrioxamine. Its action therefore appears not to be mediated by oxygen radical species. Many solvents such as dimethylsulfoxide, dioxolane, chloroform and butanol when present at 10 mM in the incubation mixture inhibited the low Km form of DENd. However, pyrazole and piperonylbutoxide were found to be the strongest inhibitors. These results establish that acetone affects the metabolism of DEN, particularly at low concentrations, in a fashion somewhat similar to dimethylnitrosamine.

Acetone↗
PubMedDate not supplied

Concentrations of acetone in venous blood samples from drunk drivers, type-I diabetic outpatients, and healthy blood donors.

Headspace gas chromatography (HSGC) was used to measure the concentrations of acetone in samples of venous whole blood from drunk drivers (n = 500), hospital outpatients with type-I diabetes mellitus (n = 250), and healthy blood donors (n = 288). The standard deviation (SD) of blood-acetone determination by HSGC was 0.048 mg/L at a mean concentration of 2.34 mg/L (2.1%). The concentration of acetone in blood did not change significantly when the samples were stored at 4 degrees C for eight days. The ratio of the concentrations of acetone in plasma and whole blood was 1.23:1 (SD 0.229, n = 22). The frequency distributions of blood-acetone concentrations were markedly skewed to the right. The median concentration of acetone in blood from drunk drivers was 2.03 mg/L and the 2.5 and 97.5 percentiles were 0.80 and 12.8 mg/L, respectively. In patients with type-I diabetes mellitus, the median blood-acetone concentration was 1.90 mg/L and the 2.5 and 97.5 percentiles were 0.40 and 11.1 mg/L, respectively. In healthy blood donors, the median blood-acetone level was 1.26 mg/L and the 2.5 and 97.5 percentiles were 0.37 and 4.69 mg/L, respectively. The concentrations of acetone in blood did not differ appreciably among these three groups of subjects.

Acetone↗