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PubMed1996

Inhibition of growth and induction of TGF-beta 1 in human hepatocellular carcinoma with androgen receptor by cyproterone acetate in male nude mice.

BACKGROUND/AIMS: Hepatocellular carcinoma possesses androgen receptor but its true role is not known. This study aimed to investigate the effect of an anti-androgen cyproterone acetate on the growth of androgen receptor-positive hepatocellular carcinoma. METHODS: Androgen receptor-positive human hepatocellular carcinoma cells (KYN-1/SM-10) were subcutaneously transplanted into male nude mice. When the tumor size was about 10 mm, animals were subcutaneously administered cyproterone acetate (0.1 mg/day and 0.8 mg/day) or solvent alone for 21 days. Animals were serially sacrificed for measurements of testicular weight, tumor size, and cytosolic and nuclear androgen receptor levels in tumor. Proliferating cell nuclear antigen, transforming growth factor-alpha, and transforming growth factor-beta 1 in tumor were investigated immunohistochemically, using monoclonal antibodies. Apoptotic activity was also studied by the in situ DNA nick end labeling method. RESULTS: Cyproterone acetate depressed testicular weight, suppressed tumor growth, and decreased both cytosolic-androgen receptor and nuclear-androgen receptor levels dose-dependently. Numbers of proliferating cell nuclear antigen-positive cells were decreased transiently with the low dose but continuously with the high dose of cyproterone acetate. Transforming growth factor-alpha expression was not influenced by cyproterone acetate, but the high dose of cyproterone acetate induced higher expression of transforming growth factor-beta 1, associated with increased numbers of apoptotic tumor cells, peaking on day 3. CONCLUSIONS: The inhibition of growth of androgen receptor-positive hepatocellular carcinoma with cyproterone acetate in male nude mice could be due to G1-phase cell cycle arrest, and to some extent apoptosis induced by increased synthesis of transforming growth factor-beta 1 in tumor, caused by the direct action of cyproterone acetate through androgen receptors, as well as decreased testosterone levels in blood due to cyproterone acetate-induced testicular atrophy.

Androgen Antagonists↗
PubMed2003

Effect of reactive cell density on net [2-14C]acetate uptake into rat brain: labeling of clusters containing GFAP+- and lectin+-immunoreactive cells.

Astrocytic proliferation is a hallmark of brain injury, but the biological functions and metabolic activities of reactive astrocytes in vivo are poorly understood. [2-14C]Acetate, which is preferentially transported into and, therefore, metabolized by astrocytes, was used to assess injury- and trophic factor-induced changes in astrocyte metabolic activity. Local rates of net [2-14C]acetate uptake and glucose utilization (CMR(glc)), determined with [14C]deoxyglucose to assay overall metabolic activity of all brain cells, were assayed 7 days after a cannula placement; adjacent brain sections were immunostained to identify glial fibrillary acidic protein-positive (GFAP(+)) astrocytes and microglia plus macrophages (lectin-positive cells). GFAP(+) cells were abundant in tissue surrounding the cannula compared to the contralateral hemisphere, whereas lectin(+) cells were restricted to the wound boundary. CMR(glc) fell 25% in regions enriched in reactive astrocytes compared to the homologous contralateral hemisphere, whereas [14C]acetate uptake increased slightly (6%) but statistically significantly; metabolism of both tracers in 13 other brain structures was unchanged. Injection of basic fibroblast growth factor (b-FGF) into cerebral cortex or superior colliculus produced fiber-rich cell clusters containing both GFAP(+) and lectin(+) cells that had a 37% increase in [14C]acetate uptake; GFAP(+)-cell density rose in the nearby neuropil but the corresponding change in [14C]acetate uptake was small (6-8%). Sensory stimulation did not alter [14C]acetate uptake into the clusters. Thus, [14C]acetate uptake was relatively stable with respect to changes in the density of reactive astrocytes that are dispersed throughout the neuropil and to changes in cellular activity arising from sensory stimulation. In contrast, b-FGF-induced cell clusters that contain mixed cell types and numerous fibers accumulated higher levels of [14C]acetate, raising the possibility that increased uptake might be due to high numbers of activated astrocytes and, perhaps, acetate metabolism by other cell types.

Acetates↗
PubMed2001

Comparison of soluble and immobilized acetate for removing Pb from contaminated soil.

Five lead (Pb) contaminated soils were used in a laboratory and modeling study to examine the effects of soluble and immobilized acetate on Pb removal from a contaminated soil as a function of pH. Soluble acetate was added as sodium acetate; immobilized acetate was added in the form of a cation exchange resin. For comparative purposes, Pb adsorption with no acetate also was measured as a function of pH. A surface complexation modeling framework was used to interpret experimental data. Experimental results showed the cation exchange resin was much more effective than soluble acetate in removing Pb from soils due to a strong affinity of the resin for Pb. In addition, concentrations of soluble Pb in resin/soil slurry were very low, minimizing the pollution threat if discharged. As deduced from modeling studies, soluble acetate performed poorly compared to the resin, in part, due to adsorption of the soluble PbAc(+) complex. The effectiveness of both soluble and immobilized acetate was diminished below pH 4 as a result of competition by H(+) for acetate. Modeling results based on resin affinity for Pb compare well with experimental data for resin/soil mixtures, suggesting that Pb partitioning in resin/soil mixtures may be predicted reasonably well if soil/Pb and resin/Pb partitioning are known. Thus, the modeling approach may be used as a screening tool to determine the performance of alternative resins.

Acetates↗
PubMed2006

Effects of oral glatiramer acetate on clinical and MRI-monitored disease activity in patients with relapsing multiple sclerosis: a multicentre, double-blind, randomised, placebo-controlled study.

BACKGROUND: Parenterally administered glatiramer acetate reduces the frequency of relapses and the formation of active brain lesions seen with MRI in multiple sclerosis. This study assessed whether two doses of glatiramer acetate given orally could improve clinical and MRI measures of inflammation and neurodegeneration in a large cohort of patients with relapsing-remitting multiple sclerosis. METHODS: 1912 patients with relapsing-remitting multiple sclerosis were screened and 1651 were randomised to receive 50 mg or 5 mg of glatiramer acetate or placebo by daily oral administration over 14 months. The intention-to-treat cohort consisted of 1644 patients who took at least one dose of study medication (50 mg glatiramer acetate [n=543], 5 mg glatiramer acetate [n=553], placebo [n=548]). After baseline investigation, clinical assessments were done every 2 months and MRI was obtained for all patients at baseline and at study exit. Additionally, MRI was undertaken every 2 months for a cohort of 486 patients. The primary outcome was the total number of confirmed relapses observed during the study period. Several prespecified clinical and MRI secondary and tertiary outcomes assessed treatment efficacy on inflammation and neurodegeneration due to multiple sclerosis. FINDINGS: The cumulative number of confirmed relapses did not differ between the two active treatment groups and the placebo group. Relative to placebo, the rate ratio for the 50 mg glatiramer acetate treated group was 0.92 (95% CI 0.77-1.08, p=0.30) and for the 5 mg glatiramer acetate treated group was 0.98 (0.83-1.15, p=0.76). No drug effect was seen for any of the secondary and tertiary endpoints. The study drug was safe and well tolerated. INTERPRETATION: 5 mg and 50 mg glatiramer acetate administered orally on a daily basis do not affect relapse rate or other clinical and MRI parameters of disease activity and burden in patients with relapsing-remitting multiple sclerosis. Treatment with oral formulations of glatiramer acetate at the doses tested cannot be recommended.

Administration, Oral↗
PubMed2005

Production of electricity from acetate or butyrate using a single-chamber microbial fuel cell.

Hydrogen can be recovered by fermentation of organic material rich in carbohydrates, but much of the organic matter remains in the form of acetate and butyrate. An alternative to methane production from this organic matter is the direct generation of electricity in a microbial fuel cell (MFC). Electricity generation using a single-chambered MFC was examined using acetate or butyrate. Power generated with acetate (800 mg/L) (506 mW/m2 or 12.7 mW/ L) was up to 66% higher than that fed with butyrate (1000 mg/L) (305 mW/m2 or 7.6 mW/L), demonstrating that acetate is a preferred aqueous substrate for electricity generation in MFCs. Power output as a function of substrate concentration was well described by saturation kinetics, although maximum power densities varied with the circuit load. Maximum power densities and half-saturation constants were Pmax = 661 mW/m2 and Ks = 141 mg/L for acetate (218 ohms) and Pmax = 349 mW/m2 and Ks = 93 mg/L for butyrate (1000 ohms). Similar open circuit potentials were obtained in using acetate (798 mV) or butyrate (795 mV). Current densities measured for stable power outputwere higher for acetate (2.2 A/m2) than those measured in MFCs using butyrate (0.77 A/m2). Cyclic voltammograms suggested that the main mechanism of power production in these batch tests was by direct transfer of electrons to the electrode by bacteria growing on the electrode and not by bacteria-produced mediators. Coulombic efficiencies and overall energy recovery were 10-31 and 3-7% for acetate and 8-15 and 2-5% for butyrate, indicating substantial electron and energy losses to processes other than electricity generation. These results demonstrate that electricity generation is possible from soluble fermentation end products such as acetate and butyrate, but energy recoveries should be increased to improve the overall process performance.

Acetates↗
PubMed2001

Butyl acetate and yeasts interact in adhesion and germination of Botrytis cinerea conidia in vitro and in fungal decay of golden delicious apple.

Butyl acetate is a volatile aroma and flavor compound in apple. Conidia of three strains of Botrytis cinerea, a fungus that causes decay of apple fruit in postharvest storage, had greater adhesion to and greater germination on polycarbonate membrane filters on water inside sealed 500 cc glass jars that were injected with 4 microliters butyl acetate than conidia not so exposed. Conidial germination was highly correlated with conidial adhesion. The yeasts Sporobolomyces roseus and Cryptococcus laurentii, but not Saccharomyces cerevisiae, reduced the adhesion and germination promoting effect of butyl acetate. Conidia did not readily utilize butyl acetate as a food source, as shown by lack of tetrazolium violet reduction, whereas S. roseus and C. laurentii, but not S. cerevisiae did. Butyl acetate added to suspensions of conidia increased the electrical conductivity of the suspensions and increased the loss of 14C from 14C-labeled conidia compared to conidia unexposed to butyl acetate. Uptake of [14C]glucose by conidia was not increased by butyl acetate. Wounds of Golden Delicious apples inoculated with conidia (strain F-J-4) in a dilute solution of butyl acetate had greater decay than unexposed wounds. S. roseus and C. laurentii, but not S. cerevisiae, added with the conidia decreased the incidence or size of decay. Results indicated that butyl acetate increased conidial adhesion, stimulating conidial germination, and some yeasts can reduce this effect.

Acetates↗
PubMed1987

Acetate relaxation of isolated vascular smooth muscle.

The vasorelaxant effects of acetate in arginine vasopressin (AVP)-contracted rat tail artery strips were examined in order to study mechanism of action. Dose-dependent relaxation by acetate was found in the clinically important range of 4 to 16 mM. Relaxation was not due to complexing of ionized calcium, persisted after mechanical removal of the endothelium, and was not altered by pretreatment with indomethacin. Although acetate also inhibited contraction by alpha-1 and alpha-2 agonists, the relaxant effect was not altered by destruction of sympathetic nerve terminals using 6-hydroxydopamine. The degree of relaxation in this model by various anions correlated with their lyotropic properties; however, the vasorelaxant effect of acetate exceeded that which would be expected on the basis of its position in the lyotropic series. The vasorelaxant effect of acetate was shared by other short-chain fatty acids that can be conjugated with coenzyme A (CoA), such as propionate and malonate. In contrast, a much lesser or absent relaxant effect was found with nonfatty-acid precursors of acetyl CoA, such as pyruvate, lactate, and alanine. The vasorelaxant effect of acetate was abolished by pretreatment with DIDS, an inhibitor of organic anion uptake, suggesting that cellular uptake of acetate is essential to its vasorelaxant action. The results suggest that the relaxant effect of acetate in vascular smooth muscle is non-specific, is not mediated by prostaglandins, does not depend upon the presence of either endothelium or the sympathetic nervous system, and may be due to metabolism of acetate to acetyl CoA with attendant conversion of ATP to AMP.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1988

Effect of gut-derived acetate on oral glucose tolerance in man.

1. Dietary fibre has a moderating impact on glucose metabolism. To test the hypothesis that this effect of fibre may be mediated by its breakdown product acetate, oral glucose tolerance tests were carried out in healthy volunteers with and without acetate. 2. Five subjects received 50 g of glucose orally while taking either acetate (15 mmol every 15 min) by mouth or chloride as control. Oral acetate made no detectable difference to glucose tolerance or to levels of free fatty acids, 3-hydroxybutyrate, lactate, insulin, glucagon and gastric inhibitory polypeptide. 3. The 50 g dose of glucose temporarily depressed acetate levels in blood. This was probably due to an interaction between glucose and acetate in the gastrointestinal lumen as the same effect was seen with 50 g of xylose in three subjects. 4. Plasma acetate concentrations were unaffected by 50 g of oral glucose in one subject when acetate was instilled into the sigmoid colon. 5. It is unlikely that the improvement of glucose tolerance by dietary fibre is mediated by acetate.

3-Hydroxybutyric Acid↗
PubMed1979

Plasma acetate concentrations during canine haemorrhagic shock.

Acetate, pyruvate, lactate and NEFA concentrations, as well as acid-base-parameters were followed during bleeding, stable hypotension and re-infusion in five dogs. Mean arterial blood pressures were kept at 30 mmHg during the shock phase. An increase in acetate concentrations (P less than 0.01) was found in arterial as well as in venous plasma samples. The maximal mean acetate concentration was 0.19 mmol/l (during reinfusion) as compared to 0.06 mmol/l prior to bleeding. There was no difference between arterial and inferior caval venous concentrations. A definite correlation (r = 0.81, P less than 0.02) was found between blood pyruvate and plasma acetate concentrations. There was no correlation between plasma glucose or NEFA and acetate concentrations or between blood excess lactate and plasma acetate. The plasma acetate accumulation was negligible compared to the concomitant lactate accumulation (1:60), and did not contribute to the metabolic acidosis of shock. The correlation between acetate and pyruvate concentrations may indicate that pyruvate is the main substrate of acetate production in hypovolemic shock.

Acetates↗
PubMed1998

Production rate of acetate during colonic fermentation of lactulose: a stable-isotope study in humans.

BACKGROUND: Breath tests are currently used to qualitatively assess colonic fermentation; no quantitative estimations are available for healthy subjects. OBJECTIVE: This study describes a stable-isotope-dilution method to measure acetate production quantitatively from colonic bacterial fermentation. DESIGN: Six volunteers received a primed, constant, intravenous infusion of [1-13C]acetate at a rate of 1.01 +/- 0.04 micromol x kg(-1) x min(-1) for 7 h. They ingested 20 g pure lactulose after 1 h of the tracer infusion. Expired air and arterialized venous blood were sampled every 15 min. RESULTS: Before lactulose intake, the breath-hydrogen concentration was 7 +/- 2 ppm and the plasma acetate concentration and isotopic enrichment were 141 +/- 14 micromol/L and 14.8 +/- 1.4 moles percent excess, respectively. Whole-body acetate turnover was 6.0 +/- 0.7 micromol x kg(-1) x min(-1). After lactulose ingestion, maximum breath hydrogen and acetate concentrations reached 63 +/- 15 ppm (P = 0.004) and 313 +/- 25 micromol/L (P = 0.002), respectively, whereas [13C]acetate enrichment decreased to 9.9 +/- 1.3 moles percent excess (P = 0.03). Whole-body acetate turnover increased to 9.8 +/- 1.5 micromol x kg(-1) x min(-1) and later decreased almost to baseline values. Colonic lactulose fermentation yielded 140 +/- 12 mmol acetate over 6 h, representing 86% of the production based on stoichiometric equations. CONCLUSION: This new method provides a quantitative estimate of colonic carbohydrate fermentation via evaluation of acetate production.

Acetates↗
PubMed2000

Acetic acid suppresses the increase in disaccharidase activity that occurs during culture of caco-2 cells.

To understand how blood glucose level is lowered by oral administration of vinegar, we examined effects of acetic acid on glucose transport and disaccharidase activity in Caco-2 cells. Cells were cultured for 15 d in a medium containing 5 mmol/L of acetic acid. This chronic treatment did not affect cell growth or viability, and furthermore, apoptotic cell death was not observed. Glucose transport, evaluated with a nonmetabolizable substrate, 3-O-methyl glucose, also was not affected. However, the increase of sucrase activity observed in control cells (no acetic acid) was significantly suppressed by acetic acid (P < 0.01). Acetic acid suppressed sucrase activity in concentration- and time-dependent manners. Similar treatments (5 mmol/L and 15 d) with other organic acids such as citric, succinic, L-maric, L-lactic, L-tartaric and itaconic acids, did not suppress the increase in sucrase activity. Acetic acid treatment (5 mmol/L and 15 d) significantly decreased the activities of disaccharidases (sucrase, maltase, trehalase and lactase) and angiotensin-I-converting enzyme, whereas the activities of other hydrolases (alkaline phosphatase, aminopeptidase-N, dipeptidylpeptidase-IV and gamma-glutamyltranspeptidase) were not affected. To understand mechanisms underlying the suppression of disaccharidase activity by acetic acid, Northern and Western analyses of the sucrase-isomaltase complex were performed. Acetic acid did not affect the de novo synthesis of this complex at either the transcriptional or translational levels. The antihyperglycemic effect of acetic acid may be partially due to the suppression of disaccharidase activity. This suppression seems to occur during the post-translational processing.

Acetic Acid↗
PubMed2001

Acetic acid feeding enhances glycogen repletion in liver and skeletal muscle of rats.

To investigate the efficacy of the ingestion of vinegar in aiding recovery from fatigue, we examined the effect of dietary acetic acid, the main component of vinegar, on glycogen repletion in rats. Rats were allowed access to a commercial diet twice daily for 6 d. After 15 h of food deprivation, they were either killed immediately or given 2 g of a diet containing 0 (control), 0.1, 0.2 or 0.4 g acetic acid/100 g diet for 2 h. The 0.2 g acetic acid group had significantly greater liver and gastrocnemius muscle glycogen concentration than the control group (P < 0.05). The concentrations of citrate in this group in both the liver and skeletal muscles were >1.3-fold greater than in the control group (P > 0.1). In liver, the concentration of xylulose-5-phosphate in the control group was significantly higher than in the 0.2 and 0.4 g acetic acid groups (P < 0.01). In gastrocnemius muscle, the concentration of glucose-6-phosphate in the control group was significantly lower and the ratio of fructose-1,6-bisphosphate/fructose-6-phosphate was significantly higher than in the 0.2 g acetic acid group (P < 0.05). This ratio in the soleus muscle of the acetic acid fed groups was <0.8-fold that of the control group (P > 0.1). In liver, acetic acid may activate gluconeogenesis and inactivate glycolysis through inactivation of fructose-2,6-bisphosphate synthesis due to suppression of xylulose-5-phosphate accumulation. In skeletal muscle, acetic acid may inhibit glycolysis by suppression of phosphofructokinase-1 activity. We conclude that a diet containing acetic acid may enhance glycogen repletion in liver and skeletal muscle.

Acetic Acid↗
PubMed2001

Comparison of histological compositions and apoptosis in canine spontaneous benign prostatic hyperplasia treated with androgen suppressive agents chlormadinone acetate and finasteride.

PURPOSE: Chlormadinone acetate and finasteride are androgen suppressive agents clinically used for benign prostatic hyperplasia but their mechanism for inducing prostatic atrophy differs. We investigated the effect of these androgen suppressive agents on prostatic histology and apoptosis using the spontaneous canine benign prostatic hyperplasia model. MATERIALS AND METHODS: Animals were treated with oral chlormadinone acetate or finasteride for 25 weeks. The prostatic volumes were analyzed every 5 weeks. Prostatic androgen and estrogen concentrations, histological composition and apoptosis were determined at the end of treatment. Apoptosis was measured by in situ labeling of 3' hydroxy ends of the DNA breaks using the terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labeling method. RESULTS: There was a similar volume reduction effect with 0.3 mg./kg. chlormadinone acetate daily and 1 mg./kg. finasteride daily. Chlormadinone acetate decreased testosterone and dihydrotestosterone but finasteride decreased only dihydrotestosterone in the prostate gland. The concentration ratio of estradiol-to-total androgen in the prostate was significantly increased in finasteride treated canines. Chlormadinone acetate and finasteride decreased the epithelial and stromal components. The extent of apoptosis observed in the prostate was significantly higher in the chlormadinone acetate group compared to that of the control and finasteride groups. CONCLUSIONS: Although a similar effect of chlormadinone acetate and finasteride was observed in the induction of prostatic regression and composition of the histological components, the sustained increase in apoptosis was observed only in chlormadinone acetate treated canines. We suggest that different intraprostatic endocrine environments created by chlormadinone acetate or finasteride, which have different intraprostatic testosterone levels and estradiol-to-androgen ratios, may be responsible for the different outcomes in the extent of apoptosis.

Androgen Antagonists↗
PubMed1998

Validation of the [1,2-13C]acetate recovery factor for correction of [U-13C]palmitate oxidation rates in humans.

1. The validity of estimations of plasma fatty acid oxidation using tracers has often been questioned. The appearance of isotopic markers in breath CO2 is delayed and incomplete. Recently suggestions have been made that substantial amounts of tracer are incorporated into products of the tricarboxylic acid cycle (e.g. glucose, glutamine and glutamate) and that an acetate correction factor can be used to correct for tracer fixation. In the present study we investigated whether the appearance of 13CO2 during a separate infusion of [1,2-13C]acetate could be used for correction of [U-13C]palmitate oxidation rates in studies lasting <2 h and we quantified the appearance of tracer in the glutamine, glutamate and glucose pools of the body. 2. An infusion of either [1,2-13C]acetate (0.104 micromol min-1 kg-1) or [U-13C]palmitate (0.013 micromol min-1 kg-1) was given to eight male subjects and continued for 2 h at rest. In six subjects the infusion of [1,2-13C]acetate was repeated to determine reproducibility of the acetate recovery. 3. Fractional recovery in breath from [1,2-13C]acetate gradually increased during the infusion period at rest from 14.1 +/- 0.6% at 60 min to 26.5 +/- 0.5% at 120 min after the start of the infusion. Intersubject coefficient of variance was 8.3 +/- 0.6% and intrasubject coefficient of variance of the acetate recovery tests was 4.0 +/- 1.5%. After 2 h of [1,2-13C]acetate infusion, 12.4 +/- 0.8 and 10.3 +/- 0.9% of infused 13C was incorporated in the glutamine and glutamate pools, respectively. 4. In conclusion, the [1,2-13C]acetate recovery factor can be used for correcting the rate of [U-13C]palmitate oxidation in infusing studies of 2 h in resting conditions. Failure to use this recovery factor leads to a substantial underestimation of the rate of plasma free fatty acid oxidation. The extent of label fixation could largely be explained by accumulation of tracer carbon in glutamine and glutamate, and the accumulation in glucose is negligible.

Acetates↗
PubMed1995

Ethanol inhibits acetate metabolism in rat hepatocytes.

The metabolism of acetate at concentrations of 1, 2.5, 5 and 10 mM was investigated in freshly isolated hepatocytes from 48 hr fasted, female rats in the absence and presence of 10 mM ethanol. The maximal capacity for acetate metabolism was 0.85 mumol/(10(8) cells.min). Ethanol caused a 20% decrease in the apparent Vmax for acetate metabolism and an increase in the apparent Km for acetate from 3.0 to 4.6 mM. At physiological concentration of acetate (approximately 1 mM) and in the absence of an inhibitory effect of ethanol, the capacity for acetate metabolism was 15-20% of the rate of acetate formation from ethanol and the inhibitory effect of ethanol further reduced it to 10-15%. The results thus explain the well-known but hitherto not understood fact that only a small fraction of acetate produced in the liver during ethanol oxidation is further metabolized by the liver, while the majority is exported for oxidation in other tissues. Finally, a new method for calculation of liver acetate uptake in the presence of ethanol is presented.

Acetates↗
PubMed1977

Influence of acetate on the metabolism of palmitate in the perfused hind-quarter of the rat.

The metabolism of 1-14C-palmitate and its metabolic interaction with U-14C-acetate were studied in the perfused hind-quarter of the rat. 9% of 1-14C-palmitate taken up was oxidized to 14CO2 accounting for 7% of total oxygen consumption by the perfused tissue. Most label from 1-14C-palmitate was found in the lipid fraction of the muscle tissue. In spite of a 40% inhibition of palmitate oxidation, acetate only caused minor changes in the overall metabolism of palmitate. U-14C-acetate was mainly oxidized to 14CO2 and the oxygen consumption due to oxidation of acetate accounted for 20-30% of the total oxygen uptake. Minor amounts of 14C-acetate were found in muscle lipids. The addition of palmitate did not alter the metabolism of acetate. It is concluded that the presence of palmitate did not affect 14C-acetate metabolism, while the presence of acetate inhibited 14C-palmitate oxidation. The possible sites of interaction are discussed. The found interaction will probably not contribute to any major extent to the disturbed lipid metabolism found in animals and man during ethanol intake. No major changes in the tissue content of high-energy phosphate compounds were found in the presence of palmitate or acetate or both.

Acetates↗
PubMed1999

Acetate-mediated growth inhibition in sterol 14alpha-demethylation-deficient cells of Candida albicans.

Candida albicans is a fungus thought to be viable in the presence of a deficiency in sterol 14alpha-demethylation. We showed in a strain of this species that the deficiency, caused either by a mutation or by an azole antifungal agent, made the cells susceptible to growth inhibition by acetate included in the culture medium. Studies with a mutant demonstrated that the inhibition was complete at a sodium acetate concentration of 0.24 M (20 g/liter) and was evident even at a pH of 8, the latter result indicating the involvement of acetate ions rather than the undissociated form of acetic acid. In fluconazole-treated cells, sterol profiles determined by thin-layer chromatography revealed that the minimum sterol 14alpha-demethylation-inhibitory concentrations (MDICs) of the drug, thought to be the most important parameter for clinical purposes, were practically identical in the media with and without 0.24 M acetate and were equivalent to the MIC in the acetate-supplemented medium. The acetate-mediated growth inhibition of azole-treated cells was confirmed with two additional strains of C. albicans and four different agents, suggesting the possibility of generalization. From these results, it was surmised that the acetate-containing medium may find use in azole susceptibility testing, for which there is currently no method capable of measuring MDICs directly for those fungi whose viability is not lost as a result of sterol 14alpha-demethylation deficiency. Additionally, the acetate-supplemented agar medium was found to be useful in detecting reversions from sterol 14alpha-demethylation deficiency to proficiency.

Acetates↗
PubMed1996

Pathways of acetate, propionate, and butyrate formation by the human fecal microbial flora.

The pathways of short-chain fatty acid (SCFA; acetate, propionate, and butyrate) formation from glucose were determined for the human fecal microbial communities of two subjects. The pathways were identified by radioisotope analysis of the SCFA and CO2 obtained after incubation of fecal suspensions with glucose under 20% CO2 with [1-14C]glucose, [3,4-14C]glucose, or 14CO2. Acetate was chemically degraded to learn the labeling of the methyl and carboxyl carbons. The labeling of CO2 and acetate showed that the major route of glucose catabolism was the Embden-Meyerhof-Parnas pathway, with production of CO2 from pyruvate carboxyl carbon. Labeling of the methyl and carboxyl carbons of acetate by 14CO2 or [3,4-14C]glucose proved that acetate was formed from CO2 by the Wood-Ljungdahl pathway. CO2 reduction accounted for about one-third of the acetate formed by suspensions from subject 1 and about one-fourth of the acetate formed by suspensions from subject 2. Propionate was formed by a CO2 fixation pathway, and butyrate was formed by classical routes of acetyl-S coenzyme A condensation. The amount of CO2 formed from [1-14C] glucose and acetate labeling patterns obtained with the other 14C precursors indicated that the Entner-Doudoroff, transketolase-transaldolase, and heterolactic pathways were not significant. Fermentation of cabbage cellulose by subject 1 followed the same pathways as were used for glucose. The results with suspensions from subject 2 suggested that some radioactive acetate was formed from the C-3 of glucose by the Bifidobacterium pathway.

Acetates↗