Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Acetone”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 271 records · Page 15Linked to original sources
PubMedDate not supplied

Reference values of urinary acetone in a Brazilian population and influence of gender, age, smoking and drinking.

BACKGROUND: Reference values for some xenobiotics naturally present in the body are important for biomonitoring, in order to compare the levels found in a population exposed to the xenobiotic with those of a reference population. Acetone in urine (UAc) is the most used bioindicator to evaluate worker exposure to acetone and isopropanol. OBJECTIVES: Since acetone is also found in individuals not occupationally exposed to these solvents, the purpose of the present study was to evaluate the basal levels of UAc and the possible influence of individual factors on such levels. METHODS: The population consisted in 207 individuals, 91 men and 116 women, between 18 and 80 years old. UAc was determined by headspace/gas chromatography/FID. RESULTS: For the total population, the reference values found were: mean (+/- SD), 1.12 (+/- 0.47) mg/l; median 1.04 mg/l; geometric mean 1.03 mg/l; 95% confidence interval 0.98-1.26 mg/l, 95th percentile 2.20 mg/l and upper reference level (mean+2 SD) 2.06 mg/l. As the values of UAc resulted in a non-Gaussian distribution, the option was to transform these values to log UAc, which drew the data closer to normal distribution (W=0. 98532, p<0.7000). CONCLUSIONS: Reference values for acetone in urine determined in a population in south Minas Gerais, Brazil, are close to the background values reported elsewhere; gender and ingestion of alcohol seem to affect the basal levels of urinary acetone, while age or smoking showed no similar effect.

Acetone↗
PubMed1988

Benzene metabolism by ethanol-, acetone-, and benzene-inducible cytochrome P-450 (IIE1) in rat and rabbit liver microsomes.

Ethanol is known to exert a synergistic effect on the toxicity of benzene. In the present investigation it was found that benzene was metabolized at a rate 20-65-fold higher in liver microsomes from ethanol- or acetone-treated rats than in microsomes from control animals. One high affinity site [Km = 19 +/- 5 (SD) microM] and one low affinity site [Km = 0.3 +/- 0.1 mM] for benzene metabolism were present in microsomes of acetone-treated rats, and similar sites were seen in microsomes from control or ethanol-treated rats. Treatment of the animals with either ethanol or acetone mainly influenced the Vmax values for benzene metabolism. Also benzene treatment of rats caused an increased rate of microsomal benzene metabolism. The hepatic microsomal NADPH-dependent metabolism of benzene was inhibited by compounds known to interact with the ethanol-inducible form of P-450 such as imidazole, ethanol, aniline, and acetone but was unaffected by addition of metyrapone. Anti-IgG against ethanol-inducible cytochrome P-450 from rat (P-450j) or rabbit liver (P-450 LMeb) inhibited the microsomal benzene metabolism effectively in rat or rabbit liver microsomes, respectively, whereas preimmune IgG was without effect. The level of rat ethanol-inducible P-450 (P-450j) was induced to an extent similar to that for the microsomal benzene metabolism, by either benzene, acetone, or ethanol. The data indicate that benzene is metabolized mainly by the ethanol-inducible P-450 form in liver microsomes and that the induction of this isozyme by ethanol can provide an explanation for the synergistic action of ethanol on benzene toxicity.

Acetone↗
PubMed1983

Acetone-treated agglutinin against Yersinia pseudotuberculosis in free-living rats.

Retrospective investigation was done on Yersinia pseudotuberculosis infection in barn rat populations living in an Yersinia endemic area and in zoo rat populations living in a nonendemic area. The OH agglutinins against Y pseudotuberculosis were normally distributed within both populations. Most of the OH agglutinin titers and many O agglutinin titers were reduced by treatment of sera with acetone. Sera with O and OH agglutinin titers were assigned to 2 groups, one with a titer less than 1:8 and the other with a titer of greater than or equal to 1:8. Rats harboring the organism did not possess O or OH agglutinin titers greater than 1:8 in acetone-treated sera. In most nontreated sera, OH agglutinin titers were higher than were the O agglutinin titers. However, in most acetone-treated sera, O agglutinin titers were equivalent to OH agglutinin titers. Differences by region and age were observed in acetone-treated O agglutinin titers of greater than or equal to 1:8 against Y pseudotuberculosis. Therefore, it is recommended that to detect antibody against Y pseudotuberculosis in rats, sera should be treated with acetone before the test and O antigen should be used.

Acetone↗
PubMed1981

A rapid quantitative colorimetric determination of blood acetone applied to the assessment of ketosis in fasted pregnant ewes.

A simple, accurate, colorimetric method for determining blood acetone as an adjunct to the enzymic method of estimating the other ketones was developed and tested on a group of fasted pregnant ewes. Acetone reacted with 2-hydroxybenzaldehyde to form a stable coloured complex that followed Beer's Law up to an acetone concentration of at least 4 mg/100 ml of the test solution at 490 nm. While the optimum incubation time of the reaction mixture was found to be 3 h at 40 degrees C, it could also be left to incubate overnight at room temperature. When tested in a blood matrix, the method gave a mean within-batch coefficient of variation of 0,7%, and a day to day variation of 0,3-1,2%, while an overall recovery of 100, 6+/-1,4% was achieved over 5 concentration ranges (2,86-10,53 mg/100 ml). The values obtained from this method corresponded closely to those from the diffusion technique previously employed and it considerably simplified the procedure. A direct linear relationship, y = 2,594x + 2,917 with a coefficient of determination r2 = 0,958 for 49 pairs of data, was found between the acetone (= x mg/100 ml) and total ketone (= y mg/100 ml) concentrations in blood samples drawn from fasted pregnant sheep. This relationship can therefore be used to estimate accurately the degree of ketosis from the blood acetone concentration alone.

Acetone↗
PubMed1978

Interaction of styrene and acetone with drug biotransformation enzymes in rat liver.

In the presence of hepatic microsomes, styrene produced a type I difference spectrum, which demonstrates that styrene binds to the catalytic site of ferricytochrome P-450. A comparison of the binding parameters for the interaction of styrene with noninduced, phenobarbital-induced, and 3-methylcholanthrene-induced microsomes indicated that styrene is predominantly bound by cytochrome P-450 and not by cytochrome P-448. Inhalation exposure to a mixture of acetone (1,000 ppm, 6 h/d) and styrene (300 ppm, 6 h/d) for 5 d caused a distinct decrease in hepatic free nonprotein sulfhydryl groups. This decrease could be observed both with and without phenobarbital treatment. Acetone inhalation alone also enhanced ethoxycoumarin O-deethylase activity in rats without pretreatments. Acetone inhalation also increased the cytochrome P-450 content of liver microsomes, but it had no effect on NADPH cytochrome c reductase or epoxide hydratase activity. Combined exposure to styrene and acetone enhanced NADPH cytochrome c reductase activity in nonphenobarbital-treated rats, but no effect was seen in the phenobarbital-treated animals. Phenobarbital treatment of animals can greatly modify the biotransformation and toxicity of styrene, phenobarbital inducible P-450 hemoprotein playing a predominant role in its metabolism. Simultaneous inhalation exposure to acetone also interacts with the metabolism of styrene.

Acetone↗
PubMed1993

[An infrared spectrophotometric method for determining acetone in the air of a work area in the presence of other solvents].

The acetone is used on a large scale in practice as solvent of nitro-cellulose and acetyl-cellulose paints and lacquer, rubber and resins. A spectrophotometric method in the infrared area for direct determination of gas phase of acetone is developed by means of 20 m.gas cuvette. The determination is performed in the specific for the acetone peaks at 1216 cm-1 and 1737 cm-1. With the method could be determined the acetone concentrations of 10 mg/m3 to 2000 mg/m3. For this purpose are worked out different standard scales of the acetone at various length of the gas cuvette. The method is specific in the presence of the most frequently used organic solvents--toluol, ethanol, butanol, mineral turpentine and cyclohexan. Ketones only stand in the way of determination.

Acetone↗
PubMed1993

The efficacy of acetone in the sterilisation of ophthalmic instruments.

Acetone has been considered a quick, effective and less expensive chemical sterilising agent and continues to be used by ophthalmic surgeons, at least in developing countries. Its utility however has been questioned recently. This study was designed to assess the efficacy of acetone against Pseudomonas aeruginosa, Bacillus subtilis and Aspergillus flavus present on ophthalmic surgical instruments (forceps, sutures). The instruments were contaminated by immersion in standard suspensions of the organisms and thereafter were either unwashed (group-I), washed and dried (group-II) or only washed (group-III) before immersion in acetone. The exposure to acetone was kept at 3, 10 and 20 minutes in each group. The results showed that acetone could eliminate Pseudomonas (vegetative bacteria) after 10 minutes exposure in unwashed group and 3 minutes exposure in washed groups. It was ineffective against spore bearing bacteria (B. subtilis) and fungus (Aspergillus flavus) even after 20 minutes of exposure.

Acetone↗
PubMed1996

Effects of acetone on the capacity of o-xylene and toluene to induce several forms of cytochrome P450 in rat liver.

The influence of acetone on the induction of P450 in lung, kidney and liver by toluene and xylene was studied in an attempt to estimate more precisely the range of P450 which are proposed to function in the activation of xylenes and toluene metabolites in the conditions of combined exposures. The addition of acetone potentiated the induction of CYP1A1/2 to 4 minutes ethoxyresorufin deethylation that from control animals after pretreatment with toluene. The level of this enzymatic activity (0.4 nmol/min/mgP) estimated in this study is consistent with the turnover number of the purified CYP1A1 (0.45 nmol/min/mgP). The assay activity results were confirmed by immunoblotting detection of the CYP1A1/2 levels. Oppositely, the addition of acetone in the inhalation protocol using o-xylene lead to a lower ethoxyresorufin deethylation activity as that in rat livers from rats pretreated with xylene alone. Pentoxyresorufin deethylation activity was enhanced strongly by toluene (3.5 times the controls) and by xylene (4 times the controls) and the addition of acetone potentiated the induction of CYP2B1 both after xylene and toluene. A 4 fold induction of CYP2E1 dependent chlorzoxazone hydroxylation after exposure to toluene and 2.5 fold after xylene corresponded to the enzyme levels of P45020E1 detected by immunoblotting. The addition of acetone consequently potentiated the induction effect of toluene and xylene and increased its levels more markedly in the case of xylene, which is a weaker inducer of CYP2E1.

Acetone↗
PubMed1996

Pattern of inhalation exposure: blood levels and acute subnarcotic effects of toluene and acetone in rats.

Solvent blood concentrations and subnarcotic effects (inhibition of electrically evoked seizures) were measured in rats exposed to constant or fluctuating air concentrations of toluene or acetone. A 4 hour exposure of resting rats to toluene at an air concentration of 1 and 2 mg/l, or to acetone at 4 and 10 mg/l, led to blood levels of 6.7 and 12.8 mg/l of toluene, or 183 and 520 mg/l of acetone: seizure inhibition amounted to 18% and 40+, or 10% and 50%, respectively. Blood level and effect attained 1/2 of the final values after 40 min and 60 min of exposure to 2 mg/l toluene, respectively, and dropped to 1/2 70 min and 90 min after exposure cessation: respective values for acetone 10 mg/l were 80 and 120 min, and more than 4 hours. A steep rise and a rapid drop was characteristic also for the course of blood level and effect during an exposure to fluctuating concentrations of toluene: ten minute fivefold jump in the air concentration induced a shortlasting seizure inhibition by more than 80%; the curves for acetone were flat.

Acetone↗
PubMed1991

Immunochemical detection of cytochrome P450 isozymes induced in rat liver by n-hexane, 2-hexanone and acetonyl acetone.

Cytochrome P450 isozymes induced in rat liver by treatment with n-hexane, 2-hexanone and acetonyl acetone (given intraperitoneally 5 mmol/kg for 4 days) were investigated using enzyme assays (benzene, toluene, 7-ethoxyresorufin and 7-pentoxyresorufin metabolism) and monoclonal antibodies (anti-P450IA1/2, anti-P450IIB1/2, anti-P450IIC11/6, anti-P450IIE1(91) and anti-P450IIE1(98)). n-Hexane treatment enhanced the activities of low-Km benzene aromatic hydroxylase and toluene side-chain oxidase, but not 7-ethoxyresorufin O-deethylase or 7-pentoxyresorufin O-depentylase. 2-Hexanone or acetonyl acetone treatment enhanced the activities of low- and high-Km benzene aromatic hydroxylases, toluene side-chain oxidase and 7-pentoxyresorufin O-depentylase, but not of 7-ethoxyresorufin O-deethylase. Immunoblot analysis showed that anti-P450IA1/2 did not bind liver microsomal protein from either control and treated rats in the region of cytochrome P450s, whereas with anti-P450IIE1(98) a clear-cut band was seen in liver microsomes from control and treated rats, with intensities in the following order: 2-hexanone = acetonyl acetone greater than or equal to n-hexane greater than control greater than phenobarbital. With anti-P450IIB1/2, a band was detected in microsomes from phenobarbital-treated rats, and to a lesser extent, in microsomes from 2-hexanone- and acetonyl acetone-treated rats. Like the immunoblot analysis, anti-P450IIE1(91) inhibited toluene side-chain hydroxylase activity in all microsomes, except in preparations from phenobarbital-treated rats and anti-P450IIB1 in microsomes from phenobarbital-, 2-hexanone- and acetonyl acetone-treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2002

Remarkable variations in the luminescence of frozen solutions of [Au[C(NHMe)(2)](2)](PF(6)) x 0.5(acetone). Structural and spectroscopic studies of the effects of anions and solvents on Gold(I) carbene complexes.

The unusual luminescence behavior of the two-coordinate gold(I) carbene complex, [Au[C(NHMe)(2)](2)](PF(6)) x 0.5(acetone), is reported. Upon freezing in a liquid N(2) bath, the colorless, nonluminescent solutions of [Au[C(NHMe)(2)](2)](PF(6)) x 0.5(acetone) become intensely luminescent. Strikingly, the colors of the emission differ in different solvents and appear only after the solvent has frozen. Solid [Au[C(NHMe)(2)](2)](PF(6)) x 0.5(acetone) is also luminescent, and the luminescence is attributed to the formation of extended chains of gold(I) centers that are connected through aurophilic attractions. Crystallographic studies of [Au[C(NHMe)(2)](2)](PF(6)) x 0.5(acetone) and [Au[C(NHMe)(2)](2)](BF(4)), which is also luminescent, reveal that both involve extended chains of cations and that the anions are hydrogen bonded to the cations through cation N-H groups. However, these chains differ in the Au...Au separations in each and in the carbene ligand orientations. In contrast, [Au[C(NMe(2))(NHMe)](2)](PF(6)) forms a colorless, nonluminescent solid, and in that solid there are no Au...Au interactions, a factor which supports the contention that aggregated species are responsible for the luminescence of [Au[C(NHMe)(2)](2)](PF(6)) x 0.5(acetone) in the solid state and in frozen solutions.

Journal Article↗
PubMed2006

Study of acetone photodissociation over the wavelength range 248-330 nm: evidence of a mechanism involving both the singlet and triplet excited states.

Measurements of the acetyl yield from acetone photolysis have been made using laser flash photolysis/laser induced fluorescence. Phi(total)(lambda,p,T) was determined over the ranges: 266 < or = lambda/nm < or = 327.5, 0.3 < or = p/Torr < or = 400 and 218 < or = T/K < or = 295. The acetyl yield was determined relative to that at 248 nm by conversion to OH by reaction with O2. Linear Stern-Volmer plots (1/[OH] vs [M]) describe the data for lambda < 300 nm, but for lambda > 300 nm, nonlinear Stern-Volmer plots were observed. This behavior is interpreted as evidence for dissociation from two excited states of acetone: S1 when the Stern-Volmer plots are linear and both S1 and T1 when Stern-Volmer plots are nonlinear. A model for acetone photolysis is proposed that can adequately describe both the present and literature data. Barriers to dissociation are invoked in order to explain the dependence of pressure quenching of the acetone photolysis yields as a function of wavelength and temperature. This pressure quenching was observed to become more efficient with increasing wavelength, but it was only above approximately 300 nm that a significant T dependence was observed, which became more pronounced at longer wavelengths. This is the first study to observe a T-dependent phi(total)(lambda,p,T). A parametrized expression for phi(total)(lambda,p,T) has been developed and is compared against the recommended literature data by running box model simulations of the atmosphere. These simulations show that acetone photolysis occurs more slowly at the top of the troposphere.

Journal Article↗
PubMed2004

Crystallization and preliminary X-ray analysis of an acetone carboxylase from Xanthobacter autotrophicus strain Py2.

Acetone carboxylase from Xanthobacter autotrophicus strain Py2 catalyzes the MgATP-dependent carboxylation of acetone to acetoacetate. Interestingly, during this reaction ATP is hydrolyzed to AMP and inorganic phosphate, suggesting a novel carboxylation mechanism. Acetone carboxylase is a heterohexameric protein comprised of three different polypeptides having molecular weights of 86 342, 78 509 and 19 773 Da arranged in an alpha(2)beta(2)gamma(2) quaternary structure. Here, the crystallization and preliminary X-ray data analysis of acetone carboxylase is reported. The acetone carboxylase isolated from the aerobic microorganism X. autotrophicus strain Py2 crystallizes in a primitive orthorhombic point group P222, with unit-cell parameters a = 76.2, b = 122.0, c = 264.2 A. The Matthews coefficient calculation indicates that one alphabetagamma half of the large protein complex is located in the asymmetric unit in this crystal form. Crystals have been obtained that diffract to better than 2.8 A resolution and data have been collected to 3.2 A resolution.

Adenosine Triphosphate↗
PubMed2007

Analysis of the inter-molecular interactions between amino acids and acetone by THz spectroscopy.

The THz spectra of amino acids after application of spots of acetone were measured. The 0.6 THz band was commonly observed in many amino acids that formed the intra-molecular salt structure. The band can be attributed to the interaction vibration from the common structural configuration of amino acids and acetone molecules. The evidence suggests that the vibration between the amino acids with intra-molecular salt structure and acetone has a peak at 0.6 THz. A model of the interaction vibration of acetone and the functional groups of amino acids is proposed.

Acetone↗
PubMed1997

Growth kinetics of preexposed and naive populations of Tetrahymena pyriformis to 2-decanone and acetone.

The growth kinetics of preexposed and naive Tetrahymena pyriformis grown in the presence of one hydrophilic and one hydrophobic nonpolar narcotic (acetone and 2-decanone, respectively) have been evaluated. The response of naive Tetrahymena exposed to nonpolar narcotics varied from a change in generation time upon exposure to hydrophilic chemical to a change in lag phase with similar generation time compared to control upon exposure to hydrophobic compounds. Tetrahymena grown in the presence of low concentrations of 2-decanone and then transferred to higher concentrations acclimated to the presence of the toxicant. Acclimation was demonstrated by reduced lag phases compared to naive cells. Results of population growth studies of Tetrahymena grown in the presence of low concentrations of acetone and then transferred to higher concentrations of acetone exhibit the same pattern, an increased generation time with increasing concentration with no lag time, as naive populations. Additionally, the observed generation times in acetone were cumulative relative to the transfer concentration as well as the acclimation concentration. The most feasible explanation for this phenomenon is the interaction of the toxicants with the plasma membrane.

Acetone↗
PubMed1997

Neurotoxicity associated with occupational exposure to acetone, methyl ethyl ketone, and cyclohexanone.

The neurotoxic effects of acetone, methyl ethyl ketone (MEK), and cyclohexanone on Romanian workers and the impact of those effects on industry environmental standards have been controversial subjects. To scientifically substantiate the standards, a study was conducted on three groups of workers to determine the changes induced by ketone solvents on the central and peripheral nervous systems. Groups of exposed workers and matched controls were studied for each solvent: acetone, 71 exposed and 86 controls from a coin printing factory; MEK, 41 exposed and 63 controls from a cable factory; and cyclohexanone, 75 exposed and 85 controls from a furniture factory. The subjects' mean age was 36 years. The mean length of exposure was 14 years. Study participants completed a questionnaire, responded to questions about alcohol consumption, submitted to a clinical examination, submitted samples for identification of biological exposure markers, and underwent motor nerve conduction velocity and neurobehavioral tests. Results showed that workers exposed to acetone were most affected in terms of human performance and evidence of neurotoxicity, followed by workers exposed to MEK and workers exposed to cyclohexanone. On the basis of the results, it was proposed that the 6-hr permissible exposure limits for acetone, MEK, and cyclohexanone be reduced to less than 500, 200, and 150 mg/m3, respectively.

Acetone↗
PubMed1996

Modulation of the development of humoral immunity by topically applied acetone, ethanol, and 12-O-tetradecanoylphorbol-13-acetate.

The effects of topically applied 12-O-tetradecanoylphorbol-13-acetate (TPA), acetone, and ethanol on systemic immune function were analyzed in SSIN mice. A total of one, four, or eight dorsal applications of solvent (50-300 microl/treatment, 2x/week) affected neither the overall cellularity of the spleen nor the relative proportions of splenic cells expressing CD4, CD8, or Ig surface markers. In contrast, overall cellularities of the spleen increased and relative T cell content of the spleen decreased in mice treated multiple times with TPA (2 microg/application in 0.2 ml acetone). The development of splenic B cells secreting IgM against sheep red blood cells (SRBC, a T-cell-dependent antigen) was retarded, and the overall duration of IgM synthesis was decreased, in mice immunized 1 hr after the last of four applications (>200 microl) of either solvent. Comparable retardations occurred in mice immunized as late as 7 days after termination of solvent treatment. However, solvent effects on the development of antibody-forming cells were not observed after eight topical applications or when TNP-LPS (a T-cell-independent antigen) was used as the immunogen. The effects of TPA on the development of IgM-secreting B cells were indistinguishable from those of the solvent used for its application. Although serum hemagglutination titers to SRBC correlated with the relative numbers of splenic B cells producing IgM, in vitro proliferative responses to B and T cell mitogens were not predictive of the effects of solvents or TPA on the development of antibody-secreting cells. Collectively, these studies demonstrate that topically applied acetone and ethanol can systemically modulate humoral immunity and emphasize the need for inclusion of nontreated controls when assessing the potential immunomodulatory activities of agents dissolved in acetone or ethanol.

Acetone↗
PubMed1996

Behaviour of urinary 2,5-hexanedione in occupational co-exposure to n-hexane and acetone.

We analysed the relationship between free 2,5-hexanedione (2,5-HD) and total 2,5-HD in the urine of 87 workers exposed to n-hexane and other solvents (hexane isomers, acetone and toluene), in relation to different working conditions. The concentration of free 2,5-HD in urine of workers exposed to n-hexane was about 12% of total urinary 2,5-HD. The most significant correlation (r = 0.936) was that of total 2,5-HD in urine with environmental n-hexane and exhaled air. With equal exposure to n-hexane, the concentrations in urine of free and total 2,5-HD increased when cutaneous absorption was involved (gloves not used), during the working week and with co-exposure to acetone. An analysis of the relationship between combined exposure to acetone and urinary concentrations of the various forms of 2,5-HD suggests that acetone might influence the toxicokinetics of n-hexane, increasing the proportion of free 2,5-HD.

Acetone↗