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PubMed1996

Evaluation of bulk milk analyses of acetone, urea, and the fat-lactose-quotient as diagnostic aids in preventive veterinary medicine.

The purpose of this study was to evaluate the use of additional acetone and urea analyses to the established milk quality system (protein, fat, lactose, and somatic cell count) in bulk milk samples twice a month. Samples were obtained from 44/93 herds in a lowland/highland area. When ranging herds with most acetone values over 0.24mmol/1 (90th percentile), only two out of 10 herds would be on a corresponding list when ranged for highest ketosis treatment incidence. Most high acetone values occur after periods with concentrated calvings, but also in periods without calvings, presumably because of feeding with inferior silage high in butyric acid. Milk fat concentration, milk lactose concentration and the interaction term between these, the fat-lactose-quotient, show the largest absolute values in all three models with ketosis treatment incidence, milk protein concentration, and milk yield as dependent variables in general linear analyses on standardized variables. Acetone and urea concentrations in bulk milk show only small absolute values or are omitted from the models. The practical conclusion from these analyses on bulk milk samples to be used by advisory personnel is small, but it seems that high bulk milk fat concentrations and low lactose concentrations are unfavourable when it comes to ketosis treatment incidence, but favourable when it comes to milk protein concentration. Bulk milk acetone concentrations as a measure of the energy supply in herds must only be interpreted after calving intensity and silage quality are assessed.

Acetone↗
PubMed1991

Infertility in rats induced by 2,5-hexanedione in combination with acetone.

The morphological changes as well as the functional consequences for the reproduction of the testis-injuring effect of 2,5-hexanedione (2,5-HD) were evaluated in rats. The potentiation by acetone and the reversibility of the effects was also studied. Male rats were dosed for 6 weeks with 0, 0.13%, 0.25% or 0.50% 2,5-HD alone or in combination with 0.50% acetone in the drinking water. During the last week of treatment the fertility of half of the treated males was studied by introducing each of them to a non-treated female rat, after which the number of matings, pregnancies and foetuses was examined. In order to evaluate the degree of reversibility of the effect on testis the same examination was made in the other half of the males after a 10 weeks dose-free period. The weight and morphology of testis from all the males was studied. The weight of testis, testis tubuli diameter and fertility was reduced by 2,5-HD and further reduced in groups dosed with 2,5-HD, 0.25% and 0.50% plus acetone 0.50%. Combined administration of acetone and 2,5-HD caused a potentiation comparable to the effect of the double dose of 2,5-HD. Minor changes were reversible within the 10 weeks dose-free period, whereas infertility and other severe changes in the highest combined group were non-reversible within this period. The number of matings was unaffected. It is concluded that 2,5-HD has a testis-injuring effect, which in high doses and combined with acetone causes non-reversible infertility and that testis is more sensitive than the nerve tissue to 2,5-HD.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetone↗
PubMed1997

The genes for butanol and acetone formation in Clostridium acetobutylicum ATCC 824 reside on a large plasmid whose loss leads to degeneration of the strain.

Degeneration is the process whereby Clostridium acetobutylicum ATCC 824 loses the capacity to produce acetone and butanol after repeated vegetative transfers or in continuous culture. Two degenerate mutants (M5 and DG1) of C. acetobutylicum ATCC 824 do not contain the four genes (ctfA, ctfB, adc, and aad) for acetone and butanol formation. Strain ATCC 824 contains a 210-kb plasmid (pSOL1) which is absent in M5 and DG1. pSOL1 carries the four acetone and butanol formation genes. A restriction map of pSOL1 was constructed by using ApaI, SmaI, SstII, and NarI digestions. M5 and DG1 could be complemented for acetone and butanol formation by expressing the corresponding genes (ctfA, ctfB, and adc for acetone; aad for butanol) on the plasmid. Degeneration of this strain thus appears to be the result of pSOL1 loss.

Acetone↗
PubMed2003

Design of antisense RNA constructs for downregulation of the acetone formation pathway of Clostridium acetobutylicum.

We investigated the effect of antisense RNA (asRNA) structural properties on the downregulation efficacy of enzymes in the acetone-formation pathway (acetoacetate decarboxylase [AADC] and coenzyme A-transferase [CoAT]) of Clostridium acetobutylicum strain ATCC 824. First, we generated three strains, C. acetobutylicum ATCC 824 (pADC38AS), 824(pADC68AS), and 824(pADC100AS), which contain plasmids that produce asRNAs of various lengths against the AADC (adc) transcript. Western analysis showed that all three strains exhibit low levels of AADC compared to the plasmid control [ATCC 824(pSOS95del)]. By using computational algorithms, the three different asRNAs directed toward AADC, along with previously reported clostridial asRNAs, were examined for structural features (free nucleotides and components). When the normalized metrics of these structural features were plotted against percent downregulation, only the component/nucleotide ratio correlated well with in vivo asRNA effectiveness. Despite the significant downregulation of AADC in these strains, there were no concomitant effects on acetone formation. These findings suggest that AADC does not limit acetone formation and, thus, we targeted next the CoAT. Using the component/nucleotide ratio as a selection parameter, we developed three strains [ATCC 824 (pCTFA2AS), 824(pCTFB1AS), and 824(pCOAT11AS)] which express asRNAs to downregulate either or both of the CoAT subunits. Compared to the plasmid control strain, these strains produced substantially low levels of acetone and butanol and Western blot analyses showed significantly low levels of both CoAT subunits. These results show that CoAT is the rate-limiting enzyme in acetone formation and strengthen the hypothesis that the component/nucleotide ratio is a predictive indicator of asRNA effectiveness.

Acetone↗
PubMed1972

Mechanism of antiviral action of acetone on rabbitpox virus replication.

Acetone added to the maintenance medium in a 1% concentration reduces the yield of infectious rabbitpox virus in L-cell monolayer cultures by 90 to 97%. This concentration of the inhibitor is not toxic for cells. It was established that there is an inhibitor-sensitive stage late in the infectious cycle. Acetone exerted no significant influence on production of early viral messenger ribonucleic acid, formation of polyribosomes, deoxyribonucleic acid (DNA) replication, or protein synthesis. In the presence of acetone, the assembly of so-called "acetone particles" occurred. These particles are similar to normal virions by morphological and sedimentation properties but are slightly different from them in buoyant density. The amount of virus-specific DNA and the optical density of the "acetone particles" are the same as those of normal virions despite a 10- to 25-fold difference in the infectivity of the preparations.

Acetone↗
PubMed1989

Neurobehavioural effects of short duration exposures to acetone and methyl ethyl ketone.

A total of 137 volunteers were recruited and tested for neurobehavioural performance before, during, and after a short duration (4 h) exposure to acetone at 250 ppm, methyl ethyl ketone (MEK) at 200 ppm, acetone at 125 ppm with MEK at 100 ppm, or a placebo. Ethanol (95%-0.84 ml/kg) was used as a positive control. Performance testing was computer controlled and took place in an environmental chamber with four test stations. The total test regimen before, during, and after exposure covered 10 hours and 32 measures were collected. The measurements were extracted from two biochemical (venous blood and alveolar breath) tests, four psychomotor (choice reaction time, visual vigilance, dual task (auditory tone discrimination and tracking), memory scanning) tests, one sensorimotor (postural sway) test, and one psychological (profile of mood states (POMS] test. The exposure to 250 ppm acetone produced small but statistically significant changes in performance from controls in two measures of the auditory tone discrimination task and on the anger hostility scale (men only) of the POMS test. Neither MEK nor the combined acetone/MEK exposures produced statistically significant interpretable results. The combination exposure provides some indication that there was no potentiation of the acetone effects with the coexposure to MEK or vice versa. More pronounced performance decrements occurred with ethanol at 0.07-0.08% BAC. Significant (less than 0.05) differences were evident on both the auditory tone and tracking tests in the dual task and there was partial significance on the visual vigilance test (0.05-0.06) and some postural sway measures (less than 0.09). These findings agree with an earlier Japanese study in showing some mild decrements on behavioural performance tests with exposures to acetone at 250 ppm.

Acetone↗
PubMed1992

Biological monitoring of workers exposed to acetone in acetate fibre plants.

Concentrations of acetone in urine, alveolar air, and blood were measured by gas chromatography with flame ionisation detection for 110 subjects occupationally exposed to acetone (mean 372 ppm) in three factories. Significant relations were found between the time weighted average environmental concentration and the concentration in the biological samples. The strongest correlation was between the concentration of acetone in urine and the degree of exposure (r = 0.71, 95% CI 0.64-0.77). This suggests that urinary acetone concentration is the best biological index of occupational exposure to acetone.

Acetone↗
PubMed1995

Physiologically based pharmacokinetic model for acetone.

OBJECTIVE: This study aimed to develop a physiologically based pharmacokinetic model for acetone and to predict the kinetic behaviour of acetone in the human body with that model. METHODS: The model consists of eight tissue groups in which acetone can be distributed: the mucous layer of the inhaled air tract, the mucous layer of the exhaled air tract, a compartment for gas exchange (alveolus of the lung), a group of blood vessel rich tissues including the brain and heart, a group of tissues including muscles and skin that have low perfusion rates, a group of fatty tissues, an organ for metabolism (liver), and a compartment for urinary excretion (kidney). A mucous layer in the model is only the outermost layer of the mucus lining the wall of the air tract during inhalation and exhalation. To check the relevance of the model, the simulated results were compared with the experimental data. Next, simulation was conducted by changing the volume of the mucous layer and the respiratory rate to clarify the effect of these variables. Finally, simulation of an occupational situation was performed. RESULTS: With an appropriate value for the volume of mucous layer, the simulated acetone concentrations in arterial blood, end exhaled air, urine, and fatty tissue were found to agree well with the experimental data. The volume of mucous layer and rate of respiration were critical for the appropriate simulation. The simulated occupational situation fitted the observed regression line in field studies quite well. The simulation also enabled predictions to be made about the characteristic kinetics for water soluble solvents. CONCLUSION: The model is useful for understanding and explaining the kinetics of acetone.

Absorption↗
PubMed1991

Influence of acetone on the severity of the liver injury induced by haloalkane mixtures.

Acetone potentiation of haloalkane-induced liver injury is a well-known phenomenon. Acetone-treated rats challenged with a trichloroethylene-CCl4 mixture exhibit a more sever liver injury than that predicted by the addition of the single potentiating effects of each. The purpose of the present study was to determine if acetone exerted similar interactions with other haloalkane mixtures. The testing protocol used was designed and performed to allow categorization of interactions occurring among two or three agents. Rats were treated (p.o.) with corn oil or acetone (10.2 mmol/kg) and were administered (i.p.) 18 h later 1,1-dichloroethylene (0.6 mmol/kg), trichloroethylene (5.6 mmol/kg), tetrachloroethylene (19.6 mmol/kg), 1,1,1-trichloroethane (10.0 mmol/kg), 1,1,2-trichloroethane (1.1 mmol/kg), 1,1,2,2-tetrachloroethane (1.0 mmol/kg), CHCl3 (6.2 mmol/kg), CCl4 (1.0 mmol/kg), or a mixture of two haloalkanes (all 28 combinations were tested). Liver injury was assessed 24 h later using plasma alanine aminotransferase activity and a quantitative histological evaluation. In corn oil pretreated rats, the hepatotoxic responses observed for the 28 mixtures were additive for 26 of 28 mixtures and supra-additive for 2 of 28, whereas in acetone-pretreated rats the responses observed were additive for 17 of 28, infra-additive for 10 of 28, and supra-additive for 1 of 28. Mixtures containing 1,1,1-trichloroethane or tetrachloroethylene resulted only in no change in toxicity or infra-additivity. Increased toxic responses (additivity and supra-additivity) were observed with certain binary mixtures containing CCl4, CHCl3, 1,1,2-trichloroethane, or 1,1-dichloroethylene.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetone↗
PubMed1995

Cytochemical localization of the acetone-inducible cytochrome P-450 isoform, CYP2E1, in murine colonic epithelium.

Immunolocalization of a toxicologically important cytochrome P-450 isoform, the alcohol-inducible CYP2E1, was examined in mouse colon. Male CD-1 mice (30-40 g) were exposed to acetone (1% v/v), a potent inducer of hepatic CYP2E1, in drinking water for 14 days. Tissue sections were fixed in 1% paraformaldehyde and incubated with anti-rat CYP2E1 polyclonal antibody. Immunohistochemical staining on tissue sections was performed using the indirect peroxidase-antiperoxidase method. In acetone-exposed mice, immunoreactivity was localized exclusively within the cytoplasm of surface epithelial cells of the proximal colon. Infrequently, only very faint staining was evident in colons of untreated control mice. Using the same monospecific antibody, the presence of CYP2E1 was confirmed by Western blot analysis. A 2-to 3-fold elevation in immunoreactivity corresponding to cytochrome P-4502E1 was found in colon microsomes isolated from acetone-exposed form acetone-exposed mice. Further evidence for colonic CYP2E1 is provided by elevation (up to 2.5-fold) in levels of chlorzoxazone 6-hydroxylase, a CYP2E1 substrate, after acetone treatment. The significance of these finding is discussed in terms of the potential for proximal colonic epithelial cells to participate directly in bioactivation of dietary promutagenic substances.

Acetone↗
PubMed1996

Acetone in urine as biological index of occupational exposure to isopropyl alcohol.

In order to investigate a role of acetone in urine (AcU, mg/l) as an indicator of occupational exposure to isopropyl alcohol (IPA, ppm), AcU was measured in 80 male workers exposed to this substance in a plastic factory. The exposure concentration of solvent was also monitored personal diffusive sampling in the individuals during morning 4-hr shift. Urine samples were collected near the end of the shift and were analyzed for acetone by head-space gas chromatography. The correlation between airbornre concentration of IPA and its urinary metabolite acetone was significant: AcU (mg/l) = 0.031 x IPA (ppm) + 0.608, r = 0.75, n = 80, P < 0.001. We established 44 ppm as the lowest airborne concentration of IPA that caused excessive urinary excretion of acetone which could be discriminated from the endogenous production of acetone in non-exposed people. This concentration was as low as one ninth to one tenth of the current exposure limit of 400 ppm. At higher concentrations than 44 ppm, AcU was found to be a useful index for monitoring occupational exposure to IPA.

1-Propanol↗
PubMed1982

Isopropyl alcohol poisoning treated with hemodialysis: kinetics of isopropyl alcohol and acetone removal.

A comatose and hypotensive patient was successfully treated with hemodialysis after ingesting 480 mL of isopropyl alcohol. Removal of isopropyl alcohol and its major metabolite acetone was measured in urine, blood, and dialysate. According to dialysate measurements, approximately 19 g of isopropyl alcohol and 7 g of acetone were removed per hour using a standard 1 m2 dialyzer. The average dialysance of isopropyl alcohol and acetone were 137 and 165 mL/min, respectively. Removal of isopropyl alcohol was 52 times and acetone 40 times more efficient through hemodialysis than through urinary excretion. Since coma and hypotension portend a bad prognosis and since urinary excretion is slow relative to hemodialysis removal, hemodialysis may be considered life-saving in patients comatose from isopropyl alcohol poisoning. There have been two previous reports of hemodialysis used for treatment of isopropyl alcohol intoxication [1, 2]. Neither of these reports describes the kinetics of isopropyl alcohol removal. This paper reports a third patient treated with hemodialysis who afforded us the opportunity to study blood, urine, and dialysate levels of isopropyl alcohol and its chief metabolite, acetone. By utilizing these results a comparison was made of urine excretion to dialysis removal of these compounds to compare their respective efficacy. In addition, the estimated removal by dialysance calculations was compared to estimated removal by measurement of dialysate volumes and concentrations.

1-Propanol↗
PubMed1991

Isopropanol ingestion: a report of six episodes with isopropanol and acetone serum concentration time data.

The disposition of isopropanol and its major metabolite acetone were observed in six isopropanol ingestion episodes among five patients. Serum admission isopropanol and peak acetone concentrations ranged from 16.5 to 220 mg/dL and 141 to 585 mg/dL respectively. Ingestions ranged from 120 to 300 mL of 70% isopropanol with concomitant ethanol ingestion in two episodes. The isopropanol and acetone apparent half-lives ranged from 2.9 to 16.2 hours (h) and 7.6 to 26.2 h respectively. Two episodes of isopropanol ingestion were observed within a 9 month period in patient one. Isopropanol terminal elimination rate constants were 0.043 and 0.085 per hour (per h) with no marked difference in acetone terminal elimination rate constants (0.025 and 0.033 per h). Discrepancy between the two isopropanol elimination rate constants reflected concomitant ethanol abuse with the first ingestion. Reductions in isopropanol and acetone half-lives were also noted among patients requiring ventilatory support.

1-Propanol↗
PubMed2000

Mixed ruminal microbes of cattle produce isopropanol in the presence of acetone but not 3-D-hydroxybutyrate.

The objective was to evaluate the ability of mixed rumen microbes to synthesize isopropanol from acetone or 3-D-hydroxybutyrate. Rumen fluid from seven mature, nonpregnant, dry Holstein cows was incubated with starch or cellulose and additions of acetone, 3-D-hydroxybutyrate, or saline. Rumen fluid was analyzed for isopropanol after 0, 3, 6, and 9 h. No isopropanol was present in any sample at 0 h, and none was present in incubations containing saline or 3-D-hydroxybutyrate at any subsequent time. Incubations that included acetone produced small amounts of isopropanol from 0 to 3 and 3 to 6 h and significantly larger amounts from 6 to 9 h. With starch as the energy substrate, production from 6 to 9 h was 3.8 micromol/min per liter of rumen fluid and 3.7 micromol/min per liter with cellulose as the energy substrate; however, these values did not differ significantly. Mixed rumen microbes could synthesize isopropanol from acetone but not from 3-D-hydroxybutyrate, and rumen microbial metabolism of acetone was the likely source of plasma isopropanol seen in ketotic ruminants.

2-Propanol↗
PubMed1986

Urinary elimination of acetone in experimental and occupational exposure.

Fifteen volunteers were exposed to an acetone vapor concentration of 964-8, 610 mumol/m3 (56-500 mg/m3) for 2-4 h in an exposure chamber. Ten subjects were at rest during the exposure, and five were exposed at alternate rest and light physical exercise. Subsequently 104 workers occupationally exposed to acetone were studied. The relative uptake averaged about 53%, and the ratio of the alveolar concentration to the environmental concentration averaged about 0.28. Both for the experimentally exposed subjects and the occupationally exposed workers the urinary acetone concentration showed a linear relationship to the corresponding environmental time-weighted average concentration. A linear equation also existed between urinary concentrations and the amounts of acetone absorbed. The findings enable a consideration of the urinary concentration of the unaltered acetone as an appropriate exposure indicator and the proposal of a "biological equivalent threshold" to be used in the field of biological monitoring.

Acetone↗
PubMed1999

Saliva as an alternate for blood to measure concentrations of acetone under exposure to isopropanol.

OBJECTIVES: In occupational medicine, blood concentrations are often measured to judge the internal burden of workers at work-place during exposure to a potentially hazardous substance. However, blood-withdrawals are invasive and can often not be taken at work-place due to hygienic reasons. Sampling of saliva is non-invasive and easy to perform even at workplace. In order to substitute blood analysis, analysis of saliva has to be as specific and sensitive as blood investigations. Therefore acetone-concentrations in blood and in saliva during exposure to isopropanol were compared. METHODS: 18 healthy non-smokers were exposed to 360 ppm isopropanol in an exposure chamber over 4 h. Once an hour during exposure and 30 min after, blood and saliva were sampled. Saliva was collected by a cotton plug over 10 minutes and stored in an airtight closed headspace tube. Concentrations of the metabolite acetone were measured by gas chromatography. - RESULTS: The concentrations of acetone in blood and saliva rose continually during exposure and dropped after exposure-cessation. High correlations between concentrations of acetone in blood and saliva were found for each individual and the entire group (entire group: r = 0.8568, p <0.0001, y = 0.8374x - 0.4404). CONCLUSIONS: Acetone-measurement in saliva is a non-invasive, easily conductable and reliable method for estimating the internal burden of isopropanol-exposure. Further studies for the standardization and validation are necessary to impose a threshold limit value on work-place isopropanol-exposure.

2-Propanol↗
PubMed2000

[Determination of residual acetone in soybean phospholipids by headspace gas chromatography].

Soybean phospholipids have many functions and alimentary actions. In our country, powder soybean phospholipids are generally got by extraction with acetone, followed by vacuum drying. There may be some residual acetone present in the soybean phospholipids, which is harmful to health. So, we must know residual acetone content in the soybean phospholipids. However we have not found a method to determine the residual acetone in the soybean phospholipids. In this paper, headspace GC was used to determine residual acetone in powder soybean phospholipids. The headspace bottle was glass with a volume of 15 milliliters. Certain amounts of water, ammonium sulfate, and sample were added into the bottle. The mixture was made into a brei as soon as possible. The bottle was put into a water bath at 40 degrees C for an hour. The GC column was a 2 m x 3 mm i.d. stainless steel tube packed with GDX-103 stationary phase. Temperatures of both injector and detector were kept at 120 degrees C. Column temperature was 160 degrees C. Injection volume was 1 mL. External standard method was used for quantitation. The RSD was 1.2%. The recoveries in the range of 25.0 micrograms/g-100 micrograms/g were 98.4%-104%.

Acetone↗
PubMed2004

[Bonding strength and interface effects of different dentin surface on acetone-based adhesives bonding].

PURPOSE: To study the influences on microstructure characteristic and bonding strength of acetone-based wet bonding systems when bonding on dry or wet dentin surface. METHODS: Three acetone-based wet bonding systems, Gluma One-Bond, Bond-1 and One-Step, were used to bond Chrisma composite resin to dry or moist dentin surface, and the bonding interface was observed with HITACHI S-2700 scanning electron microscope. Microtensile strengths of different groups were measured with Instro 1195. RESULTS: All three bonding systems can infiltrate well into dentin bonding interface in the wet groups. A hybrid layer of about 5microm could be observed with resin tags traversing from the resin layer above into the undemineralized dentin below and the lateral branch of dentinal tubule. In the dry groups, three zones, a surface and a basal hybrid layer sandwiching a middle hybridoid region, could be observed. The hybrid layer was very thinner. Microtensile strength had significantly decreased while bonding on dry dentin surface with acetone-based wet bonding systems, with the maximum decrease of 39% in Bond-1. CONCLUSION: Incompletely infiltrated adhesive on dentin bonding interface could be observed and microtensile strength had significantly decreased while bonding on dry dentin surface with acetone-based wet bonding systems. Moist dentin surface, which can maintain collagen-rich fibrous network of demineralized dentin, is necessary when bonding with acetone-based wet bonding systems. Microtensile strength approaches to the real dentin bonding strength.

Acetone↗