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PubMed2002

Breath acetone is a reliable indicator of ketosis in adults consuming ketogenic meals.

BACKGROUND: Ketogenic diets are used therapeutically to treat intractable seizures. Clinically, it appears that the maintenance of ketosis is crucial to the efficacy of the diet in ameliorating seizures. To understand how ketosis and seizure protection are related, a reliable, noninvasive measure of ketosis that can be performed frequently with minimal discomfort is needed. OBJECTIVE: The objective was to determine which index, breath acetone or urinary acetoacetate, is more strongly related to the plasma ketones acetoacetate and beta-hydroxybutyrate. DESIGN: After fasting overnight for 12 h, 12 healthy adults consumed 4 ketogenic meals over 12 h. Blood, breath, and urine samples were collected hourly. Blood was analyzed for plasma acetoacetate and beta-hydroxybutyrate, breath for acetone, and urine for acetoacetate. RESULTS: By the end of the 12-h dietary treatment, plasma acetoacetate, plasma beta-hydroxybutyrate, and breath acetone had increased 3.5-fold, whereas urinary acetoacetate increased 13-fold when measured enzymatically and 25-fold when measured with urinary ketone dipsticks. Plasma acetoacetate was best predicted by breath acetone (R(2) = 0.70, P < 0.0001). Plasma beta-hydroxybutyrate was equally predicted by breath acetone and urinary acetoacetate (R(2) = 0.54, P = 0.0040). CONCLUSIONS: Breath acetone is as good a predictor of ketosis as is urinary acetoacetate. Breath acetone analysis is noninvasive and can be performed frequently with minimal discomfort to patients. As an indicator of ketosis in epilepsy patients consuming a ketogenic diet, breath acetone may be useful for understanding the mechanism of the diet, elucidating the importance of ketosis in seizure protection, and ultimately, enhancing the efficacy of the diet by improving patient monitoring.

3-Hydroxybutyric Acid↗
PubMed1994

Relationship between milk acetone and milk yield in individual cows.

Correlations between acetone in milk and milk production during the first nine weeks postpartum were calculated in ten individual cows and for a whole herd. The decrease in milk production due to ketonaemia was evaluated using a mathematical model of the KaleidaGraph integrate area program. For determination of milk components, a milk sample was obtained twice a week from one to nine weeks postpartum. Milk yield was negatively correlated with acetone concentration in milk. In non-clinical ketotic cows the calculated loss of milk yield due to elevation of milk acetone was 2-9% and in clinical ketotic cow it was as high as 26%. The correlation between milk components and acetone level varied at different stages of ketosis. Thus the stage of lactation and of ketosis should be taken into consideration when the correlation between milk parameters and milk production is evaluated. Prior to clinical ketosis, milk acetone was negatively correlated with milk yield, percentage of protein and percentage of lactose, whereas it was positively correlated with percentage of fat and urea concentration. In addition, high levels of acetone tended to be associated with high cell count. It is concluded that 1) ketotic cows do not achieve the maximum potential milk yield and 2) high levels of milk acetone are harmful to the udder. For high milk production, the concentration of acetone in milk should not exceed 0.05 mmol/l at any stage of lactation.

Acetone↗
PubMed2005

A behavioral and pharmacological validation of the acetone spray test in gerbils with a chronic constriction injury.

UNLABELLED: Cold and mechanical allodynia are important symptoms in patients with neuropathic pain. The study of cold allodynia in animals can help us to understand the underlying pathophysiological mechanisms of neuropathic pain and to validate drugs. The evaluation of cold allodynia in gerbils with a chronic constriction injury of the sciatic nerve on the cold plate is not always stable. We developed a new application method of acetone using a specific spray technique with an Eppendorf multistepper pipette. The chronic constriction injury of the sciatic nerve in gerbils resulted in a long-lasting mechanical and acetone spray-induced hyperreactivity throughout the testing period, which is clearly different from what was seen in sham-operated animals. The acetone spray test incorporates a multimodal stimulus different from direct cold stimulation. The reactivity to the acetone spray coincides in time and strength with the reactivity observed in mechanical allodynia in gerbils and with mechanical and thermal allodynia in other species. Furthermore, a pharmacological validation of the acetone spray test by different reference compounds was performed. Different compounds effective in neuropathic pain models in rodents influence the hyperreactivity to the acetone spray after acute and chronic administration. This study indicates that the multimodal acetone spray test is a valuable tool in the study of neuropathic pain in rodents. IMPLICATIONS: The acetone spray test is a multimodal and valuable tool in the evaluation of neuropathic pain behavior in gerbils.

Acetone↗
PubMed1982

Distribution and elimination of 2-[14C]-acetone in mice after inhalation exposure.

This study was undertaken to determine the tissue distribution and elimination of acetone and its metabolic radioactive fragments in mice after exposure to about 1,200 mg/m3 (500 ppm) of 2-[14C]-acetone vapor. The tissue concentrations of acetone seemed to reach steady state plateaus within 6 h of exposure. In the adipose tissue the maximal concentration was about one-third of that in the highly perfused nonadipose tissues, in which acetone was rather evenly distributed. The contents of radioactivity also reached a plateau within 6 h of exposure in all tissues except the liver and brown adipose tissue. In these tissues the radioactivity increased during exposures up to 24 h. Prolonging the exposure time from 6 h to 6 h/d for three and five consecutive days gave no or only a small additional accumulation of radioactivity in all tissues except adipose tissue. The half-times of acetone after 6 h of exposure were between 2 and 5 h in all tissues. Almost equal amounts of acetone were excreted via the lungs unmetabolized or metabolized to carbon dioxide. In all tissues endogenous levels of acetone were reached within 24 h after exposure. Thus, acetone did not accumulate after prolonged or repeated exposure to concentrations of 1,200 mg/m3.

Acetone↗
PubMedDate not supplied

Studies on inhibition and induction of metabolism of ethyl carbamate by acetone and related compounds. Evidence for metabolism by cytochromes P-450.

Ethanol and a variety of other compounds previously have been shown to acutely inhibit the metabolism of ethyl carbamate (EC) when given concurrently in mice. On the other hand, ethanol pretreatment (10% in drinking water for the period 48 to 12 hr prior to EC treatment) is known to have the opposite effect and enhance the clearance of EC from blood of mice. In the present work, acetone has been shown to act similarly. Concurrent acetone treatment inhibits the metabolism of EC (11.1 mg/kg po) in male A/JAX mice in a dose-response manner. Blood clearance (Cl) of this po dose of EC from mice following concurrent acetone treatment (50 mg/kg, 0.86 mmol/kg ip) averaged 185 +/- 5.4 (SE) ml hr-1 kg-1 vs. controls of 804 +/- 24.6 ml hr-1 kg-1. Comparing doses that produce equal effects on the blood clearance values of EC, acetone is approximately 50-fold more potent as an inhibitor than ethanol. Pretreatment of mice with acetone (2 g/kg ip) 48 hr and 24 hr before EC administration po increased the clearance of EC approximately 3-fold (CI = 2623 +/- 123 ml hr-1 kg-1). 2-Propanol was found to be at least as potent as inhibitor as acetone, but with a longer duration of inhibition; this longer duration was explained by the longer persistence of acetone in blood from conversion of 2-propanol to acetone.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Propanol↗
PubMed1989

The role of water in the radiation sensitization of acetone.

These experiments were aimed at the better understanding of the mechanism of the enhancement of radiation damage brought about by acetone in spores of Bacillus megaterium. Particularly, the intention was to examine the extent of involvement of water content in this action of acetone. The radiosensitization of acetone increased with increasing oxygen concentration and ultimately became zero at 2.1% O2 in N2. The extent of sensitization increased with rising concentration of acetone up to the first peak (50% acetone in water) under anaerobic condition. Further increase in acetone concentration resulted a maximum response seen at 90% acetone in water. To investigate the role of hydroxyl radical in the radiation sensitization caused by acetone two different types of hydroxyl radical scavengers (t-butanol and iso-propanol) were used.

1-Propanol↗
PubMed1986

Pathways of acetone's metabolism in the rat.

Distributions of 14C were different from those of 13C in glucoses formed by livers of rats in diabetic ketosis and perfused with [2-14C]acetone and [2-13C]lactate. There was 32-73% of the 14C and 8-12% of the 13C in carbons 3 and 4 of the glucoses with the remaining 14C and 13C distributed about equally in the other carbons. Incorporations of 14C from [2-14C]acetone (14-39%) also exceeded those from [2-14C]pyruvate (8-10%) into carbons 3 and 4 of glucoses formed by hepatocytes from rats fed acetone or fasted. [2-14C]Acetone and [2-14C]pyruvate were infused into rats that were fed, fasted, given acetone in their drinking water, or in diabetic ketosis. Thirty-seven to 52% of the 14C in the glucoses formed was in their carbons 3 and 4 when the acetone was infused and 8 to 14% when the pyruvate was infused. [1,3-14C]Hydroxybutyrate was formed by the rats in diabetic ketosis given [2-14C]acetone. It is concluded that acetone is metabolized in rats to a large extent by a pathway in which lactate or its metabolic equivalent is not an intermediate and that pathway is via acetyl-CoA. via acetyl-CoA.

Acetone↗
PubMed1984

Metabolism of acetone to isopropyl alcohol in rats and humans.

Isopropyl alcohol and acetone have been detected in autopsy blood samples of individuals not previously exposed to these compounds. Since some of these individuals had a history of diabetes mellitus, it has been suggested that in these cases, reduction of acetone to isopropyl alcohol might be a metabolic pathway for its production. This hypothesis was investigated in a study of normal and diabetic rats. Acute administration of acetone resulted in measureable levels of isopropyl alcohol in blood. Metabolism of acetone to isopropyl alcohol was different in normal and diabetic animals. Blood levels of isopropanol reached a maximum at the second highest dose in normal rats, but there was a two-phase response in diabetic rats. In a second series of experiments, acetone was administered on alternate days for a week. In spite of this chronic administration (and persistence of high blood acetone), there was no enhancement of acetone metabolism to isopropyl alcohol. These experiments indicate that high levels of blood acetone could result in transformation to isopropyl alcohol.

1-Propanol↗
PubMed1994

Smell acuity for acetone and its relationship to taste ability to phenylthiocarbamide in a Nigerian population.

Acetone smell sensitivity and phenylthiocarbamide taste sensitivity thresholds have been measured simultaneously for 970 Nigerians (542 males and 428 females) using modified sorting techniques. The distribution was bimodal in both cases and the frequency of subjects with high smell acuity for acetone was 9.6% while that of non-tasters was 12.60% with a gene frequency, as computed by maximum likelihood methods, of 0.355 +/- 0.015. Females showed a higher frequency for smell sensitivity to acetone but a slightly lower frequency of non-tasters compared to males. Acetone smell sensitivity and PTC with high smell acuity for acetone were tasters while 30.28% of subjects least sensitive taste ability decreased with age in the overall population. All the subjects least sensitive to acetone were non-tasters, a significantly higher proportion than in the overall population. The correlation between acetone smell acuity and phenylthiocarbamide taste ability demonstrates a strong allelic association. All the 94 individuals with high smell acuity for Acetone were tasters for phenylthiocarbamide.

Acetone↗
PubMed1995

In situ hybridization analysis of hepatic cytochrome P450 2E1 messenger ribonucleic acid in mice. Modulation of expression by acetone.

BACKGROUND: Cytochrome P450 2E1 is a distinct enzyme induced by diverse agents and notably by solvents including acetone. The P450 2E1 apoprotein is predominantly localized in the centrilobular region of the hepatic lobule in the constitutive state and after induction with acetone. In this study, we investigated the level and pattern of distribution of the 2E1 mRNA within the hepatic lobule in control mice and in mice exposed to acetone under acute and chronic conditions. EXPERIMENTAL DESIGN: Male CD-1 mice were administered acetone acutely (5 ml/kg) or chronically (1% in drinking water for 8 days). Cytochrome P450 2E1 mRNA was detected in liver tissues, using in situ hybridization with a 3H-labeled RNA probe coupled with quantitative image analysis. RESULTS: Acetone exposure did not alter the distance spanning a central vein and an adjacent portal vein. In control mice, 2E1 mRNA transcripts were localized most abundantly in the centrilobular zone of the hepatic lobule; intermediate levels were found in the midzonal region, and minimal levels were found in the periportal region. In acetone-treated mice, 2E1 mRNA expression within the hepatic lobule was significantly reduced and was manifested, firstly, in a decreased hepatocyte population with high expression, as assessed by reduction of total acinar areas containing 2E1 mRNA transcripts, and, secondly, in reduced 2E1 mRNA content within the hepatocytes. These alterations were observed to a significantly greater extent in mice after chronic versus acute acetone exposure. CONCLUSIONS: Our results showed that acetone exposure in mice results in both a reduction and a more restricted distribution of 2E1 mRNA within the hepatic lobule. Furthermore, these findings suggest that 2E1 enzyme induction is associated with post-transcriptional events that are more marked after chronic than after acute exposure.

Acetone↗
PubMedDate not supplied

Induction and regulation of CYP2E1 in murine liver after acute and chronic acetone administration.

The effects of acute and chronic acetone administration on hepatic Cyp2e1 were investigated in mice. Acute treatment consisted of a single dose of acetone (5 ml/kg) given intragastrically, whereas the chronic regimen consisted of 1% acetone in drinking water for 8 days. We examined 1) relative induction of Cyp2e1 protein by immunoblotting, 2) relative induction of enzyme catalytic activity (p-nitrophenol hydroxylation), and 3) Cyp2e1 mRNA levels associated with acute and chronic treatment regimens. Western immunoblotting, using a monoclonal antibody (Mab 1-98-1) specific for rat ethanol-inducible P-450, detected a band of M(r) 51,000 in liver microsomes of both control and acetone-treated mice. Densitometric quantitation showed significant enhancement of the intensity of this band by 4.4- and 5.3-fold after acute and chronic acetone treatments, respectively. Hydroxylation of p-nitrophenol was increased 2.3-fold in microsomes from livers exposed acutely to acetone, as compared with an increase of 3.7-fold in microsomes from livers exposed chronically. The induction of Cyp2e1 protein, as well as of catalytic activity, by acetone was not accompanied by significant alterations in the levels of Cyp2e1 mRNA. These results demonstrate a difference in induced increases of Cyp2e1 between acute and chronic acetone treatments: significantly higher induction of both protein and catalytic activity is induced by treatment under chronic vs. acute conditions.

Acetone↗
PubMed1993

Breath acetone analyzer: diagnostic tool to monitor dietary fat loss.

Acetone, a metabolite of fat catabolism, is produced in excessive amounts in subjects on restricted-calorie weight-loss programs. Breath acetone measurements are useful as a motivational tool during dieting and for monitoring the effectiveness of weight-loss programs. We have developed a simple, easy-to-read method that quantifies the amount of acetone in a defined volume of exhaled breath after trapping the sample in a gas-analyzer column. The concentration of acetone, as measured by the length of a blue color zone in the analyzer column, correlates with results obtained by gas chromatography. Using the breath acetone analyzer to quantify breath acetone concentrations of dieting subjects, we established a correlation between breath acetone concentration and rate of fat loss (slope 52.2 nmol/L per gram per day, intercept 15.3 nmol/L, n = 78, r = 0.81). We also discussed the possibility of using breath acetone in diabetes management.

Acetone↗
PubMed2003

Reactions of lead cluster ions with acetone.

Reactions of lead cluster cations and anions with acetone have been studied using a homemade reflectron time-of-flight mass spectrometer. Association with acetone to form Pb(k)(CH(3)COCH(3))(n)(+), high-energy pathway reactions forming Pb(k)CH(3)(+), and intraheterocluster reaction of Pb(k)(CH(3)COCH(3))(n+1)(+) to give Pb(k)CH(3)(CH(3)COCH(3))(n)(+) were the main reaction pathways for lead cluster cations with acetone. Decomposition of acetone by Pb(k)(-) to give Pb(k)C(m)(-) ions and their further association with acetone, Pb(k)C(m)(CH(3)COCH(3))(-), were the dominant reactions of lead cluster anions with acetone. Pb(7)(-), Pb(10)(-), and Pb(k)C(5)(-) were 'magic numbers' with special structural stabilityin Pb(k)(-) and Pb(k)C(m)(-), respectively. In addition, Pb(k)H(-), CH(2)COCH(3)(CH(3)COCH(3))(n)(-) and Pb(k)CH(2)COCH(3)(CH(3)COCH(3))(n)(-) were also observed in the reaction of lead cluster anions. Some reaction mechanisms are proposed for these reactions. To investigate the isotope effect for the reaction of lead cluster cations and anions with acetone and to verify the structural assignments of the observed ions, reactions of lead cluster cations and anions with deuterated acetone-d(6) were also performed.

Journal Article↗
PubMed1991

NTP technical report on the toxicity studies of Acetone in F344/N Rats and B6C3F1 Mice (Drinking Water Studies) (CAS No. 67-64-1).

Toxicity studies were conducted by administering acetone (greater than 99%percnt; pure) in drinking water to groups of F344/N rats and B6C3F1 mice of each sex for 14 days or 13 weeks. Fourteen-Day Studies: All rats and mice receiving concentrations as high as 100,000 ppm acetone in drinking water lived to the end of the 14-day studies. The mean body weights of male rats receiving 50,000 or 100,000 ppm and female rats given 100,000 ppm were lower than those of controls. Body weights of all groups of mice were similar. Kidney and liver weight to body weight ratios for exposed rats and mice were greater than those for controls. Histopathologic changes were not seen in these organs in rats or in the kidney in mice. Centrilobular hepatocellular hypertrophy was noted in male and female mice receiving 20,000 and 50,000 ppm acetone, respectively. Thirteen-Week Studies: All rats lived to the end of the 13-week studies (drinking water concentrations as high as 50,000 ppm). The final mean body weights of rats receiving 50,000 ppm were 19%percnt; lower than that of controls for males and 7%percnt; lower for females. Water consumption by all rats that received 50,000 ppm acetone and females that received 20,000 ppm or more was notably lower than that by controls. Liver and kidney weight to body weight ratios were increased for male and female rats receiving 20,000 ppm or greater. Caudal and right epididymal weights and sperm motility were decreased for male rats given 50,000 ppm, and the percentage of abnormal sperm was increased. Leukocytosis and thrombocytopenia were observed at 20,000 ppm and above (males and females), and reticulocytopenia and erythrocytopenia were seen at 5,000 ppm and above (males). These changes, in addition to increase in erythrocyte size (MCV), are consistent with macrocytic anemia. Splenic pigmentation (hemosiderosis) noted in dosed male rats was apparently related to these changes. The increased incidence and severity of nephropathy observed in dosed male rats were considered the most prominent chemically related findings in this study. All mice lived to the end of the 13-week studies (drinking water concentrations up to 20,000 ppm for males and up to 50,000 ppm for females). The final mean body weights of dosed and control mice were similar. Water consumption by female mice that received 50,000 ppm acetone was notably lower than that by controls. The absolute liver weight and the liver weight to body weight ratio were significantly increased for females receiving 50,000 ppm, and the absolute spleen weight and the spleen weight to body weight ratio were significantly decreased. Results from the hematologic analyses did not show any biologically significant effects. Centrilobular hepatocellular hypertrophy of minimal severity was seen in 2110 female mice receiving 50,000 ppm. No compound-related lesions were found in male mice. In summary, the results from these studies show that acetone is mildly toxic to rats and mice when administered in drinking water for 13 weeks. Minimal toxic doses were estimated to be 20,000 ppm acetone for male rats and male mice and 50,000 ppm acetone for female mice. No toxic effects were identified for female rats. The testis, kidney, and hematopoietic system were identified as target organs in male rats, and the liver was the target organ for male and female mice. Synonyms: 2-propanone; dimethyl ketone; pyroacetic acid. (NOTE: These studies were supported in part by funds from the Comprehensive Environmental Response, Compensation, and Liability Act trust fund (Superfund) by an interagency agreement with the Agency for Toxic Substances and Disease Registry, U.S. Public Health Service.)

Journal Article↗
PubMed1983

Topical treatment of acne rosacea with benzoyl peroxide acetone gel.

A group of patients with acne rosacea was treated with 5 percent benzoyl peroxide acetone gel for four weeks and then with 10 percent benzoyl peroxide acetone gel for an additional four weeks. A parallel group of patients was treated with a matching placebo (acetone gel vehicle). At the end of the first four weeks of treatment the dropout rate due to lack of improvement was 23 and 63 percent for benzoyl peroxide acetone gel and placebo, respectively. Benzoyl peroxide acetone gel was superior to placebo with respect to improvement in the overall severity of the lesions when judged by photographs, and by reduction of erythema, papules, and pustules. Results after treatment with benzoyl peroxide acetone gel were better during weeks five to eight than during weeks one to four for all lesions except telangiectasia. Benzoyl peroxide acetone gel was superior to placebo when the overall responses were compared. In addition, the benzoyl peroxide acetone gel-treated group, but not the placebo-treated group, showed a significantly better response during weeks five to eight compared to weeks one to four.

Administration, Topical↗
PubMed2002

Odorant differentiated pattern of cerebral activation: comparison of acetone and vanillin.

Whether different odorous compounds (odorants) are processed by different cerebral circuits is presently unknown. A first step to address this complicated issue is to investigate how the cerebral regions mediating signals from olfactory (i.e., unimodal) odorants, differ from those mediating the olfactory + trigeminal (i.e., bimodal) odorants. [15O]-H2O-PET scans were conducted in 12 healthy females during three separate conditions: birhinal, passive smelling of: 1) the unimodal odorant vanillin; 2) the bimodal odorant acetone; and 3) odorless air. Significant activations were calculated contrasting vanillin to air, acetone to air, and deactivations, running these contrasts in the opposite direction. Smelling of vanillin activated bilaterally the amygdala and piriform cortex. These regions were only engaged slightly by acetone. Instead, strong activations were found in the anterior and central insula and claustrum, the posterior portion of anterior cingulate, the somatosensory cortex (SI for face), cerebellum, ventral medial (VMPo) and dorsal medial (MDvc) thalamus, the lateral hypothalamus, and pons/medulla. In parallel, the somatosensory (SI, below central representation of face), secondary visual and auditory cortices, as well as the supplementary motor area and the parahippocampal gyri were deactivated. No deactivations were observed with vanillin, although the odor components of acetone and vanillin were rated similarly intense (75 +/- 17 mm vs. 61 +/- 22 mm, NS). The differentiated pattern of cerebral activation during odorant perception seems to be dependent on the signal transducing cranial nerves involved. In contrast to vanillin, which solely activates the olfactory cortex, acetone engages predominantly trigeminal projections from the nasal mucosa. Acetone's limited activation of the olfactory cortex may result from a cross-modal interaction, with inhibition of acetone's odor component by its trigeminal component.

Acetone↗
PubMedDate not supplied

Acetone potentiation of chronic liver injury induced by repetitive administration of carbon tetrachloride.

The ability of ketonic compounds to modify the chronic liver injury (cirrhosis) induced by haloalkanes is unknown. To investigate this problem, male Sprague-Dawley rats were treated p.o. twice weekly for 12 weeks with acetone (25 mmoles per kg in corn oil) or corn oil alone (10 ml per kg). The rats were treated p.o. with corn oil (10 ml per kg) or CCl4 (5 mmoles per kg in corn oil) 18 hr after each pretreatment. Animals were killed after 4, 8, 10 or 12 weeks of treatment. Liver-kidney/body weight ratios were computed; biochemical analyses were performed on plasma (ALT, bilirubin and blood urea nitrogen) and liver (collagen) samples. For the 10-week group, liver injury was assessed by a morphometric analysis. Body weight gain was slower in acetone-treated rats given CCl4; 35% died. Compared to corn oil + CCl4-treated rats, acetone + CCl4-treated animals showed significantly lower liver weight/body weight ratios and higher kidney weight/body weight ratio values at all four times. Significantly higher levels occurred at all four times for bilirubin concentrations, and at 4, 8 and 10 weeks for collagen contents. No significant differences were observed in ALT activities between corn oil- and acetone-treated rats challenged with CCl4. Light microscopy revealed that after 10 weeks of treatment, acetone + CCl4-treated animals showed a fully developed cirrhosis, whereas a much less severe lesion was observed in corn oil + CCl4-treated rats. Evidence of nephrotoxicity was observed in the acetone + CCl4 group as exemplified by significantly elevated blood urea nitrogen values. We conclude that acetone treatment increases the extent of fibrosis and accelerates the appearance of cirrhosis induced by CCl4.

Acetone↗
PubMed1990

Anaerobic degradation of acetone by Desulfococcus biacutus spec. nov.

From anaerobic digestor sludge of a waste water treatment plant, a gram-negative, strictly anaerobic sulfate-reducing bacterium was isolated with acetone as sole organic substrate. The bacterium was characterized as a new species, Desulfococcus biacutus. The strain grew with acetone with doubling times of 72 h to 120 h; the growth yield was 12.0 (+/- 2.1) g x [mol acetone]-1. Acetone was oxidized completely, and no isopropanol was formed. In labelling studies with 14CO2, cell lipids (including approx. 50% PHB) of acetone-grown cells became labelled 7 times as high as those of 3-hydroxy-butyrate-grown cells. Enzyme studies indicated that acetone was degraded via acetoacetyl-CoA, and that acetone was channeled into the intermediary metabolism after condensation with carbon dioxide to a C4-compound, possibly free acetoacetate. Acetoacetyl-CoA is cleaved by a thiolase reaction to acetyl-CoA which is completely oxidized through the carbon monoxide dehydrogenase pathway. Strain KMRActS was deposited with the Deutsche Sammlung von Mikroorganismen, Braunschweig, under the number DSM 5651.

3-Hydroxybutyric Acid↗