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At least 19 recordsLinked to original sources

PubMed1992

Curvi-linear relation between acetone in breathing zone air and acetone in urine among workers exposed to acetone vapor.

An occupational health study was conducted on 45 acetone-exposed male workers in combination with 343 non-exposed men to examine the quantitative relationship between the intensity of acetone vapor exposure and the concentration of acetone in urine. The time-weighted average acetone concentrations were measured by means of diffusive samplers with water as absorbent, whereas urine samples were collected at the end of the shift as well as before the shift on the next morning. Acetone concentration in shift-end urine did not increase when the workers were exposed to acetone up to approx. 15 ppm, and this was followed by a gradual increase at a higher atmospheric acetone concentration, in a manner dependent to acetone vapor concentration. The comparison in acetone concentrations between the urine samples collected at the shift-end and those before the shift of the next morning showed that the levels in two sets of samples were the same among those exposed to 15 or less ppm acetone, whereas acetone in the shift-end samples was significantly higher than the counterpart levels in the pre-shift samples among those exposed to acetone at more than 15 ppm.

Acetone↗

PubMed2005

ATP-dependent enolization of acetone by acetone carboxylase from Rhodobacter capsulatus.

Acetone carboxylase catalyzes the carboxylation of acetone to acetoacetate with concomitant hydrolysis of ATP to AMP and two inorganic phosphates. The biochemical, molecular, and genetic properties of acetone carboxylase suggest it represents a fundamentally new class of carboxylase. As the initial step in catalysis, an alpha-proton from an inherently basic (pK(a) = 20) methyl group is abstracted to generate the requisite carbanion for attack on CO(2). In the present study alpha-proton abstraction from acetone has been investigated by using gas chromatography/mass spectrometry to follow proton-deuteron exchange between D(6)-acetone and water. Acetone carboxylase-catalyzed proton-deuteron exchange was dependent upon the presence of ATP, Mg(2+), and a monovalent cation (K(+), Rb(+), NH(4)(+)), and produced mixtures of isotopomers, ranging from singly exchanged H(1)D(5)- to fully exchanged H(6)-acetone. The initial rate of isotopic exchange was higher than k(cat) for acetone carboxylation. The time course of isotopic exchange showed that multiple exchange events occur for each acetone-binding event, and there was a 1:1 stoichiometric relationship between molecules of ATP hydrolyzed and the sum of new acetone isotopomers formed. ADP rather than AMP was formed as the predominant product of ATP hydrolysis during isotopic exchange. The stimulation of H(+)(-)D(+) exchange and ATP hydrolysis by K(+) followed saturation kinetics, with apparent K(m) values of 13.6 and 14.2 mM for the two activities, respectively. The rate of H(+) exchange into D(6)-acetone was greater than the rate of D(+) exchange into H(6)-acetone. There was an observable solvent (H(2)O vs D(2)O) isotope effect (1.7) for acetone carboxylation but no discernible substrate (H(6)- vs D(6)-acetone) isotope effect. It is proposed that alpha-proton abstraction from acetone occurs in concert with transfer of the gamma-phosphoryl group of ATP to the carbonyl oxygen, generating phosphoenol acetone as the activated nucleophile for attack on CO(2).

Acetone↗

PubMed1994

Serum acetone and liver acetone monooxygenase activity in pregnant rats, fetuses, and neonates: reversible pretranslational reduction of cytochrome P450IIE1 (P450IIE1) during pregnancy.

Serum acetone in neonates was found to increase from < 20 microM at 20 days gestation to 377 +/- 107 microM 1 day after birth. This increase in acetone occurs concurrently with the initial expression of liver P450IIE1 in rat (Song et al., 1986, J. Biol. Chem. 261:16689-16697). Treating pregnant rats with drinking water containing 1% acetone did not result in a premature induction of liver acetone monooxygenase, a P450IIE1 catalyzed activity, in fetuses sacrificed at 20 days gestation. The data indicate that increased serum acetone levels are not responsible for the initial induction of P450IIE1 in neonates. However, acetone monooxygenase activity in their mothers was significantly less than acetone-treated females which were not pregnant, indicating a reduced activity of P450IIE1 during pregnancy although its induction by acetone was still observed. Acetone monooxygenase activity in 20 day pregnant rats given untreated drinking water was also less than in nongravid rats. These findings are supported by immunoblot data which show significant and progressive reductions in liver P450IIE1 in both untreated and acetone-treated rats during pregnancy. Northern mRNA blot analysis further revealed that the decreases in P450IIE1 activity and protein content were mainly due to pretranslational suppression with reduced level of its mRNA. However, their levels rapidly returned to the control level after parturition (within 1 day). Repeated administration of several exogenous hormones (estriol, pregnanediol, thyroxine) or peptide hormones (placental lactogen, prolactin, chorionic gonadotropin) failed to suppress P450IIE1 in nonpregnant rats, indicating a possibility of another factor(s) responsible for the P450IIE1 suppression during pregnancy.

Acetone↗

PubMed1997

Acetone odor and irritation thresholds obtained from acetone-exposed factory workers and from control (occupationally unexposed) subjects.

Sensitivity of olfaction (smell) and chemesthesis (irritation) was evaluated for 2-propanone (acetone) and 1-butanol in acetone-exposed workers (AEW; N = 32) during a workday and unexposed subjects (microES; N = 32). Irritation sensitivity was assessed using a method that relies on the ability of individuals to localize irritants on the body. When a volatile compound is inhaled into one nostril and air into the other, the stimulated side can be determined (lateralized) only after the concentration reaches a level that stimulates the trigeminal nerve (irritation); compounds stimulating olfaction alone cannot be lateralized. Intranasal lateralization thresholds offer an objective measure of sensory irritation elicited by volatile compounds. Test results indicated that neither olfactory nor lateralization thresholds for butanol differed between AEW and microES. Olfactory thresholds to acetone in AEW (855 ppm) were elevated relative to those of microES (41 ppm), as were lateralization thresholds (36,669 ppm and 15,758 ppm, respectively). Within AEW, level of occupational exposure was not correlated with thresholds. Other measures revealed that microES used more irritation descriptors than did AEW on trials where the acetone concentration was below the lateralization threshold. This is noteworthy because microES received lower concentrations of acetone to evaluate than did AEW. These results suggest that exposures to acetone induce changes in acetone sensitivity that are specific to acetone. The acetone concentrations eliciting sensory irritation using the lateralization technique were all well above current occupational exposure standards. The current study indicates that acetone is a weak sensory irritant and that sensory adaptation is an important factor affecting its overall irritancy.

1-Butanol↗

PubMed1986

Hydroxylation of acetone by ethanol- and acetone-inducible cytochrome P-450 in liver microsomes and reconstituted membranes.

Acetone oxidation in rat liver microsomes was induced 5- or 8-fold by the treatment of the animals with ethanol or acetone, respectively. The apparent Km of the reaction was 0.9 mM, a value lower than the concentration reported for plasma acetone under starvation conditions. The major acetone metabolite was identified as acetol by GC-MS. Acetone oxidation in microsomes was inhibited by typical P-450 inhibitors as well as by compounds (e.g. imidazole) known to interact with the ethanol-inducible P-450 form. Antibodies against this P-450 isozyme were inhibitory for the reaction in rabbit liver microsomes and this isozyme was the only one that showed acetone hydroxylation activity in reconstituted membranes. Imidazole inhibited the conversion of [14C]acetone into low-Mr compounds (e.g. glucose) in vivo. It is suggested that the ethanol- and acetone-inducible P-450 make use of acetone as an endogenous substrate in the utilization of the compound for, e.g. glucose production under conditions of starvation and diabetic ketoacidosis.

Acetone↗

PubMed1995

Acetone excretion into urine of workers exposed to acetone in acetate fiber plants.

To develop a proper protocol for biological exposure monitoring of acetone, we evaluated whether exposure to acetone on the previous day affects the biological monitoring value at the end of a work day. One hundred and ten male workers exposed to acetone in three acetate fiber manufacturing plants were monitored using a liquid passive sampler on two consecutive working days after 2 days without exposure. Urine samples were collected at the start of the workshift and the end of the shift on both days for each subject. For ten exposed workers urine samples were collected approximately every 2 h during and after the first working day until the following morning. Acetone concentrations in urine (Cu) at the start of the first working day were 1.3 +/- 2.4 (range: ND-14.1) mg/l in nonexposed workers and 2.4 +/- 5.6 (range: ND-40.3) mg/l in exposed workers. The urinary acetone concentration at the beginning of the second working day indicated that urinary levels of acetone do not decline to background level by the following morning when exposure concentration exceeds 300 ppm. However, linear regression analysis demonstrated that the relationship between environmental exposure level and urine level was similar on the 1st day and the 2nd day. Thus, although urine acetone levels did not return completely to baseline after high exposures, under the present exposure levels the exposure on the previous day did not significantly affect urinary acetone at the end of the workshift of the next day.

Acetone↗

PubMed1990

Urinary excretion of unmetabolized acetone as an indicator of occupational exposure to acetone.

Acetone concentrations in urine samples from 28 workers exposed to acetone in a fiber-reinforced plastics factory were determined by directly injecting urine supernate into a gaschromatograph with FID detectors. Acetone concentrations in the urine from ten nonexposed subjects were also determined. The 8-h time-weighted exposure intensity of individual workers was monitored by means of diffusive sampling. Acetone concentration in urine and acetone concentration in the breathing zone showed a linear correlation to each other. The study results indicate that the correlation coefficient is high enough to enable use of the urinary level of acetone as an indicator of occupational exposure to acetone.

Acetone↗

PubMed1998

Effects of variation in exposure to airborne acetone and difference in work load on acetone concentrations in blood, urine, and exhaled air.

Using a physiologically based pharmacokinetic (PBPK) model, the effects of variation of exposure concentration of acetone on three biological indicators--acetone concentrations in blood, urine, and exhaled air--were investigated. The effect of the difference in work load was also examined. It was confirmed that the model could be used to estimate acetone concentrations during fluctuating exposure by comparing simulated acetone concentrations with the corresponding values observed in field surveys. By inputting the exposure situations into the PBPK model, the variabilities of the biological indicators were simulated. The variation of acetone exposure was expressed by seven 1-hour time-weighted averages (CEXPs). The arithmetic means of the CEXPS were 200 and 750 ppm. The geometric standard deviations (GSDs) were 1.5, 2.0, and 3.0, representing low, moderate, and high variations, respectively. Work loads were set at 15 and 50 W. Consequently, there were 12 exposure situations. The acetone concentrations in venous blood (CB) and exhaled alveolar air (CA) at 1 minute after the end of the work shift were selected as biological indicators of exposure because they were predicted to decrease rapidly at the end of exposure and become relatively stable after 1 minute. The acetone concentration in urine excreted during the last 2 hours of the work shift (CU) was also used as a biological indicator. Simulation was repeated 100 times with randomly permuting CEXPs for each situation. The mean values of CB, CU, and CA showed almost no variation regardless of the difference in the GSD of CEXPs. The coefficients of variation increased with the GSD of CEXPs but were less than 0.2. Consequently, these variables were acceptable as biological indicators of daily average exposure for the same work load. However, the difference in work load greatly changed the mean values of CB, CU, and CA, thus making it difficult to use these variables as indicators of daily average exposure for different work loads.

Acetone↗

PubMedDate not supplied

Comparative analysis of pulpal circulatory reaction to an acetone-containing and an acetone-free bonding agent as measured by vitalmicroscopy.

Despite great progress in the production of new dental polymers, application of these products is still controversial. The unlined utilization of cytotoxic adhesive materials on pulpal dentin can adversely influence the pulp, leading to alterations in local microcirculation that can be an early sign of pathological changes. In a previous study by the authors, the effect of an acetone-free bondmaterial was examined on the vascular diameter of pulpal vessels by means of vitalmicroscopy. In this study, experiments comparing experimental data provided by an acetone-containing bondmaterial to these earlier findings with acetone-free ones have been performed. Thirty male Sprague-Dawley rats (weighing 333+/-9 g) were used for this investigation. The first lower incisor was prepared for vitalmicroscopy. Changes in vessel diameter were recorded prior to and 5, 15, 30 and 60 minutes after the investigated materials (Scotchbond Multi-Purpose Dental Adhesive System or Prime & Bond 2.1) were administered on dentin as recommended by the manufacturer. In control rats (saline administration), the vessel diameter was stable during the experiment. In the presence of acetone-free bondmaterial (Scotchbond), the vessel diameter was increased during the experimental period in relation to the baseline (12.15+/-2.85%; 16.36+/-2.39%; 14.16+/-3.48%; 12.12+/-3.72%). In the presence of acetone-containing bondmaterial (Prime & Bond 2.1), a similar result was observed (10.56+/-2.27%; 16.13+/-2.94%; 17.88+/-2.54%; 14.54+/-3.16%). The differences between the control values and those registered with test groups were significant (p<0.05; ANOVA). There was no significant difference among the test groups. The results of this study suggest that dental bond materials applied on a very thin layer of dentin may affect the blood supply to the dental pulp. However, no stasis or prestasis has been detected, indicating a possible reversible effect. The authors could not show any statistical difference between the vasodilatation caused by the acetone-containing and the acetone-free bond material.

Acetone↗

PubMed1987

Production of acetone and conversion of acetone to acetate in the perfused rat liver.

The utilization of millimolar concentrations of [2-14C]acetone and the production of acetone from acetoacetate were studied in perfused livers from 48-h starved rats. We devised a procedure for determining, in a perfused liver system, the first-order rate constant for the decarboxylation of acetoacetate (0.29 +/- 0.09 h-1, S.E., n = 8). After perfusion of livers with [2-14C]acetone, labeled acetate was isolated from the perfusion medium and characterized as [1-14C]acetate. No radioactivity was found in lactate or 3-hydroxybutyrate. After 90 min of perfusion with [2-14C]acetone, the specific activity of acetate was 30 +/- 4% (n = 13) of the initial specific activity of acetone. We conclude that, in perfused livers from 2-day starved rats, acetone metabolism occurs for the most part via free acetate.

Acetates↗

PubMed1988

Pyrazole is different from acetone and ethanol as an inducer of the polysubstrate monooxygenase system in mice: evidence that pyrazole-inducible P450Coh is distinct from acetone-inducible P450ac.

The induction of liver microsomal monooxygenase activities elicited by pyrazole, ethanol, and acetone, all shown to be inducers of rat P450j and rabbit P450LM3a, has been compared in inbred strains of DBA/2N, AKR/J, and Balb/c mouse. Pyrazole strongly increases coumarin 7-hydroxylase (COH) activity in DBA/2N but much less in other strains. The effect of pyrazole on aniline p-hydroxylase and ethanol oxidase activities is also strain dependent: an increase was seen only in the DBA/2N strain. Ethanol and acetone were unable to induce COH, whereas aniline p-hydroxylase and ethanol oxidase were elevated about 1.4- to 3.3-fold in all strains. No strain difference could be detected in aniline p-hydroxylase or ethanol oxidase inducibility. There was a strong correlation between aniline p-hydroxylase and ethanol oxidase activities in every strain, whereas no positive correlation could be found between COH and aniline p-hydroxylase activities. Immunoinhibition experiments showed that a polyclonal antibody against purified pyrazole-inducible COH (P450Coh) blocked about 90% of COH activity, but only about 10% of aniline p-hydroxylase or ethanol oxidase in mouse liver microsomes. Monoclonal antibody 1-91-3 (raised against rat acetone-inducible P450ac) did not inhibit COH, whereas aniline p-hydroxylase was blocked 46-76% and ethanol oxidase 25-70%, depending on the source of microsomes. In immunoblots, anti-P450Coh recognized only its own antigen but not the P450ac, whereas monoclonal antibody 1-98-1 against P450ac detected P450ac and a corresponding form in the D2 mouse liver, but not the P450Coh. The purified P450ac and P450Coh had molecular masses of 52 and 50 kDa, respectively, on sodium dodecyl sulfate-polyacrylamide gel electrophoresis. These antigens were expressed differentially in response to pyrazole, ethanol, and acetone: P450Coh was increased only after pyrazole treatment, but 1-98-1-detectable protein was elevated in D2 mouse liver microsomes by ethanol and acetone, but not by pyrazole. We conclude that mouse P450Coh and rat P450ac are not corresponding forms of the same isozyme, and that a P450ac-like protein, responsible for most of aniline p-hydroxylation and ethanol oxidation, is present in the D2 mouse liver. These two P450 isozymes are also dissimilarly expressed in the mouse liver in response to inducer administration.

Acetone↗

PubMed2002

Solvation of copper ions by acetone. structures and sequential binding energies of Cu+(acetone)x, x = 1-4 from collision-induced dissociation and theoretical studies.

Collision-induced dissociation of Cu+(acetone)(x), x = 1-4, with Xe is studied as a function of kinetic energy using guided ion beam mass spectrometry. In all cases, the primary and lowest energy dissociation channel observed is endothermic loss of one acetone molecule. The primary cross section thresholds are interpreted to yield 0 and 298 K bond energies after accounting for the effects of multiple ion-neutral collisions, internal energy of the complexes, and dissociation lifetimes. Density functional calculations at the B3LYP/6-31G* level of theory are used to determine the structures of these complexes and provide molecular constants necessary for the thermodynamic analysis of the experimental data. Theoretical bond dissociation energies are determined from single point calculations at the B3LYP/6-311+G(2d,2p) and MP2(full)/6-311+G(2d,2p) levels, using the B3LYP/6-31G* optimized geometries. The experimental bond energies determined here are in good agreement with previous experimental measurements made in a high-pressure mass spectrometer for the sum of the first and second bond energy (i.e., Cu+(acetone)2 --> Cu+ + 2 acetone) when these results are properly anchored. The agreement between theory and experiment is reasonable in all cases, but varies both with the size of the cluster and the level of theory employed. B3LYP does an excellent job for the x = 1 and 3 clusters, but is systematically low for the x = 2 and 4 clusters such that the overall trends in sequential binding energies are not parallel. In contrast, all MP2 values are somewhat low, but the overall trends parallel the measured values for all clusters. The trends in the measured Cu+(acetone), binding energies are explained in terms of 4s-3d sigma hybridization effects and ligand-ligand repulsion in the clusters.

Journal Article↗

PubMed1999

[Comparison of the effect of acetone-containing and acetone-less bonding materials on dental pulp blood vessels in rats].

No data are available on the direct acute vascular effect of dental bond materials in the dental pulp. The purpose of the present study was to investigate the effect of composite resin bonding systems on the pulpal vascular diameter. Three groups of male Sprague-Dawley rats (weighing 300-490 g), each of 10 animals were used for this investigation. The left lower incisor of the rats was prepared for vitalmicroscopy. Changes in vessel diameter were recorded prior to; and 5, 15, 30, 60 minutes after the application of saline (control) or the bonding agents (test1: acetone containing--/Prime/Bond2.1, DeTrey/; test2: acetone free /Scotchbond Multi-Purpose Adhesive System, 3M/ bond material) on pulpal dentin as recommended by the manufacturer. In control rats, the vessel diameter was stable during the experiment. However, in the presence of bonding materials an enhancement was registered in vascular diameter (p < 0.05). The bond materials applied directly onto a very thin layer of dentin show acute vasodilating effect on the rat pulpal microvessels, but no stasis or prestasis has been detected, indicating a possible reversible effect. We could not show any statistical difference between the vasodilatation caused by the acetone containing and the acetone free bonding material.

Acetone↗

PubMed2002

Biological activity of palladium(II) and platinum(II) complexes of the acetone Schiff bases of S-methyl- and S-benzyldithiocarbazate and the X-ray crystal structure of the [Pd(asme)2] (asme=anionic form of the acetone Schiff base of S-methyldithiocarbazate) complex.

Palladium(II) and platinum(II) complexes of general empirical formula, [M(NS)(2)] (NS=uninegatively charged acetone Schiff bases of S-methyl- and S-benzyldithiocarbazate; M=Pt(II) and Pd(II)) have been prepared and characterized by a variety of physicochemical techniques. Based on conductance, IR and electronic spectral evidence, a square-planar structure is assigned to these complexes. The crystal and molecular structure of the [Pd(asme)(2)] complex (asme=anionic form of the acetone Schiff base of S-methyldithiocarbazate) has been determined by X-ray diffraction. The complex has a distorted cis-square planar structure with the ligands coordinated to the palladium(II) ions as uninegatively charged bidentate NS chelating agents via the azomethine nitrogen and the mercaptide sulfur atoms. The distortion from a regular square-planar geometry is attributed to the restricted bite angles of the ligands. Antimicrobial tests indicate that the Schiff bases exhibit strong activities against the pathogenic bacteria, Bacillus subtilis (mutant defective DNA repair), methicillin-resistant Staphylococcus aureus, B. subtilis (wild type) and Pseudomonas aeruginosa and the fungi, Candida albicans (CA), Candida lypotica (2075), Saccharomyces cerevisiae (20341) and Aspergillus ochraceous (398)-the activities exhibited by these compounds being greater than that of the standard antibacterial and antifungal drugs, streptomycin and nystatin, respectively. The palladium(II) and platinum(II) complexes are inactive against most of these organisms but, the microbe, Pseudomonas aeruginosa shows strong sensitivity to the platinum(II) complexes. Screening of the compounds for their cytotoxicities against T-lymphoblastic leukemia cancer cells has shown that the acetone Schiff base of S-methyldithiocarbazate (Hasme) exhibits a very weak activity, whereas the S-benzyl derivative (Hasbz) is inactive. However, the palladium(II) complexes exhibit strong cytotoxicities against this cancer; their activities being more than that of the standard anticancer drug, tamoxifen. The [Pt(asme)(2)] complex exhibits a very weak cytotoxicity, whereas [Pt(asbz)(2)] is inactive against leukemic cells.

Acetone↗

PubMed1955