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PubMed2001

Effect of barrier disruption by acetone treatment on the permeability of compounds with various lipophilicities: implications for the permeability of compromised skin.

The permeability of compromised skin barrier was investigated in vitro using acetone-disrupted hairless mouse skin as a model membrane. The effect of compound lipophilicity was studied using sucrose, caffeine, hydrocortisone, estradiol, and progesterone as model compounds. The results demonstrated that permeability barrier disruption by acetone treatment significantly enhanced the permeability of the skin to both hydrophilic and amphipathic compounds, including sucrose, caffeine and hydrocortisone. This effect was more prominent with caffeine and hydrocortisone at different transepidermal water loss (TEWL) levels. Acetone treatment, however, didn't appear to alter the percutaneous penetration of highly lipophilic compounds, such as estradiol and progesterone. The characteristics of skin permeability were described by parabolic relationships between log P(WS) (permeability coefficient of whole skin) and log K(O/W) (octanol/water partition coefficient) at different degrees of permeability barrier disruption. The optimal log K(O/W) of compounds for skin penetration appeared to decrease with an increase in TEWL levels. The maximal permeability achieved was similar through skin displaying different TEWL levels. In an attempt to explore the underlying mechanisms for the changes in skin permeability, the stratum corneum/normal saline partition coefficients of water, caffeine, and hydrocortisone either decreased or remained unaffected with an increase in TEWL. Electron microscopic examinations have revealed reductions in stratum corneum lipid content and alterations in intercellular membrane structures as a result of acetone treatment, whereas negligible changes in the number of horny layers were observed by safranin staining of the stratum corneum. We have concluded that the enhancement in skin permeability to both hydrophilic and amphipathic compounds by acetone treatment arose mainly because of the increase in stratum corneum diffusivity at higher TEWL levels. The results imply the possibility of using both TEWL and drug lipophilicity to predict alterations in skin permeability and hence the dose adjustment of topically applied medication for patients with impaired skin barrier function.

Acetone↗
PubMed2005

Rapid determination of acetone in human blood by derivatization with pentafluorobenzyl hydroxylamine followed by headspace liquid-phase microextraction and gas chromatography/mass spectrometry.

In the current work, a simple, rapid, accurate and inexpensive method was developed for the determination of acetone in human blood. The proposed method is based on derivatization with O-(2,3,4,5,6-pentafluorobenzyl)hydroxylamine hydrochloride (PFBHA), followed by headspace liquid-phase microextraction (HS-LPME) and gas chromatography/mass spectrometry (GC/MS). In the present method, acetone in blood samples was derivatized with PFBHA and acetone oxime formed in several seconds. The formed oxime was enriched by HS-LPME using the organic solvent film (OSF) formed in a microsyringe barrel as extraction interface. Finally, the enriched oxime was analyzed by GC/MS in electron ionization (EI) mode. HS-LPME parameters including solvent, syringe plunger withdrawal rate, sampling volume, and extraction cycle were optimized and the method reproducibility, linearity, recovery and detection limit were studied. The proposed method was applied to determination of acetone in diabetes blood and normal blood. It has been shown that derivatization with HS-LPME and GC/MS is an alternative method for determination of the diabetes biomarker, acetone, in blood samples.

Acetone↗
PubMed2000

13C NMR lineshapes of acetone adsorbed on silica.

13C NMR data, obtained as a function of temperature with magic-angle spinning (MAS) and either cross polarization or direct polarization, are reported on acetone and a sample of acetone (an approximately equal mixture with 13C labels at C-1 or C-2) adsorbed on dry silica gel. Various contributions to the observed linewidths and T2C values are considered in terms of a previously established model of the acetone/SiO2 system; in that model, acetone species are in equilibrium between a physisorbed-acetone (non-hydrogen-bonded) state and a state consisting of acetone units that are hydrogen bonded to silanol moieties on the silica surface. Spin dynamics simulations are useful in interpreting the effects of variations of experimental parameters. It is concluded that the main linewidth contributions, which increase at lower temperatures, are: (a) a dispersion of chemical shifts in the hydrogen-bonded state, associated with the inhomogeneous character of the silica surface; (b) the interference between MAS averaging of the chemical shift anisotropy (especially for the carbonyl carbon) and molecular motion and/or chemical exchange; and (c) chemical exchange broadening. Prominence of the last of these contributions is most consistent with data obtained as a function of magnetic field strength, MAS speed, and temperature.

Acetone↗
PubMed1982

Increased acetone exhalation induced by metabolites of halogenated C1 and C2 compounds.

Rats were exposed, in a closed desiccator jar chamber, to concentrations of various halogenated C1 and C2 compounds at which the metabolizing capacities were saturated (Vmax conditions). Within the exposure period of 50 h concentrations of the xenobiotic and of exhaled acetone were monitored in the gas phase of the system. The quantitative extent of acetone exhalation was dependent on the individual compound examined. Acetone exhalation was stimulated in presence of vinyl chloride, vinyl bromide, vinyl fluoride, vinylidene fluoride, cis- and trans-1,2-dichloroethylene, trichloroethylene, perchloroethylene, methylene chloride, chloroform, carbon tetrachloride and 1,1,2-trichloroethane. No stimulation of acetone exhalation occurred with 1,1,1-trichloroethane and with the reference hydrocarbon n-hexane. Also, acetone exhalation was evoked by infusions of either fluoroacetate or chloroacetate, two anticipated or proven metabolites of some haloethylenes; the infusion rates of which were based on calculations of the metabolic rates of vinylidene fluoride and of vinyl chloride, respectively.

Acetone↗
PubMed1990

Biological monitoring of occupational exposure to isopropyl alcohol vapor by urinalysis for acetone.

The relationship of the intensity of occupational vapor exposure to isopropyl alcohol (IPA) with urinary excretion of acetone and unmetabolized IPA was studied in 99 printers of both sexes, who were exposed to up to 66 ppm IPA (as time-weighted average), together with toluene, xylenes, methyl ethyl ketone and/or ethyl acetate. Acetone and IPA concentrations in urine were studied also in 34 non-exposed subjects. Acetone was detectable in the urine of most of the non-exposed, and the urinary acetone concentration increased in proportion to the IPA exposure intensity (r = 0.84 for observed, non-corrected values), whereas the correction for creatinine concentration or specific gravity of urine did not give a larger correlation coefficient. IPA itself was not found in the urine of the non-exposed, and was detectable in urine of only those who were exposed to IPA above a certain level, e.g. 5 ppm. The present study results suggest that urinary acetone is a valuable index for biological monitoring of occupational exposure to IPA as low as 70 ppm.

1-Propanol↗
PubMed1976

Generation of an esterolytic and kinin-forming kallikrein-alpha2-macroglobulin complex in human serum by treatment with acetone.

Kinin-forming and esterolytic activity in human citrate plasma has been activated by treatment of the plasma with acetone. By far most of the esterolytic activity if not all of it was recovered in an alpha2-macroglobulin (alpha2M) kallikrein complex (SI) which was characterized and purified by chromatography. Little if any esterolytic activity was present which could be ascribed to free plasma kallikrein. The alpha2M-kallikrein complex had kinin-releasing activity though much less than free plasma kallikrein, relative to esterolytic potency. This explains that a considerable fraction of the kinin-forming potential of acetone-activated plasma resides in free plasma kallikrein although it represents only a very small portion of the total kallikrein store. Like free plasma kallikrein the alpha2M complex releases kinin from LMW-kininogen less efficiently than from HMW, in systems of purified components. In whole plasma, the efficiencies change: whereas plasma kallikrein is rapidly inactivated by endogenous inhibitors, the alpha2M complex is protected from further inactivation and capable of releasing kinin continuously if slowly, attacking also LMW-kininogen after HMW-kininogen has been consumed by free kallikrein. While the alpha2M-complex in this respect differs functionally from free plasma kallikrein and explains earlier observations suggesting the presence of two kininogenases, it seems doubtful now that two truly different kininogenases exist in human plasma. The results suggest that acetone predominantly inactivates full inhibitors of kallikrein such as C1INH whereas alpha2M is somewhat more resistant and (pre-)-kallikrein even more. Depending on the time and temperature of acetone treatment one obtains more or less total kallikrein and varying proportions of free to bound enzymes. It is likely that acetone does not turly trigger an activation of prekallikrein but supports spontaneous activation by slowing down the control of the feedback reinforcement of this activation, by damaging inhibitors.

Acetone↗
PubMed1987

Quantitative aspects of two methods to dissolve collagen-free muscle proteins from acetone dry powders of Guelders ring sausage.

The purpose of this study was to find experimental conditions for the complete solubility of collagen-free muscle proteins (CFMP) using acetone powder of Guelders ring sausage. Preliminary experiments were carried out to choose the best procedure for preparing the acetone dry powder. Two different methods of acetone extraction of minced sausage were compared. The acetone dry mass (ADM) method using continuous extraction in a Soxhlet [2] apparatus gave better results than the acetone powder (ACP) method, which used a blender [1]. The ADM method was used for further investigations. ADM was extracted with two types of sodium dodecyl sulphate (SDS), containing solvents A and B. Solvent A contains a Tris-boric acid buffer (pH 8.2) with 1.5% (m/v) SDS and 0.05% (m/v) dithioerythreitol [3]. Solvent B is a borate-chloric acid buffer (pH 9.0) with 2.0% (m/v) SDS and 1.0% (m/v) mercapto-ethanol [2]. Both solvents showed a linear relationship between the quantities of CFMP in ADM and the dissolved CFMP. The linear relationships were found between quantities of 10.0 and 30.0 mg (solution A) and of 5.0 and 30.0 mg ADM (solution B) per ml solvent. The solubility of CFMP was better in solvent B than in solution A. Completely dissolved CFMP from ADM was only obtained in the case of 5.0 mg ADM in 1.0 ml solution B. These conditions will be used in liquid chromatography experiments, the results of which will be reported later.

Acetone↗
PubMed1975

[Breath acetone and ketonemia in normal- and overweight subjects during total fasting (author's transl)].

In subjects of ideal weight (7 males and 7 females) total whole blood ketones and breath acetone were determined during a 6 day fast, and in obese subjects (8 males, 18 females) during 6-28 days of fasting. Development of starvation ketosis was significantly slower in overweight than in normal weight subjects. Breath acetone concentration was up to blood ketone levels of 4 mMol/1 a linear function of the blood ketone concentration, beyond that level, however, an additional exponential component became apparent. The highest acetone elimination found was 4.46 mg/min, corresponding to 6.4 g acetone and 11.2 g acetoacetic acid in 24 hours. Hence the decarboxylation of acetoacetic acid to acetone may be an additional mechanism for the lowering of ketoacidosis in starvation.

Acetone↗
PubMed1993

Toluene metabolism in isolated rat hepatocytes: effects of in vivo pretreatment with acetone and phenobarbital.

Hepatocytes isolated from control, acetone- and phenobarbital-pretreated rats were used to study the metabolic conversion of toluene to benzyl alcohol, benzaldehyde, benzoic acid and hippuric acid at low (< 100 microM) and high (100-500 microM) toluene concentrations. The baseline formation rates of toluene metabolites (benzyl alcohol, benzoic acid and hippuric acid) were 2.9 +/- 1.7 and 10.0 +/- 2.3 nmol/mg cell protein/60 min at low and high toluene concentrations, respectively. In vivo pretreatment of rats with acetone and phenobarbital increased the formation of metabolites: at low toluene concentrations 3- and 5-fold, respectively; at high toluene concentrations no significant increase (acetone) and 8-fold increase (phenobarbital). Apparent inhibition by ethanol, 7 and 60 mM, was most prominent at low toluene concentrations: 63% and 69%, respectively, in control cells; 84% and 91% in acetone-pretreated cells, and 32% (not significant) and 51% in phenobarbital-pretreated cells. Ethanol also caused accumulation of benzyl alcohol. The apparent inhibition by isoniazid was similar to that of ethanol at low toluene concentrations. Control and acetone-pretreated cells were apparently resistant towards metyrapone; the decrease was 49% and 64% in phenobarbital-pretreated cells at low and high toluene concentrations, respectively. In these cells, the decrease in presence of combined ethanol and metyrapone was 95% (low toluene concentrations). 4-Methyl-pyrazole decreased metabolite formation extensively in all groups. Benzaldehyde was only found in the presence of an aldehyde dehydrogenase inhibitor. Increased ratio benzoic/hippuric acid was observed at high toluene concentrations. These results demonstrate that toluene oxidation may be studied by product formation in isolated hepatocytes. However, the influence of various enzymes in the overall metabolism could not be ascertained due to lack of inhibitor specificity.

Acetone↗
PubMed1979

Volatile hydrocarbon and carbonyl products of lipid peroxidation: a comparison of pentane, ethane, hexanal, and acetone as in vivo indices.

A study was undertaken to determine whether respiratory hexanal and acetone as well as pentane and ethane could be measured as potential indices of lipid peroxidation in vivo. The tests of induction of lipid peroxidation in rats included injection of iron-dextran and the vitamin E deficiency status. Injection of 460 mg of iron/100 g body wt over a 28-day period increased pentane and ethane production 4- and 6-fold, respectively. Hexanal production was increased 7-fold after injection of 60 mg of iron/100 g body wt, and then it fell back to the preinjection level in spite of continued injection of iron-dextran. Acetone production was lower in iron-injected rats than in controls, and it was ca. 10-fold higher in fasted vitamin E-deficient rats than in vitamin E-supplemented rats, being ca 48 and 5 nmol/100 g/min, respectively. It was observed that halomethane injection did not increase hexanal production, while acetone and pentane production were increased. Pentane and hexanal, but not acetone, were found to arise from decomposition of linoleic acid hydroperoxide in vitro. It was concluded that hydrocarbon gases are better indices of lipid peroxidation than hexanal, which is enzymatically metabolized, and acetone, the production of which is dominated by factors such as altered carbohydrate metabolism.

Acetone↗
PubMed1984

A purge-and-trap method for the analysis of acetone in biological tissues.

A method for the detection and quantitation of acetone in biological tissues is described. The solvent was extracted with nitrogen gas from the biological specimen and adsorbed on a porous polymer (Porapak Q). The acetone content of the adsorbent was determined by conventional gas chromatographic analysis (FID) after heat desorption. The reliability of the method was tested both with in vitro- and in vivo-exposed specimens. A complete recovery was obtained after in vitro additions of acetone. The method error was about 9% as calculated from both in vitro and in vivo experiments. Acetone concentrations ranging between 17 nmol/g tissue in nonexposed animals and 1.8 mumol/g tissue in mice exposed to acetone vapor were determined.

Acetone↗
PubMed1980

Characteristics of an acetone powder preparation of the vitamin K-dependent gamma-glutamyl carboxylase.

An acetone powder, prepared from the liver microsomes of vitamin K-deficient rats, retains an active vitamin K-dependent gamma-glutamyl carboxylase. While the basic requirements of the enzyme are similar to those of the carboxylase of either resuspended microsomes or detergent-solubilized microsomes, the acetone powder preparation reveals some additional properties of the carboxylase. Carboxylation of the synthetic pentapeptide substrate phenylalanylleucyl-glutamyl-glutamyl-valine can occur in the absence of nonionic detergent; however, when vitamin K hydroquinone drives the acetone powder carboxylation nonionic detergent is require for maximal activity. Experiments are described in which the acetone powder is incubated with the pentapeptide, pelleted by centrifugation, resuspended with fresh reactants, and incubated again. They suggest that the low V for the carboxylase, observed by all investigators, is, at least in part, not the result of irreversible enzyme inactivation nor depletion of reactants, but rather accumulation of a yet to be identified inhibitor(s). The acetone powder prepared from microsomes derived from livers of nutritionally normal cows contains vitamins vitamin K-dependent gamma-glutamyl carboxylase. This enzyme can be solubilized from the powder using Triton X-100 and could provided a large supply of starting material for enzyme purification.

Acetone↗
PubMed1978

Stimulation of microsomal dimethylnitrosamine-N-demethylase by pretreatment of mice with acetone.

To further investigate the relationship between in vivo microsomal enzyme modifiers and in vitro dimethylnitrosamine (DMN) metabolism, male C57BL/6J mice were pretreated with acetone or Aroclor 1254, two compounds known to influence DMN-N-demethylase activity. Pretreatment with acetone enhanced the in vitro microsomal activity of DMN-N-demethylase, as measured by formaldehyde production from DMN. Accompanying this acetone-enhanced demethylase activity was an increase in the covalent binding of [14C]DMN to RNA, protein and DNA. Four distinct Km values dependent on the substrate concentration were observed for the N-demethylase present in control microsomes. Only one Km value was observed for the demethylase in microsomes from acetone-treated animals, but it was significantly lower than the lowest Km observed in the control microsomes. At DMN concentrations of 1 and 10 mM, acetone significantly increased N-demethylation of DMN as compared to control, but not at 100 mM DMN. Aroclor 1254 pretreatment repressed DMN-N-demethylase at 1 mM DMN but enhanced it at 100 mM. These results suggest that there may be multiple forms of DMN-N-demethylase which are dependent on DMN concentration and respond differently to modifiers of the microsomal drug-metabolizing enzymes.

Acetone↗
PubMed1983

Induction of a high affinity nitrosamine demethylase in rat liver microsomes by acetone and isopropanol.

The effects of acetone and isopropanol on the microsomal monooxygenase system have been investigated to study the role of this enzyme system in the metabolism of nitrosamines. Treatment of rats with acetone or isopropanol (2.5-5 ml/kg, i.g.) causes a 3-4.5-fold enhancement in the NADPH-dependent nitrosodimethylamine demethylase (NDMAd) activity. This is accompanied by only moderate increases in the gross cytochrome P-450 (P-450) content and NADPH-cytochrome c reductase activity. Several other monooxygenase activities were increased to different extents from an 8% increase in aryl hydrocarbon hydroxylase to a 261% increase in ethoxycoumarin O-dealkylase activities. Kinetic analysis indicates that a low Km form of NDMAd (Km = 0.07 mM) is induced by these treatments. In the microsomes of the treated rats, this high affinity form becomes predominant, in contrast to control microsomes which possess at least three Km-values for NDMAd. The treatment also enhances the metabolism of nitrosomethylethylamine, nitrosomethylbenzylamine and nitrosomethylaniline although to lesser extents than with nitrosodimethylamine. Several lines of observations suggest that the enhanced NDMAd is due to the induction of one or more specific P-450 isozyme(s) by pretreatment with acetone or isopropanol: (a) The treatment induces proteins with molecular weights (Mr) of 50 000 and 52 000 which are in the range of known P-450 isozymes. (b) The induction of these proteins and NDMAd activity was inhibited by CoCl2 and cycloheximide. (c) The induced microsomes had a peak at 450.6 nm different from the 450.0 nm peak of control microsomes. When added to the incubation mixture, both acetone and isopropanol inhibit NDMAd activity. Isopropanol is more potent than acetone and is shown to be a competitive inhibitor with a Ki-value of 0.151 mM.

1-Propanol↗
PubMed1986

Deposition of ethanol and acetone vapors in the upper respiratory tract of the rat.

The deposition of nonreactive gases in the lungs is well studied and is dependent on the ventilation-perfusion relationships of that organ. The current investigation was undertaken to determine if pulmonary ventilation-perfusion models could be successfully applied to quantitatively describe upper respiratory tract (URT) deposition of acetone and ethanol vapors. Toward this end, the deposition of these vapors was measured in the surgically isolated URT of the anesthetized rat at selected inspiratory flow rates (ranging from 70 to 500 ml/min) and exposure times (ranging from 3.3 to 13.3 min). The deposition of acetone in the URT followed apparent quasi-steady-state conditions, suggestive of a ventilation-perfusion relationship. Pulmonary ventilation-perfusion models predict the ratio of the amount deposited to the amount not deposited should be linearly related to the inverse of the inspiratory flow rate. Such a relationship was observed for URT acetone (r = 0.988, N = 16,p less than 0.0001) and ethanol (r = 0.963, N = 20, p less than 0.0001) deposition. From the deposition-flow relationships estimates of 0.31 and 0.33 ml/min were obtained for nasal blood flow in the ethanol and acetone studies, respectively. The 95% confidence limits for these estimates overlapped. The successful application of a ventilation-perfusion model to describe URT deposition suggests that acetone and ethanol vapors equilibrate between the inspired airstream and the capillary blood of the URT and that their deposition is dependent on both the URT ventilation and perfusion rates.

Acetone↗
PubMed1988

Assessment of the minimal effective dose of acetone for potentiation of the hepatotoxicity induced by trichloroethylene-carbon tetrachloride mixtures.

Administration of acetone to rats in amounts larger than or equal to a minimal effective dosage (MED) is known to potentiate the severity of the liver damage produced by CCl4 alone. It has been reported that CCl4-induced hepatotoxicity is also enhanced by the previous administration of trichloroethylene (TCE). In addition, TCE-CCl4 mixture-induced liver injury is potentiated by acetone. The present study was undertaken to determine if the acetone MED is decreased when the haloalkane challenge is a mixture of TCE-CCl4 instead of CCl4 alone. The effect of varying mixture compositions was also evaluated. In a first series of experiments, male Sprague-Dawley rats received corn oil or acetone (0.05-0.25 ml/kg, po); 18 hr later, they received an ip injection of either CCl4 (0.1 ml/kg) or [TCE (0.25 ml/kg)-CCl4 (0.1 ml/kg)]. In a second series, rats received corn oil or acetone (0.75 ml/kg), and were challenged with TCE (1.5 ml/kg), CCl4 (0.25 ml/kg), or a mixture of TCE-CCl4, where TCE and CCl4 dosages were equal to 25-75%, 50-50%, and 75-25%, respectively, of those used for the administration of the solvents alone. In both series, rats were killed 24 hr after the haloalkane challenge. Liver injury was assessed biochemically (plasma ALT activities and bilirubin concentrations) and morphologically. When TCE was added to a solution of CCl4, smaller doses of CCl4 were required to produce equally severe liver injury.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetone↗
PubMed1980

Hemin-catalyzed generation of triplet acetone.

Hemin can substitute for horseradish peroxidase as a catalyst for the aerobic oxidation of isobutanal to acetone and formate. Previous studies have shown that the chemiphosphorescent emission observed in the enzyme-catalyzed reaction is due to the production of acetone in its triplet state. Although no chemiphosphorescence is observed with the model system (hemin), generation of triplet acetone in this system is indicated by an analysis of data for energy transfer to the 9,10-dibromoanthracene-2-sulfonate ion and for interception of the excited species by the sorbate ion, a known triplet quencher. These data are compared to those obtained with triplet acetone generated by thermal cleavage of tetramethyldioxetane in aqueous solution. The results are in agreement with the hypothesis that the quenching of triplet acetone by oxygen is less efficient in the enzyme catalyzed reaction, pointing to a protective role for the apoenzyme in that system.

Acetone↗
PubMed1986

Lipid composition of liver microsomes from rats treated with acetone.

The metabolism of certain compounds by rat hepatic microsomal preparations obtained from acetone-treated rats is greater than that measured in microsomes obtained from control rats. Since the lipid composition of membranes can significantly influence metabolism catalyzed by membrane-bound enzymes, studies were conducted in order to determine whether acetone-induced alterations in microsomal metabolism are associated with changes in the lipid composition of these membranes. Phospholipid and cholesterol concentrations were measured in extracts of rat liver microsomes obtained from rats treated with acetone, sodium phenobarbital, or vehicle. Acetone treatment did not alter the phospholipid and cholesterol content of the microsomes, whereas sodium phenobarbital (positive control) caused a significant decrease in cholesterol content/mg microsomal protein. These data indicate that acetone-induced alterations in microsomal metabolism may not be attributed to changes in the phospholipid and cholesterol content of the microsomes.

Acetone↗