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 361 records · Page 20Linked to original sources
PubMed1993

Biological monitoring of workers exposed to styrene and acetone.

Twenty-two workers exposed to styrene and acetone in two fiberglass industries were monitored on Monday and Thursday for 8 hours using passive dosimeters. Urine samples were collected at the end of the workshift and before the start of the work on the next morning (Tuesday and Friday). The charcoal disks of the passive dosimeters were analysed by gas-chromatography. Mandelic acid (MA) and phenylglyoxylic acid (PGA) were measured using a HPLC method; values were expressed in mg/g of creatinine. The 8-h TWA exposure values for styrene and acetone ranged respectively from 22 to 522 mg/m3 and 40-1581 mg/m3 on Monday; 25-423 mg/m3 and 55-579 mg/m3 on Thursday. Styrene TWA exposure values significantly correlate with the sum of metabolites at the end of workday (r = 0.70 on Monday and r = 0.95 on Thursday) and also at the next morning (r = 0.86 on Tuesday and r = 0.85 on Friday). A styrene exposure level of 213 mg/m3 (ACGIH-TLV) was associated with an excretion of metabolites (MA+PGA) higher on Thursday (803 mg/g creat) than on Monday (570 mg/g creat). The same result was found on Friday (459 mg/g creat) compared with Tuesday (305 mg/g creat). Moreover our data show that the simultaneous exposure to acetone does not modify the excretion of MA. In conclusion the TLV of styrene is associated with different values of metabolites at the beginning and at the end of the work-week.

Acetone↗
PubMed1976

Acetone production by methylobacteria.

An accumulation of acetone was observed during the metabolism of ethane and products of ethane oxidation by washed suspensions of Methylosinus trichosporium OB3B. This strain possessed an acetoacetate decarboxylase and 3-hydroxybutyrate dehydrogenase, and a decline in poly-beta-hydroxybutyric acid occurred under the same conditions as acetone formation. A pathway of acetone production from poly-beta-hydroxybutyric acid via 3-hydroxybutyrate and acetoacetate was suggested.

Acetoacetates↗
PubMed1990

Pulmonary toxicity of inhaled styrene in acetone-, phenobarbital- and 3-methylcholanthrene-treated rats.

Pulmonary changes in glutathione (GSH) indicated by the concentration of non-protein sulphydryls showed a decrease of 43% in rats exposed for 5 h per day three times to 500 cm3/m3 (2100 mg/m3) styrene vapour. In these rats, only a marginal decrease was observed in the pulmonary cytochrome P450 oxidative metabolism. Following a single 24-h inhalation exposure to 500 cm3/m3 styrene, the decreases in GSH were 66% in lung but only 16% in liver. On the other hand, a multifold increase in the disposition of thioether compounds was found in urine. Pulmonary cytochrome P450-dependent metabolism was decreased, shown by low residual activities of 7-ethoxyresorufin (less than 20%), 7-ethoxycoumarin (53%) and 7-pentoxyresorufin O-dealkylases (76%). Epoxide hydrolase and GSH S-transferase enzyme activities which catalyze styrene detoxification were not decreased. Styrene exposure (24 h) of acetone-, phenobarbital- or 3-methylcholanthrene-pretreated rats resulted in pulmonary effects different from each other and from those of styrene alone. Acetone potentiated the lung effect and elevated 1.5-fold urine thioether output. Inducer pretreatment seemed to be a factor aggravating styrene toxicity; in effect this was clearest in acetone-induced rats. In general, GSH depletion accompanied by inhibition of cytochrome P450-dependent oxidative drug metabolism were the earliest biochemical lesions manifested in styrene-exposed lung.

Acetone↗
PubMed1983

Changes in alkaline and acid phosphatases of the rabbit cornea following experimental exposure to ethanol and acetone: a biochemical and histochemical study.

Alkaline and acid phosphatases were studied in the rabbit cornea following acetone and ethanol exposure to the eye. Changes in enzyme activities were investigated in homogenates of epithelium and stroma quantitatively and in frozen cryostat sections on days 1, 4, 7, 14, and 28. Biochemical and histochemical findings showed a remarkable increase in alkaline phosphatase of the epithelium beginning on day 7. This activation persisted until day 28 after instillation of both noxae with maximum activity on day 14. However, acetone was proved to be significantly more effective than ethanol. In addition, a different topochemistry of alkaline phosphatase was found in the epithelium of treated corneas, i.e., enzyme activity was observed not only superficially but in all epithelial layers of the cornea as compared to a normal one. The effect of acetone and ethanol on a regenerating corneal epithelium is discussed.

Acetone↗
PubMed2002

Attraction of the tropical bont tick, Amblyomma variegatum, to human breath and to the breath components acetone, NO and CO2.

Ticks are of medical and veterinary importance and employ several cues in search of a host. Olfaction is one modality by which ticks locate a blood-meal and breath is the major vent of gaseous and volatile metabolites from the host that could contribute to this search. We studied the responses of a hunter tick, Amblyomma variegatum, to diluted human breath and five of its components (acetone, CO2, NO, isoprene and NH3) while walking in an air stream on a locomotion compensator. Diluted breath elicited the greatest responses of all treatments in terms of time to onset of upwind walk, attraction, speed and local search behaviour after stimulus off. Acetone, NO and CO2 also attracted, but with a reduced speed in the case of acetone and NO. Neither isoprene nor NH3 induced any response. Our study indicates that breath was the most adequate stimulus tested. It also attracted two other ixodid tick species, Rhipicephalus sanguineus and Ixodes ricinus, as well as the argasid tick, Ornithodorus moubata. It appears that the evolution of resource tracking in ticks included sensory and behavioural adaptations for recognition and orientation to host metabolites that are regularly expelled in breath.

Acetone↗
PubMed2003

Isopropanol and acetone induces vinyl chloride degradation in Rhodococcus rhodochrous.

In situ bioremediation of vinyl chloride (VC)-contaminated waste sites requires a microorganism capable of degrading VC. While propane will induce an oxygenase to accomplish this goal, its use as a primary substrate in bioremediation is complicated by its flammability and low water solubility. This study demonstrates that two degradation products of propane, isoproponal and acetone, can induce the enzymes in Rhodococcus rhodochrous that degrade VC. Additionally, a reasonable number of cells for bioremediation can be grown on conventional solid bacteriological media (nutrient agar, tryptic soy agar, plate count agar) in an average microbiological laboratory and then induced to produce the necessary enzymes by incubation of a resting cell suspension with isopropanol or acetone. Since acetone is more volatile than isopropanol and has other undesirable characteristics, isopropanol is the inducer of choice. It offers a non-toxic, water-soluble, relatively inexpensive alternative to propane for in situ bioremediation of waste sites contaminated with VC.

2-Propanol↗
PubMed1984

Studies on the mechanisms of induction of N-nitrosodimethylamine demethylase by fasting, acetone, and ethanol.

Previous work has shown that induction of a high-affinity NADPH-dependent nitrosodimethylamine demethylase (NDMAd) in liver microsomes occurs in rats due to fasting, ethanol consumption, and streptozotocin-induced diabetes. Several lines of observations suggest that this is due to the induction of specific cytochrome P-450 isozymes. Induction of P-450 species by ethanol has also been observed by other investigators. Since each of the above altered metabolic states has in common elevated levels of ketone bodies, the possible role of acetone, a known inducer of NDMAd, in the induction of the demethylase activity was investigated. Levels of endogenous acetone in fasted rats correlated (r = 0.72) with a three- to fourfold increase in NDMAd activity. However, a dose-response experiment showed endogenous levels of acetone to be capable of causing at most 40% of the induction in fasted rats. This suggests that other ketone bodies or factors may have contributed to the induction. The induction of NDMAd by ethanol was enhanced by alcohol dehydrogenase inhibitors pyrazole and acetaldehyde oxime, suggesting that ethanol, rather than its metabolites, was responsible for the induction.

Acetone↗
PubMed1983

Production of formaldehyde and acetone by hydroxyl-radical generating systems during the metabolism of tertiary butyl alcohol.

t-Butyl alcohol is not a substrate for alcohol dehydrogenase or for the peroxidatic activity of catalase and, therefore, it is used frequently as an example of a non-metabolizable alcohol. t-Butyl alcohol is, however, a scavenger of the hydroxyl radical. The current report demonstrates that t-butyl alcohol can be oxidized to formaldehyde plus acetone by hydroxyl radicals generated from four different systems. The systems studied were: (a) two chemical systems, namely, the iron catalyzed oxidation of ascorbic acid and the Fenton reaction between H2O2 and iron; (b) an enzymatic system, the coupled oxidation of xanthine by xanthine oxidase; and (c) a membrane-bound system, NADPH-dependent microsomal electron transfer. The oxidation of t-butyl alcohol appeared to be mediated by hydroxyl radicals, or by a species with the oxidizing power of the hydroxyl radical, because the production of formaldehyde plus acetone was (a) inhibited by competing scavengers of the hydroxyl radical; (b) stimulated by the addition of iron-EDTA; and (c) inhibited by catalase. The last observation suggests that H2O2 served as the precursor of the hydroxyl radical in all three systems. A possible mechanism is hydrogen abstraction to form the alkoxyl radical [CH3)3-C-O.), spontaneous fission of the alkoxyl radical to produce acetone and the methyl radical (CH3.), interaction of the methyl radical with O2 to form the methyl peroxy radical (CH300.), and decomposition of the later to formaldehyde. These results extend the alcohol oxidizing capacity of the microsomal alcohol oxidizing system to a tertiary alcohol. Since t-butyl alcohol is not a substrate for alcohol dehydrogenase or catalase, the ability of microsomes to oxidize t-butyl alcohol lends further support for a role for hydroxyl radicals in the microsomal alcohol oxidation system. In view of the production of formaldehyde, and the reactivity as well as further metabolism of this aldehyde, caution should be used in interpreting experiments in which t-butyl alcohol is used as a presumed "non-metabolizable" alcohol. t-Butyl alcohol may be a valuable probe for the detection of hydroxyl radicals in intact cells and in vivo.

Acetone↗
PubMed1995

Effect of propylthiouracil treatment on NADPH-cytochrome P450 reductase levels, oxygen consumption and hydroxyl radical formation in liver microsomes from rats fed ethanol or acetone chronically.

The antithyroid drug propylthiouracil (PTU) has been shown previously to reduce hepatic oxygen utilization and to protect the liver from ethanol-induced injury. The present study examined the effect of PTU on hepatic microsomal oxygen consumption and on the activities of NADPH-cytochrome P450 reductase (CYP-reductase) and cytochrome P4502E1 (CYP2E1) in rats receiving ethanol or acetone chronically. Liver microsomes from rats treated with ethanol for 29 days displayed increases in (i) O2 consumption (70%), (ii) hydroxyl radical (.OH) production (49%) and (iii) ethanol oxidation (50%). Microsomal CYP2E1 levels were increased markedly by chronic ethanol administration, while CYP-reductase was affected marginally, but not significantly (P = 0.06). Chronic treatment with acetone for 14 days, produced similar effects, except that .OH production was not enhanced. Administration of PTU (25 mg/kg/day) to ethanol- or acetone-fed rats, for 10 and 14 days, respectively, led to a marked reduction in the levels and activity of CYP-reductase, and to a decrease in the rates of microsomal O2 consumption, .OH production and ethanol oxidation, but did not lower the levels of CYP2E1 or the metabolism of the CYP2E1 substrate N,N-nitrosodimethylamine. These data suggest that the ability of PTU to protect the liver from ethanol-induced injury may be due to a reduction in the levels of CYP-reductase, thereby minimizing the enhancement of microsomal oxygen consumption and free radical generation associated with ethanol-induced CYP2E1 activity.

Acetone↗
PubMed1983

Increased specificity of plasma glucagon radioimmunoassay by use of acetone extraction.

The specificity of glucagon determinations with two pancreatic-type glucagon antisera has been determined by means of gel permeation chromatography before and after treatment of human plasma with acetone and ethanol. Acetone precipitates the interfering high molecular mass substances apparent in the void volume and cross-reacting precursor fragments, while pancreatic glucagon is extracted to slightly more than 50%. Hence, acetone treatment is suggested as a suitable means of obtaining specific glucagon results in single samples. Ethanol also precipitates the high molecular mass substances, but partly extracts the precursor fragments in addition to the glucagon. Ethanol treatment is therefore suggested for chemical diagnosis of the glucagonoma syndrome in which the tumor often produces precursor fragments.

Acetone↗
PubMed1989

Amniotic fluid phospholipids. Study of the cold acetone precipitation effect.

Amniotic fluid phospholipids were extracted and separated with chloroform: methanol (2:1 by vol). These phospholipids were also precipitated with cold acetone and the percentage of each phospholipid precipitated was calculated. The precipitation percentage of the six phospholipids studied ranged from 33.78 +/- 0.70 (mean +/- SEM) for lecithin to 93.77 +/- 1.40 for phosphatidylserine. The variation of L/S, PG/S and PI/S ratios depending on the precipitation step was also studied. We observed that cold acetone precipitation decreased L/S and PG/S ratios, whereas PI/S remained unchanged. Our results indicated that: (1) cold acetone precipitation affected each phospholipid in a different way; (2) the precipitation step was not an effective way of completely separating surfactant and non-surfactant material; (3) a new predictive value should be established if the L/S ratio without precipitation is to be used in the clinic on a daily basis.

Acetone↗
PubMed1994

High-performance liquid chromatographic method for the simultaneous detection of malonaldehyde, acetaldehyde, formaldehyde, acetone and propionaldehyde to monitor the oxidative stress in heart.

Lipid peroxidation (LPO) is the oxidative deterioration of polyunsaturated fatty acids (PUFA) with the production of lipid hydroperoxides, cyclic peroxides, cyclic endoperoxides, and finally fragmentation to ketones and aldehydes (including malonaldehyde, MDA). Estimation of LPO through MDA formation measured by assaying thiobarbituric acid (TBA) reactive products remains the method of choice to study the development of oxidative stress in tissues. However, MDA estimation by TBA reactive products is non-specific and often gives erroneous results. In this report we describe a method using high-performance liquid chromatographic separation to estimate MDA, formaldehyde (FDA), acetaldehyde (ADA), acetone, and propionaldehyde (PDA), the degradation products of oxygen-derived free radicals (ODFR) and PUFA, as presumptive markers for LPO. Oxidative stress was induced in the tissue by perfusing an isolated rat heart with hydroxyl radical generating system (xanthine + xanthine oxidase + FeCl3 + EDTA). The coronary effluents were collected, derivatized with 2,4-dinitrophenylhydrazine (DNPH), and extracted with pentane. Aliquots of 25 microliters in acetonitrile were injected onto a Beckman Ultrasphere C18 (3 microns) column. The products were eluted isocratically with a mobile phase containing acetonitrile-water-acetic acid (40:60:0.1, v/v/v), measured at three different wavelengths (307, 325 and 356 nm) using a Waters M-490 multichannel UV detector and collected for gas chromatography-mass spectrometry (GC-MS) analysis. The peaks were identified by cochromatography with DNPH derivatives of authentic standards, peak addition, UV pattern of absorption at the three wavelengths, and by GC-MS. The retention items of MDA, FDA, ADA, acetone, and PDA were 5.3, 6.6, 10.3, 16.5, and 20.5 min, respectively. The results of our study indicated progressive increase of all five lipid metabolites as a function of the duration of ODFR perfusion. Hydroxyl radical scavengers, superoxide dismutase plus catalase, completely inhibited the formation of these lipid metabolites, demonstrating that the release of lipid metabolites from the isolated heart was indeed in response to oxidative stress. Since MDA, FDA, ADA, acetone, and PDA are the products of ODFR-PUFA interactions, this method allows proper estimation of LPO which monitors the oxidative stress developed during the reperfusion of ischemic myocardium.

Acetaldehyde↗
PubMed1979

Effects of acetone and toluene vapors on multiple schedule performance of rats.

Six rats were trained to press a lever for a liquid food reward on a multiple fixed ratio--fixed interval (FR--FI) schedule of reinforcement. When lever-pressing rates became relatively stable, the animals were exposed to 150 ppm of either acetone or toluene for duration times of 1/2, 1, 2 and 4 hr. Exposures were conducted at least three weeks apart. Acetone produced minimal changes on the FR--FI responding during the 1/2 hr exposure. During the 1 hr exposure period, both FR and FI rates increased while during the 2 hr exposure, both FR and FI responses decreased below control levels. During the 4 hr exposure FI responses approximated control levels for 2 rats and were above the control level for the third animal while FR rates were below controls for 2 of the 3 subjects. Rate changes under toluene were generally qualitatively similar to those produced by acetone. An initial enhancement of FR and FI rates occurred during the shorter exposure periods followed by a decrease in rates during the longer exposure periods.

Acetone↗
PubMed1995

Antimutagenicity of an acetone extract of yogurt.

Reconstituted non-fat dry milk powder, fermented by a mixture of Streptococcus thermophilus CH3 and Lactobacillus bulgaricus 191R to produce yogurt, was freeze-dried and extracted in acetone. After evaporation of the acetone, the extract was dissolved in dimethyl sulfoxide (DMSO) and tested for antimutagenicity. In the Ames test, significant dose-dependent activity was observed against N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), 4-nitro-quinoline-N-oxide (4NQO), 3,2'-dimethyl-4-aminobiphenyl (DMAB), 9,10-dimethyl-1,2-benz[a]anthracene (DMBA), and 3-amino-1-methyl-5H-pyrido[4,3-b]indole acetate (Trp-P-2). Weak activity was observed against 1,2,7,8-diepoxyoctane (DEO), and no activity was observed against methyl methanesulfonate (MMS), ethyl methanesulfonate (EMS), or aflatoxin B1 (AFB1). In a related assay (Saccharomyces cerevisiae D7), significant antimutagenic activity was detected against MNNG and 4NQO. Activity against the experimental colon carcinogens MNNG and DMAB was examined further, as assayed in the Ames test (Salmonella typhimurium TA100). Compounds responsible for both activities were less soluble in aqueous solutions than in DMSO. Adjustment of yogurt pH to 3, 7.6, or 13 prior to freeze-drying and acetone extraction did not significantly alter the amount of anti-MNNG activity recovered. In contrast, extractability of anti-DMAB activity was significantly greater at acidic pH. Conjugated linoleic acid, a known dairy anticarcinogen, failed to inhibit mutagenesis caused by either mutagen, suggesting that other yogurt-derived compound(s) are responsible. Unfermented milk was treated with lactic acid, yogurt bacteria without subsequent growth, or both, to determine if formation of antimutagenic activity required bacterial growth. Extracts of the milk treatments exhibited the same weak antimutagenicity observed in unfermented milk, approximately 2.5-fold less than in the yogurt extracts, suggesting that antimutagenic activity is associated with bacterial growth.

4-Nitroquinoline-1-oxide↗
PubMed1986

Species differences in upper respiratory tract deposition of acetone and ethanol vapors.

Regional deposition patterns determine the dose of inhaled gaseous toxicant received by various areas of the respiratory tract. To study potential species differences in upper respiratory tract (URT) deposition of acetone and ethanol vapors, and to determine if deposition of these vapors could be described by a ventilation-perfusion (V-P) model, URT deposition efficiencies of these vapors were measured over a 12- to 18-min period at selected flow rates in the surgically isolated URT of urethane-anesthetized Fischer rats and Hartley guinea pigs. For both gases in both species, deposition efficiencies were significantly dependent upon inspiratory flow rate (p less than 0.0005). The V-P model predicts a linear relationship will exist between the ratio of the deposited to the nondeposited fraction and the inverse of the inspiratory flow rate. Such relationships were observed for deposition of acetone (r = 0.93, p less than 0.0005) and ethanol vapors (r = 0.95, p less than 0.0005) in the guinea pig and for deposition of acetone vapor (r = 0.95, p less than 0.0005) in the rat. In contrast, a linear relationship was not observed for ethanol in the rat suggesting that deposition mechanism(s) differ for this vapor in this species. Despite the fact that the surface area of the URT of the guinea pig is greater than that of the rat, URT deposition of these vapors was as much as twice as efficient in the rat as in the guinea pig (p less than 0.0005). This effect was not due to different blood:air partition coefficients as they were identical in both species. In toto, these results suggest there may be important anatomic and/or physiologic differences in the URT of the Hartley guinea pig and Fischer rat. Such differences may have to be considered when comparing the response(s) of these species to toxic gases or when extrapolating data obtained from these species to the human.

Acetone↗
PubMed1987

Effects of butyric and acetic acids on acetone-butanol formation by Clostridium acetobutylicum.

The actions of butyric and acetic acids on acetone-butanol fermentation are investigated. Production of butyric and acetic acids are controlled by the extracellular concentrations of both acids: acetic acid added to the medium inhibits its own formation but has no effect on butyric acid formation, and added butyric acid inhibits its own formation but not that of acetic acid. The ratio of end metabolites depends upon acetic and butyric acid quantities excreted during the fermentation. In contrast to acetic acid, which specifically increases acetone formation, butyric acid increases both acetone and butanol formations. Acetate and butyrate kinase activities were also examined. Both increase at the start of fermentation and decrease when solvents appear in the medium. Coenzyme A transferase activity is weak in the acidogenic phase and markedly increases in the solvent phase. Acetic and butyric acids appear to be co-substrates. On the basis of these results, a mechanism of acetic and butyric acid pathways, coupled to solvent formation by C. acetobutylicum glucose fermentation is proposed.

Acetate Kinase↗
PubMed1989

Carcinogenic activity associated with halogenated acetones and acroleins in the mouse skin assay.

Several chlorinated acetones have been identified in drinking water and these, as well as a number of chlorinated acroleins, are produced by chlorination of humic acid solutions. Many of these chlorinated compounds and the brominated acrolein analog were positive in the Ames Assay in the laboratory. To determine if carcinogenic activity was associated with these chemicals the following acetone derivatives: monochloro (MCA); 1,1-dichloro (1,1-DCA), 1,3-dichloro (1,3-DCA), 1,1,1-trichloro (1,1,1-TCA), 1,1,3-trichloro (1,1,3-TCA), and substituted acroleins: 2-chloro (CAC), 3,3-dichloro (DCAC), 2,3,3-trichloro (TCAC) and 2-bromo (BAC), were applied topically to SENCAR mice (25, 30, or 40/group) at the following dose levels: 50 mg/kg (MCA and 1,1,3-TCA); 50, 75 and 100 mg/kg (1,3-DCA); 100, 200 and 400 mg/kg (CAC, DCAC, and TCAC); 200 and 300 mg/kg (BAC); and 400, 600, and 800 mg/kg (1,1-DCA, and 1,1,1-TCA). Doses were applied six times over a 2-week period in 0.2 ml ethanol per application. 1,3-DCA was also tested with single doses of 37.5, 75, 150 and 300 mg/kg in 0.2 ml ethanol. Control animals received 0.2 ml ethanol per application as a single dose or multiple doses to match corresponding studies. Two weeks after the final dose, 1.0 microgram TPA in 0.2 ml acetone was applied three times weekly for 20 weeks. After 24 weeks the percentage of animals with tumors for dose groups above were: MCA (8); 1,1,3-TCA (10); 1,3-DCA, multiple doses (48, 45, 32); CAC (30, 28, 38); DCAC (3, 0, 0); TCAC (10, 5, 0); BAC (54, 43); 1,1-DCA (0, 5, 0); 1,1,1-TCA (10, 5, 0); 1,3-DCA, single doses (47, 47, 63, 20); controls (12--Table 3, 9--Table 4 average). These data show that 1,3-DCA, CAC and BAC, when applied topically, initiate tumors in the mouse skin. These chemicals administered orally in a 2% emulphor solution, at doses described in Table 3, did not initiate tumors in the mouse skin.

Acetone↗
PubMed1985

Stimulation of the mouse hepatic microsomal aniline p-hydroxylases by acetone and polyamines.

The effects of acetone +/- spermine on the high (AH-I) and low (AH-II) affinity forms of aniline hydroxylases in the mouse hepatic microsomes were investigated under in vitro conditions. The addition of either acetone or spermine alone stimulated both AH-I and AH-II activities at low concentration while some decline in stimulation was noted at higher concentrations. In the presence of both the modifiers the observed monoxygenation rates were greater than those produced by any one enhancer alone for AH-I and more than additive for AH-II. The results suggest that the enhancement of aniline p-hydroxylation by the acetone and spermine in the mouse hepatic microsomes involves at least two separate and possibly interdependent mechanisms.

Acetone↗