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PubMed1990

Kinetics of the methanogenic fermentation of acetate.

Inhibition of the fermentation of acetate to methane and carbon dioxide by acetate was analyzed with an acetate-acclimatized sludge and with Methanosarcina barkeri Fusaro under mesophilic conditions. A second-order substrate inhibition model, q(ch(4) ) = q(m)S/[K(s) + S + (S/K(i))], where S was the concentration of undissociated acetic acid, not ionized acetic acid, could be applicable in both cases. The analysis resulted in substrate saturation constants, K(s), of 4.0 muM for the acclimatized sludge and 104 muM for M. barkeri. The threshold concentrations of undissociated acetic acid when no further acetate utilization was observed were 0.078 muM (pH 7.50) for the acclimatized sludge and 4.43 muM (pH 7.45) for M. barkeri. These kinetic results suggested that the concentration of undissociated acetic acid became a key factor governing the actual threshold acetate concentration for acetate utilization and that the acclimatized sludge in which Methanothrix spp. appeared dominant could utilize acetate better and survive at a lower concentration of undissociated acetic acid than could M. barkeri.

Journal Article↗

PubMed2006

A kinetic study of isoamyl acetate synthesis by immobilized lipase-catalyzed acetylation in n-hexane.

The objective of this work was to propose a reaction mechanism and to develop a rate equation for the synthesis of isoamyl acetate by acylation of the corresponding alcohol with acetic anhydride using the lipase Novozym 435 in n-hexane. The reaction between isoamyl alcohol and acetic anhydride occurred at high rate in first place. Then, if excess alcohol was used, produced acetic acid further reacted with remaining alcohol, leading to yields higher than 100% (based on initial acetic anhydride content). This reaction was much slower and took place only when acetic anhydride had been totally consumed. Optimal pH for Novozym 435 was 7.7. Acetic acid strongly inactivated the enzyme but it was partially caused by the pH drop in the biocatalyst aqueous microenvironment. Acetic anhydride also showed an important inhibition effect. On the contrary, isoamyl alcohol and isoamyl acetate had no negative effect on the lipase. The analysis of the initial rate data showed that reaction followed a Ping-Pong Bi-Bi mechanism with inhibition by acetic anhydride. The kinetic constants were obtained by multiple regression analysis of experimental findings. Equation predictions and experimental reaction rate values matched very well at conditions where acetic acid concentration in the medium was low.

Acetic Acid↗

PubMed1992

The vasorelaxant effects of acetate: role of adenosine, glycolysis, lyotropism, and pHi and Cai2+.

The mechanism of acetate vasorelaxation is unknown. In the rat caudal artery, acetate has a vasorelaxant effect and also increases cyclic AMP. Here we evaluate the role of adenosine, of possible glycolysis inhibition by acetate, of the lyotropic properties of acetate and other anions, and of intracellular calcium and pH. Adenosine per se did not relax the caudal artery in the range of 10(-8) to 10(-2) M. Preincubation with adenosine deaminase (ADA, 5.0 U/ml) or with 8-phenyltheophylline (8-PT, 10(-6) to 10(-4) M) increased, rather than blocked the vasorelaxant effect of acetate. Oxypurinol (10(-3) M) or the nucleoside transport inhibitor NBMPR (10(-4) M) had no effect on acetate relaxation. Whereas acetate increased tissue cyclic AMP content, 10(-3) M adenosine or 10(-6) M PIA had no effect. In strips studied under conditions of inhibited glycolysis (no glucose, with 11 mM 2-deoxyglucose, 1.0 mM pyruvate, and 0.5 mM 5-iodoacetate), acetate-induced relaxation, as well as acetate-induced cyclic AMP generation, tended to be reduced but not significantly so. Other anions relaxed vascular strips in relation to their lyotropic number, but only at higher doses, and they did not stimulate cyclic AMP formation. Acetate (10 mM) caused a transient fall in Ca2+i followed by a slight, sustained rise. A concomitant decrease in pHi was seen. DIDS, which blocks the relaxant and cyclic AMP effects of acetate, had no effect on the pHi decrease, but did decrease the rate of pHi recovery.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗

PubMed1996

Prognosis of small hepatocellular carcinoma (less than 3 cm) after percutaneous acetic acid injection: study of 91 cases.

To assess the efficacy of ultrasound (US)-guided percutaneous acetic acid (in concentrations of 15%, 20%, 30%, 40%, and 50%) injection for small hepatocellular carcinomas (HCCs) for long-term prognosis, percutaneous acetic acid injection using 15% to 50% acetic acid was performed in 91 patients with one to four HCCs smaller than 3 cm during the past 6.5 years. During the series of treatment sessions for each patient, the same concentration of acetic acid was used. All tumors could be treated successfully with percutaneous acetic acid injection despite the differences in acetic acid concentration used. The number of treatment sessions to treat similar size of tumor was less when the higher concentration of acetic acid was used. No serious complications occurred as a direct sequela to percutaneous acetic acid injection. None of the tumor treated regrew. The 1-, 2-, 3-, 4-, and 5-year survival rates for 91 patients were 95%, 87%, 80%, 63%, and 49%, respectively. The 1-, 2-, 3-, 4-, and 5-year cancer-free survival rates of these patients were 83%, 54%, 50%, 37%, and 29%, respectively. Both liver function and size of tumor affected both survival rate and cancer-free survival rate significantly, but the number of tumors did not. The concentration of acetic acid did not affect the survival rate. Percutaneous acetic acid using 15% to 50% acetic acid will be effective therapy for small HCCs for long-term prognosis.

Acetates↗

PubMed1990

Control of diauxic growth of Azotobacter vinelandii on acetate and glucose.

Batch cultures of Azotobacter vinelandii were inoculated with cells pregrown on either acetate or glucose. When they were subsequently grown on a mixture of acetate and glucose, typical diauxic growth was observed, with preferential uptake of acetate in the first and glucose in the second phase of growth. Extracts from acetate-pregrown cells exhibited high acetate kinase activity in the first phase of growth. This activity decreased and activities of the two glucose enzymes glucose 6-phosphate dehydrogenase and glyceraldehyde 3-phosphate dehydrogenase increased in the second phase. Extracts from glucose-pregrown cells exhibited high initial activities of the two glucose enzymes, which decreased while acetate kinase activity increased in the first phase of growth. Again, in the second phase, activities of the two glucose enzymes increased and acetate kinase activity decreased. In any case, isocitrate dehydrogenase activity varied only slightly and unspecifically. The differences in enzyme activity and the constancy of isocitrate dehydrogenase were confirmed by experiments with either acetate- or glucose-limited chemostats. In chemostats in which both of the substrates were limiting, all of the enzymes displayed significant activities. Glucose 6-phosphate dehydrogenase activity was inhibited by acetyl coenzyme A and acetyl phosphate but not by acetate. It is proposed that diauxic growth is based on the control of enzymes involved in acetate or glucose dissimilation by which acetate or its metabolites control the expression and activity of glucose enzymes.

Acetate Kinase↗

PubMed1991

Central nervous system effects of acetate: contribution to the central effects of ethanol.

Acetate, resulting from ethanol metabolism in the liver, is released into the circulation and is utilized in a number of tissues, including the brain. In its metabolism, acetate leads to the production of adenosine, a powerful physiological mediator. We have investigated the effect of acetate on central nervous system (CNS) function in rodents. Sodium acetate in doses resulting in blood concentrations comparable to those attained after the administration of 1 to 2 g/kg ethanol, had significant CNS effects. Both ethanol and acetate produced a dose-dependent impairment of motor coordination. This effect of acetate was fully blocked by the adenosine receptor blocker 8-phenyltheophylline (8PT), whereas the dose-response relationship for ethanol was shifted to the right by about 30%. The inspired concentration of sevoflurane to achieve anesthesia was significantly reduced by both these agents. General anesthesia was potentiated in a dose-dependent fashion by ethanol and by acetate. The effect of acetate on anesthetic requirements was fully blocked by 8PT. The effect of ethanol on sevoflurane anesthetic requirements was inhibited by 22 to 35% by 8PT. Locomotor activity in mice was reduced by acetate in a dose-dependent fashion, an effect that was also fully blocked by 8PT. On the other hand, ethanol at a dose of 1 to 2 g/kg increased locomotor activity. This likely results from a direct stimulatory effect of ethanol, opposed by an inhibitor effect of acetate. The administration of 8PT enhanced the stimulation of locomotor activity induced by ethanol. In conclusion, acetate, a product of ethanol metabolism has significant CNS effects that can either potentiate or antagonize the effects of the ethanol molecule per se.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetates↗

PubMed1999

Depot medroxyprogesterone acetate use in inner-city, minority adolescents: continuation rates and characteristics of long-term users.

OBJECTIVE: To identify continuation rates of depot medroxyprogesterone acetate (Depo-Provera) and characteristics of long-term users in a population of inner-city, minority adolescents with high pregnancy rates. DESIGN: Retrospective medical record review. SETTING: An inner-city adolescent clinic and an adolescent pregnancy program. METHODS: A review of the medical records of 250 females aged 13 to 20 years (mean +/- SD, 16.8 +/- 1.1 years), 62.9% Hispanic and 34.2% African American, receiving a first depot medroxyprogesterone acetate injection for contraception between August 1993 and June 1996 was conducted using a standardized form. The mean +/- SD age at menarche of the subjects was 11.6 +/- 1.4 years, and the mean +/- SD age at first intercourse was 14.1 +/- 1.3 years; the mean number of lifetime sex partners was 2.4. Of the subjects, 73.6% had used condoms, 32.0% used oral contraceptives, and none used implants. Of the 201 subjects for whom there were data in the medical records regarding prior fertility, 172 (85.6%) had been pregnant, and 145 (72.1%) had a child. Life table analysis was used to measure depot medroxyprogesterone acetate continuation rates and to compare subgroups of adolescents. RESULTS: Depot medroxyprogesterone acetate continuation rates were found to be 70.3% at 6 months, 48.3% at 9 months, 31.5% at 12 months, and 12.8% at 24 months. The most common reason for depot medroxyprogesterone acetate discontinuation was missed appointments (41.7%). Subjects were followed up for a mean +/- SD of 1.3 +/- 0.7 years after discontinuation of depot medroxyprogesterone acetate use; 46.7% became pregnant. Among those 156 adolescents who discontinued depotmedroxyprogesterone acetate use, 40.0% restarted the method at some later time. Continuation of depot medroxyprogesterone acetate use was more likely if age at first intercourse was younger than 13 years (P = .04). Continuation rates were not related to age, ethnicity, age at menarche, number of sex partners, use of other contraceptives, prior pregnancy, or having a child. CONCLUSIONS: In this study, just less than one third of the adolescents continued depot medroxyprogesterone acetate use for 1 year or longer. This suggests that depot medroxyprogesterone acetate does not function as a long-term method for most inner-city adolescents. The only characteristic that was associated with successful continuation of depot medroxyprogesterone acetate use was young age at first intercourse, implying that experience may be the main determinant of continuation.

Adolescent↗

PubMed1984

Modulation by retinyl acetate of microfilament bundle formation in C3H/10T1/2 cells.

Retinyl acetate has been previously shown to inhibit carcinogen-induced neoplastic transformation in 10T1/2 cells and to accentuate many aspects of the nontransformed phenotype. Scanning electron microscopy of logarithmic phase 10T1/2 cells treated for 3 days with 0.3 micrograms/ml retinyl acetate revealed that this treatment caused extensive flattening of cells to the plastic substrate. In contrast the tumor promoter tetradecanoyl phorbol acetate, which antagonizes the antineoplastic activity of retinyl acetate, caused cell rounding and completely inhibited the action of retinyl acetate on cell morphology. During this same time course, the formation of microfilament bundles was also found to be modulated by retinyl acetate. Transmission electron micrographs of unsectioned peripheral regions of flattened cells showed that while the unit density of microfilament bundles was not influenced, the thickness of bundles, particularly those with a diameter of 100 nm or more, was increased by retinyl acetate. Tetradecanoyl phorbol acetate had little effect on microfilament bundle diameters but did partially antagonize the action of retinyl acetate. To determine if this increase was associated with an increase in total actin/cell, total cell proteins, and proteins not extractable by glycerol-triton extraction, were subjected to sodium dodecylsulfate/ polyacrylamide gel electro-phoresis. It was found that while total cellular actin was not increased by retinyl acetate, the proportion of nonextractable actin (which includes microfilament bundles) increased from 65% to 88% of total actin. This increase was not inhibited by inhibitors of protein or RNA synthesis. These studies again demonstrate that retinyl acetate accentuates the nontransformed phenotype of 10T1/2 cells; it is hypothesized that these actions are related to the antineoplastic activity of retinoids.

Actins↗

PubMed1997

A comparison of the acute behavioral effects of inhaled amyl, ethyl, and butyl acetate in mice.

The acute neurobehavioral effects of three acetates (amyl, ethyl, and n-butyl acetate) were investigated after 20-min inhalation exposures in mice using locomotor activity and a functional observational battery (FOB). Ethyl and n-butyl acetate produced significant decreases in locomotor activity at the highest concentrations examined, while amyl acetate was without effect. Minimally effective concentrations for activity-decreasing effects were 2000 ppm for ethyl acetate and 8000 ppm for n-butyl acetate. The potency order was similar in the FOB where ethyl acetate was more potent in disrupting the neurobehavioral measures. The FOB profile of effects for all three acetates included changes in posture, decreased arousal, increased tonic/clonic movements, disturbances in gait, delayed righting reflexes, and increased sensorimotor reactivity. Furthermore, handling-induced convulsions were produced in some mice acutely exposed to each of these acetates. Recovery from the acute effects of these acetates was rapid and began within minutes of removal from the exposure chamber. The acetates produced a profile of neurobehavioral effects that were different from those reported for depressant solvents (i.e., toluene, 1,1,1-trichloroethane) that are subject to abuse. Evidence is emerging for qualitative differences in the acute neurobehavioral effects of various volatile chemicals.

Acetates↗

PubMedDate not supplied

Coronary vasoactivity of acetate in dog and guinea-pig.

This study compares the coronary vasoactivity of acetate in the blood-perfused heart of the open-chest dog and in the buffer-perfused guinea-pig heart. In the dog acetate is a weak but probably fully efficacious coronary agonist. Direct intracoronary infusions of isosmolar Na acetate caused dose-dependent coronary vasodilation and decreased transcoronary O2 extraction, resulting in an increase in cardiac O2 usage of up to 40%. Acetate raised coronary flow to at least 50% above control in 63 of 67 dogs but caused maximum coronary vasodilation (400% of control) in only 39 of the 67. The frequency distribution of the acetate EC-20 decreased monotonically from a mode at less than 1 mM over a range extending to greater than 6 mM, suggesting a single population of animals characterized by a rather wide range of sensitivity to acetate. Theophylline antagonized acetate vasodilation, in support of the idea that adenosine mediates the coronary effects of acetate. In the guinea-pig heart, acetate in concentrations up to 10 mM caused minimal increases in coronary flow that were completely accounted for by the small change in O2 usage that resulted from switching from glucose to acetate the main energy source. Acetate (10 mM) elicited a small release of adenosine and its degradation products.

Acetates↗

PubMedDate not supplied

Acetic acid production from lactose by an anaerobic thermophilic coculture immobilized in a fibrous-bed bioreactor.

An anaerobic thermophilic coculture consisting of a heterofermentative bacterium (Clostridium thermolacticum) and a homoacetogen (Moorella thermoautotrophica) was developed for acetic acid production from lactose and milk permeate. The fermentation kinetics with free cells in conventional fermentors and immobilized cells in a recycle batch fibrous-bed bioreactor were studied. The optimal conditions for the cocultured fermentation were found to be 58 degrees C and pH 6.4. In the free-cell fermentation, C. thermolacticum converted lactose to acetate, ethanol, lactate, H(2) and CO(2), and the homoacetogen then converted lactate, H(2), and CO(2) to acetate. The overall acetate yield from lactose ranged from 0.46 to 0.65 g/g lactose fermented, depending on the fermentation conditions. In contrast, no ethanol was produced in the immobilized-cell fermentation, and the overall acetate yield from lactose increased to 0.8-0.96 g/g lactose fermented. The fibrous-bed bioreactor also gave a higher final acetate concentration (up to 25. 5 g/L) and reactor productivity (0.18-0.54 g/L/h) as compared to those from the free-cell fermentation (final acetate concentration, 15 g/L; productivity, 0.06-0.08 g/L/h). The superior performance of the fibrous-bed bioreactor was attributed to the high cell density (20 g/L) immobilized in the fibrous-bed and adaptation of C. thermolacticum cells to tolerate a higher acetate concentration. The effects of yeast extract and trypticase as nutrient supplements on the fermentation were also studied. For the free-cell fermentation, nutrient supplementation was necessary for the bacteria to grow in milk permeate. For the immobilized-cell fermentation, plain milk permeate gave a high acetate yield (0.96 g/g), although the reactor productivity was lower than those with nutrient supplementation. Balanced growth and fermentation activities between the two bacteria in the coculture are important to the quantitative conversion of lactose to acetic acid. Lactate and hydrogen produced by C. thermolacticum must be timely converted to acetic acid by the homoacetogen to avoid inhibition by these metabolites.

Acetic Acid↗

PubMed1983

Contribution of dialysate acetate to energy metabolism: metabolic implications.

During hemodialysis large amounts of acetate enter the bloodstream. Generally, it is assumed that this exogenous acetate load is oxidized immediately to carbon dioxide and water; however, the rate of plasma acetate oxidation and the effect of acetate oxidation on energy metabolism during hemodialysis has not been determined previously. The rates of plasma acetate turnover and oxidation were determined during hemodialysis in seven chronic renal failure patients by the primed continuous infusion of [1-14C] acetate. The plasma acetate turnover rate (57.2 +/- 2.9 mumoles/min X kg) agreed closely with the mass transfer rate of dialysate acetate into the bloodstream (55.3 +/- 3.2 mumoles/min X kg). Of the acetate entering the bloodstream, 54.5 +/- 5.2% or 31.6 +/- 3.77 mumoles/min X kg was oxidized immediately accounting for 40.3 +/- 4.8% of the patient's caloric expenditure. Although the oxidation of acetate during dialysis supplied a major portion of the patient's caloric need, a significant quantity of acetate was eliminated by pathways other than direct oxidation. An average overall respiratory quotient (RQ) of 1.0 +/- 0.02 indicated that fat oxidation was spared to maintain energy homeostasis during hemodialysis. The calculated non-protein RQ exceeded unity suggesting that net fat synthesis actually occurred.

Acetates↗

PubMed2004

Contribution of acetate to butyrate formation by human faecal bacteria.

Acetate is normally regarded as an endproduct of anaerobic fermentation, but butyrate-producing bacteria found in the human colon can be net utilisers of acetate. The butyrate formed provides a fuel for epithelial cells of the large intestine and influences colonic health. [1-(13)C]Acetate was used to investigate the contribution of exogenous acetate to butyrate formation. Faecalibacterium prausnitzii and Roseburia spp. grown in the presence of 60 mm-acetate and 10 mm-glucose derived 85-90 % butyrate-C from external acetate. This was due to rapid interchange between extracellular acetate and intracellular acetyl-CoA, plus net acetate uptake. In contrast, a Coprococcus-related strain that is a net acetate producer derived only 28 % butyrate-C from external acetate. Different carbohydrate-derived energy sources affected butyrate formation by mixed human faecal bacteria growing in continuous or batch cultures. The ranking order of butyrate production rates was amylopectin > oat xylan > shredded wheat > inulin > pectin (continuous cultures), and inulin > amylopectin > oat xylan > shredded wheat > pectin (batch cultures). The contribution of external acetate to butyrate formation in these experiments ranged from 56 (pectin) to 90 % (xylan) in continuous cultures, and from 72 to 91 % in the batch cultures. This is consistent with a major role for bacteria related to F. prausnitzii and Roseburia spp. in butyrate formation from a range of substrates that are fermented in the large intestine. Variations in the dominant metabolic type of butyrate producer between individuals or with variations in diet are not ruled out, however, and could influence butyrate supply in the large intestine.

Acetates↗

PubMed2004

Reliability of the [13C]-acetate breath test in the measurement of gastric emptying of ethanol solutions: a methodological study.

BACKGROUND: The [13C]-acetate breath test is a clinically well-established test for measuring gastric emptying of liquids and correlates significantly with scintigraphy. However, no studies have been undertaken to examine the relationship between gastric emptying measured by the [13C]-acetate breath test and ultrasonography. Furthermore, it is not known how ethanol may affect gastric emptying as measured by the [13C]-acetate breath test. This is particularly important because of the additional steps of absorption, metabolism and exhalation of the tracer involved in the [13C]-acetate breath test compared to the simple measurement of gastric emptying by ultrasonography. The aim of the present study was to examine the relationship between the gastric half emptying times measured by the [13C]-acetate breath test and by ultrasonography and to determine the effect of ethanol on the comparability between both methods. METHODS: On separate days, 10 healthy, fasted randomly selected subjects received the following solutions by gastric tube: 500 mL water, 4% and 10% (v/v) ethanol, 5.5% and 11.4 % (w/v) glucose. Gastric half emptying times of the test solutions were simultaneously determined using the [13C]-acetate breath test and ultrasonography of the fundus and the antrum. RESULTS: The gastric emptying rates determined by ultrasonography of the fundus correlated significantly with the results obtained using the [13C]-acetate breath test for all test solutions (r = 0.64-0.92, P < 0.05 for all), whereas ultrasonography of the antrum correlated significantly with the breath test only when water (r = 0.94, P = 0.001) was used. The difference between the mean half-emptying times obtained using the [13C]-acetate breath test and ultrasonography of the fundus was 55 +/- 1.8 min. This difference was significantly longer when 4% and 10% (v/v) ethanol solutions were given (61.2 +/- 3.3 and 71.2 +/- 2.9 min) compared to water (P < 0.05). CONCLUSIONS: A good correlation was found between gastric emptying as measured by the [13C]-acetate breath test and ultrasonography of the fundus. Measurements that were obtained using the [13C]-acetate breath test demonstrate a longer gastric half emptying time compared with those obtained using ultrasonography. This difference is even more marked when ethanol solutions are used. Presumably, this is because ethanol affects the absorption and/or the hepatic metabolism of the tracer. The [13C]-acetate breath test is therefore not a reliable gastric emptying test for comparison of different solutions, especially when ethanol-containing liquids are used.

Acetates↗

PubMed1998

Whole-body, peripheral and intestinal endogenous acetate turnover in dogs using stable isotopes.

Acetate metabolism supplies about 10% of energy requirements in food-deprived nonruminant animals. This study used a stable isotope dilution method to investigate the fate of acetate in 24-h food-deprived dogs free of colonic fermentation. Three dogs received intravenous bolus injections of 40 or 70 micromol/kg of [1-13C] acetate, and carotid blood was then sampled during a 15-min period to estimate the acetate distribution volume. Ten dogs received intravenous [1-13C] acetate infusions of 1.05 +/- 0.02 or 2.10 +/- 0. 10 micromol/(kg.min) for 120 or 200 min after a prime of 200 or 70 micromol/kg, respectively. Cephalic venous and carotid arterial blood were sampled for all dogs, and portal blood for five. Acetate distribution volume was 0.27 +/- 0.16 L/kg (mean +/- SEM). The concentrations of acetate in arterial (144 +/- 17 micromol/L), venous (155 +/- 20 micromol/L) and portal plasma (131 +/- 16 micromol/L) were not significantly different during infusion, whereas isotopic enrichments [mole percent excess (MPE): labeled acetate/all acetate molecules] in portal (1.2 +/- 0.2 MPE) and venous plasma (1.7 +/- 0.3 and 2.6 +/- 0.7 MPE) were lower than in arterial plasma for both infusion rates (4.9 +/- 0.6 and 7.6 +/- 0.8 MPE, respectively, P < 0.005). Whole-body acetate turnover was 24.4 +/- 2.4 micromol/(kg.min). Fractional acetate extractions for forelimb and intestine were 62 +/- 7 and 72 +/- 6%, respectively, and the production for each organ was 0.3 and 1.1 micromol/(kg.min) respectively, similar to that of utilization (P > 0.05). It is concluded that the forelimb and intestine produce and utilize acetate as an energy source in 24-h food-deprived dogs free of colonic fermentation.

Acetates↗

PubMed1988

Changes in blood acetaldehyde concentrations during acetate haemodialysis.

Hyperacetataemia during acetate haemodialysis has been associated with the development of a variety of unpleasant symptoms, although a direct toxic effect of acetate is hard to prove. Acetaldehyde, which is produced during the metabolism of ethanol to acetate, has various toxic effects including some of those reported during acetate dialysis such as nausea, headache and palpitations. Using a novel, recently developed method we studied blood acetaldehyde concentrations during acetate dialysis in 15 patients and found significant increases in five, with a mean peak value in these patients of 1.36 mumol/l (normal less than 0.4 mumol/l). These five patients also developed high blood acetate concentrations during a subsequent acetate dialysis and showed a significant correlation between blood acetaldehyde and acetate concentrations (r = 0.55, P less than 0.05). Blood acetaldehyde did not change during bicarbonate dialysis in these patients. Our results suggest that significant accumulation of acetaldehyde may occur during acetate dialysis, especially in those patients whose metabolic capacity for acetate is somehow impaired, and that acetaldehyde may contribute to some of the symptoms previously ascribed to 'acetate' intolerance.

Acetaldehyde↗

PubMed2006

Activation of nitric oxide synthesis in human endothelial cells using nomegestrol acetate.

OBJECTIVE: Recent clinical trials indicate that synthetic progestins may be unexpectedly relevant for the development of cardiovascular disease. The aim of this study was to establish whether nomegestrol acetate induces signaling events in human endothelial cells that differ from those of other progestins, such as natural progesterone or medroxyprogesterone acetate. METHODS: We used human endothelial cells to study the action of nomegestrol acetate (either alone or in the presence of estradiol [E2]) on the synthesis of nitric oxide (NO) and on the activity or expression of endothelial nitric oxide synthase (eNOS). We compared the effects of nomegestrol acetate with those of progesterone or medroxyprogesterone acetate. In addition, we characterized the signaling events recruited by these compounds. RESULTS: Progesterone and nomegestrol acetate increase NO synthesis by transcriptional and nontranscriptional mechanisms, whereas medroxyprogesterone acetate lacks such effects. When used together with physiological E2 concentrations, progesterone and nomegestrol acetate do not interfere with (or even enhance) E2 effects, whereas medroxyprogesterone acetate impairs E2 signaling. A marked difference in the recruitment of mitogen-activated protein kinase and phosphatidylinositol-3 kinase explains the divergent effects of the three gestagens. CONCLUSION: Our findings show significant differences in the signal transduction pathways recruited by progesterone, nomegestrol acetate, and medroxyprogesterone acetate in human endothelial cells that may have relevant clinical implications.

Cells, Cultured↗

PubMed1982

Synthesis of acetylcholine from acetate in a sympathetic ganglion.

The present experiments tested whether acetate plays a role in the provision of acetyl-CoA for acetylcholine synthesis in the cat's superior cervical ganglion. Labeled acetylcholine was identified in extracts of ganglia that had been perfused for 20 min with Krebs solution containing choline (10(-5) M) and [3H], [1-14C], or [2-14C]acetate (10(-3) M); perfusion for 60 min or with [3H]acetate (10(-2) M) increased the labeling. The acetylcholine synthesized from acetate was available for release by a Ca2+-dependent mechanism during subsequent periods of preganglionic nerve stimulation. When ganglia were stimulated via their preganglionic nerves or by exposure to 46 mM K+, the labeling of acetylcholine from [3H]acetate was reduced when compared with resting ganglia. The reduced synthesis of acetylcholine from acetate during stimulation was not due to acetate recapture, shunting of acetate into lipid synthesis, or the transmitter release process itself. In ganglia perfused with [2-14C]glucose, the amount of labeled acetylcholine formed was clearly enhanced during stimulation. An increase in acetylcholine labeling from [3H]acetate was shown during a 15-min resting period following a 60-min period of preganglionic nerve stimulation (20 Hz). It is concluded that acetate is not the main physiological acetyl precursor for acetylcholine synthesis in this sympathetic ganglion, and that during preganglionic nerve stimulation there is enhanced delivery of acetyl-CoA to choline acetyltransferase from a source other than acetate.

Acetates↗