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PubMed1991

Effect of acetate on blood metabolites and glucose tolerance during haemodialysis in uraemic non-diabetic and diabetic subjects.

We examined changes in blood concentrations of glucose, acetate and other blood intermediary metabolites as well as the disposal of an intravenous glucose load during successive glucose-free acetate and control bicarbonate haemodialysis in random order, in non-diabetic and diabetic subjects. Plasma acetate levels increased about 10-fold in both the diabetic and non-diabetic subjects during the 1st hour of acetate dialysis. This was accompanied by about 5-fold increase in the levels of the ketone bodies-acetoacetate and 3-hydroxybutyrate. Ketone body levels did not change during bicarbonate dialysis. Additionally, the changes in blood levels of glucose, non-esterified fatty acids, pyruvate, lactate, glycerol and insulin were similar with either bicarbonate or acetate treatment in each subject group. The KG rate constant of glucose disposal after intravenous glucose (10 g/m2 body surface area) given after the 1st hour of a 5-hour haemodialysis was similarly unchanged with acetate or bicarbonate dialysis, despite the additional caloric load likely from the high blood levels of acetate obtained during acetate haemodialysis. We conclude that the major metabolic effect of acetate during haemodialysis is an increase in blood ketone body levels. Glucose utilisation, as assessed from the KG rate constant of glucose disposal or changes in blood lactate and pyruvate levels, was not affected by the high acetate levels attained during dialysis.

Acetates↗
PubMed1994

Randomized trials of megestrol acetate for AIDS-associated anorexia and cachexia.

Involuntary weight loss is a frequent complication of acquired immune deficiency syndrome (AIDS) and ultimately affects the majority of patients. The deleterious effects of weight loss on immune function and the physical and psychological sequelae of severe weight loss are well recognized. Megestrol acetate induces appetite stimulation and nonfluid weight gain in patients with advanced hormone nonresponsive cancers. In a pilot study, megestrol acetate produced nonfluid weight gain in patients with AIDS. Two double-blind randomized placebo-controlled trials of megestrol acetate for the treatment of AIDS-related anorexia and cachexia have shown improvements in body weight with treatment. In a multicenter trial reported by Flynn et al. at the 7th International Conference on AIDS (1992), 65 patients with AIDS and weight loss of > 10% of ideal body weight were randomized to placebo or megestrol acetate 800 mg/day. Megestrol acetate-treated patients had a significantly greater mean maximum weight gain (p = 0.027) and appetite stimulation (p = 0.021) than did placebo-treated patients. In a second, larger randomized placebo-controlled trial, 271 patients with AIDS, anorexia and cachexia were randomized to receive placebo or multiple doses of megestrol acetate at 100, 400 or 800 mg/day for 12 weeks. A maximum weight gain of at least 5 lb (2.25 kg) was observed in 64.2% of patients in the 800-mg megestrol acetate group compared with 21.4% in the placebo group (p < 0.0001). Mean maximum weight change from baseline to last evaluation was +8.3 lb in the 800-mg group and -1.1 lb in the placebo group (p < 0.001). Mean change in lean body mass from baseline to last evaluation was +2.5 lb in the 800-mg group versus -1.7 lb in the placebo group (p < 0.001). A significant improvement in appetite was seen in patients receiving 800 mg megestrol acetate compared with patients receiving placebo. No significant toxicity was observed with megestrol acetate therapy. Megestrol acetate is an effective treatment for some patients with AIDS-related anorexia and cachexia.

Acquired Immunodeficiency Syndrome↗
PubMed1979

Effect of acetate on hypoglycemic seizures in mice.

In order to determine the effects of acetate on signs and symptoms of hypoglycemic seizures, Swiss Webster albino mice were injected intraperitoneally with solutions of NaCl, NaHCO3, NH4Cl, Na-acetate, or NH4-acetate, followed by subcutaneous injection of 7 U of insulin/kg body wt. Administration of Na- or NH4-acetate delayed and reduced the incidence of hypoglycemic reactions. Reinjection with Na-acetate or repeated injections with NH4-acetate caused a return to normal behavior patterns for 60 and 75%, respectively, of the affected hypoglycemic experimental animals. Injections of control animals with NaHCO3 or NH4Cl showed that the results were not due to alkalosis or acidosis. Acetate administration significantly increased plasma acetate and citrate, but not glucose, lactate, beta-hydroxybutyrate, or acetoacetate concentrations. The results indicate that intraperitoneal administration of acetate directly acted to prevent signs of hypoglycemia from occurring and reversed its manifestations when they were present. The protective effect of acetate suggests that it may serve as a fuel for the brain.

Acetates↗
PubMed1995

Induction of adrenal suppression by megestrol acetate in patients with AIDS.

OBJECTIVE: To investigate the development of secondary adrenal suppression in a patient with the acquired immunodeficiency syndrome (AIDS) who was receiving megestrol acetate. DESIGN AND PATIENTS: Case report of one patient abruptly withdrawn from long-term therapy with megestrol acetate; prospective study of four patients with AIDS who were starting therapy with megestrol acetate for cachexia. SETTING: Outpatient clinic of a university hospital. INTERVENTIONS: Study patients received megestrol acetate, 80 mg three times daily. MEASUREMENTS: Study patients had cosyntropin-stimulation testing and oral glucose tolerance testing before and after starting therapy with megestrol acetate. RESULTS: The patient described in the case report developed symptoms of adrenal insufficiency after withdrawal of megestrol acetate after 4 years of treatment. His basal cortisol and adrenocorticotropic hormone (ACTH) levels were low. He showed an abnormally diminished response to a short cosyntropin-stimulation test but did respond to a 3-day cosyntropin-stimulation test. The morning cortisol levels of the study patients decreased significantly (from 11.0 +/- 1.8 micrograms/dL to 1.5 +/- 0.9 micrograms/dL; P < 0.01), and the ACTH levels of these patients decreased to below normal (from 16.6 +/- 5.5 pg/mL to 6.3 +/- 3.3 pg/mL; P = 0.02) during treatment with megestrol acetate. Cortisol levels after administration of cosyntropin decreased significantly (from 27.3 +/- 3.3 pg/mL to 9.3 +/- 6.3 pg/mL; P = 0.01) during treatment with megestrol acetate. The results of oral glucose tolerance testing in two patients were consistent with the development of insulin resistance, and daily insulin requirements increased 10-fold in a patient who had preexisting diabetes. CONCLUSIONS: Prolonged administration of megestrol acetate can induce clinically significant secondary adrenal suppression, and abrupt withdrawal of megestrol acetate after prolonged administration can cause adrenal insufficiency.

Acquired Immunodeficiency Syndrome↗
PubMed2002

11C-acetate PET imaging of prostate cancer.

UNLABELLED: 11C-Acetate can act as a probe of tissue metabolism through entry into catabolic or anabolic metabolic pathways as mediated by acetyl-coenzyme A. The uptake of (11)C-acetate in prostate cancer was investigated to determine whether this tracer has potential in tumor identification. METHODS: Twenty-two patients with prostate cancer underwent PET after intravenous administration of 740 MBq (11)C-acetate. Eighteen of the 22 patients were also investigated with (18)F-FDG PET. Standardized uptake values (SUVs) for each tumor were investigated for tracer activity at 10-20 min after (11)C-acetate and 40-60 min after (18)F-FDG administration. RESULTS: Adenocarcinoma of the prostate showed variable uptake of (11)C-acetate, with SUVs ranging from 3.27 to 9.87. In contrast, SUVs for (18)F-FDG ranged from 1.97 to 6.34. By visual inspection, (11)C-acetate accumulation in primary prostate tumors was positive in all patients, whereas (18)F-FDG accumulation was positive in only 15 of 18 patients. (11)C-Acetate PET in a patient with lymph node metastasis showed high intrapelvic accumulation corresponding to metastatic sites. Similarly, 2 patients with bone metastases were (11)C-acetate avid. CONCLUSION: (11)C-Acetate shows marked uptake in prostate cancer and is more sensitive in detection of prostate cancer than is (18)F-FDG PET. (11)C-Acetate represents a new tracer for detection of prostate cancer with PET, measuring radiopharmaceutical uptake pathways that are different from those measured by (18)F-FDG.

Acetates↗
PubMed1990

[Vapor-phase gas chromatographic determination of acetate in the blood].

The suggested gas chromatographic vapor phase analysis of the blood for the direct determination of the blood acetate concentration is performed with Soviet equipment and is based on expulsion of acetic acid from its salts and other derivatives after addition of potassium bisulfate and heating of the blood sample at +105 degrees C for an hour in a hermetically sealed flask. To directly measure acetate, a certain vapor phase volume is let into the gas chromatographic evaporator after equal distribution of acetate in the gas and liquid phases is achieved. This method was used to measure the blood acetate levels in the patients with renal insufficiency treated by hemodialysis. The total content of the blood acetate in health is 1.6 +/- 0.3 mmol/l; this value essentially grows in acetate hemodialysis. In some patients acetate levels persist increased between the dialysis courses. The suggested method may be useful for monitoring the blood acetate levels in the patients treated with hemodialysis and for the detection of subjects with acetate intolerance.

Acetates↗
PubMed1986

The acid-base status does not influence the rate of acetate metabolism in hemodialyzed patients.

The present study was undertaken to evaluate whether the acid-base status influences the rate of acetate metabolism in patients chronically hemodialyzed against acetate. Ten patients (5 "intolerant" and 5 "tolerant" to acetate) received in a randomized order and for three consecutive dialyses each of the six following infusions in the venous line of the dialyzer: NaHCO3 (22, 44 or 88 mEq/h), NaCl (22 or 44 mEq/h) or Dextrose 5% in water (30 mmol/h). Plasma acetate was measured at the end of the dialysis. Bicarbonate infusions increased significantly blood pH and plasma bicarbonate but did not change the plasma acetate concentration at the end of dialysis. We conclude that the rate of acetate metabolism is not modified by changes in the acid-base status within the range usually observed in hemodialyzed patients. A significant hypoxemia per dialysis was noted only in AT patients with lower plasma acetate and rapid acetate metabolism. We conclude that acetate metabolism (and not plasma acetate concentration) plays a significant role in dialysis-induced hypoxemia.

Acetates↗
PubMed1994

Effects of chlormadinone acetate, acetazolamide and oxygen on awake and asleep gas exchange in patients with chronic obstructive pulmonary disease (COPD).

The purpose of this study was to assess the short-term effects of chlormadinone acetate (CMA), a synthetic progestogen, acetazolamide (ACET) and oxygen on awake and asleep blood gas values. The study was conducted according to a randomized, double-blind and placebo-controlled design in 53 hypoxaemic patients with chronic obstructive pulmonary disease. On the first two consecutive nights, all patients received either room air or oxygen, via a nasal cannula, in random order. They then received either CMA (25 mg), ACET (250 mg) or placebo twice a day, all in identical capsules. On the third study night, after one week of drug treatment, the patients were tested breathing room air. CMA and ACET therapy decreased mean daytime arterial carbon dioxide tension (PaCO2) by 0.7 and 0.5 kPa, respectively, and night-time end-tidal carbon dioxide tension (PETCO2) by 0.5 and 0.3 kPa, respectively. Supplemental oxygen caused increased CO2 retention during the day and night (0.6 and 0.3 kPa, respectively. Daytime arterial oxygen tension (PaO2) increased to the same extent during ACET (1.9 kPa) and oxygen (2.5 kPa). Asleep oxygen saturation improved most with oxygen supplementation (7%), although ACET also caused significant improvement (4%). CMA administration had virtually no effect on mean awake and asleep hypoxaemia. ACET therapy significantly improved subjective sleep quality. On CMA, minute ventilation increased in association with an augmentation of the hypercapnic ventilatory response. ACET treatment increased both hypercapnic and hypoxic ventilatory responses. We conclude from the group of patients with COPD studied, that the short-term effects of ACET treatment on gas exchange compare favourably with those of CMA. Oxygen therapy improves oxygenation slightly more than ACET, but aggravates CO2 retention.

Acetazolamide↗
PubMed1987

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

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

Acetate Kinase↗
PubMed2004

Zuclopenthixol acetate for acute schizophrenia and similar serious mental illnesses.

BACKGROUND: Medication used for acute aggression in psychiatry must have rapid onset of effect, low frequency of administration and low levels of adverse effects. Zuclopenthixol acetate is said to have these properties. OBJECTIVES: To estimate the clinical effects of zuclopenthixol acetate for the management of acute aggression or violence thought to be due to serious mental illnesses, in comparison to other drugs used to treat similar conditions. SEARCH STRATEGY: We supplemented past searches of Current Controlled Trials (10/2000), the Cochrane Library (1997) and MEDLINE (1966-1997) and appeals for unpublished data with an update search of the Cochrane Schizophrenia Group's Register of trials (September 2003). SELECTION CRITERIA: All randomised clinical trials involving people thought to have serious mental illnesses comparing zuclopenthixol acetate with other drugs. DATA COLLECTION AND ANALYSIS: Data were extracted independently by two reviewers and cross-checked. We calculated fixed effects relative risks (RR) and 95% confidence intervals (CI) for dichotomous data. Where possible, the number needed to treat/harm statistic (NNT/H) was calculated. We analyzed by intention-to-treat. Mean differences were used for continuous variables. MAIN RESULTS: We found no data for the primary outcome, tranquilisation. Compared with haloperidol, zuclopenthixol acetate was no more sedating at two hours (n=40, 1 RCT, RR 0.60 CI 0.27 to 1.34). People given zuclopenthixol acetate were not at reduced risk of being given supplementary antipsychotics (n=134, 3 RCTs, RR 1.49 CI 0.97 to 2.30) although additional use of benzodiazepines was less (n=50, 1 RCT, RR 0.03 CI 0.00 to 0.47, NNT 2 CI 2 to 4). People given zuclopenthixol acetate had fewer injections over seven days compared with those allocated to haloperidol IM (n=70, 1 RCT, RR 0.39 CI 0.18 to 0.84, NNT 4 CI 3 to 14). We found no data on more episodes of aggression or harm to self or others. One trial (n=148) reported no significant difference in adverse effects for people receiving zuclopenthixol acetate compared with those allocated haloperidol at one, three and six days (RR 0.74 CI 0.43 to 1.27). Compared with haloperidol or clotiapine, people allocated zuclopenthixol did not seem to be at more risk of a range of movement disorders (<20%). Three studies found no difference in the proportion of people getting blurred vision/ dry mouth (n=192, 2 RCTs, RR at 24 hours 0.90 CI 0.48 to 1.70). Similarly dizziness was equally infrequent for those allocated zuclopenthixol acetate compared with haloperidol (n=192, 2 RCTs, RR at 24 hours 1.15 CI 0.46 to 2.88). There was no difference between treatments for leaving the study before completion (n=522, RR 0.85 CI 0.31 to 2.31). REVIEWERS' CONCLUSIONS: Recommendations on the use of zuclopenthixol acetate for the management of psychiatric emergencies in preference to 'standard' treatment have to be viewed with caution. Most trials present important methodological flaws and findings are poorly reported. This review did not find any suggestion that zuclopenthixol acetate is more or less effective in controlling aggressive acute psychosis, or in preventing adverse effects than intramuscular haloperidol, and neither seemed to have a rapid onset of action. Well-conducted pragmatic randomised controlled trials are needed.

Acute Disease↗
PubMed1997

Studies of the esterase activity of cytosolic aldehyde dehydrogenase with resorufin acetate as substrate.

Resorufin acetate is a very good substrate for sheep liver cytosolic aldehyde dehydrogenase, both from the point of view of practical spectrophotometry and in terms of information provided about the nature of the catalysis shown by this enzyme. p-Nitrophenyl (PNP) acetate competes against resorufin acetate for the enzyme's active site (although relatively weakly as the latter substrate has the lower Michaelis constant), but acetaldehyde (in the presence of NAD+) inhibits the hydrolysis of resorufin acetate only at very high aldehyde concentration. In the absence of cofactor, the rate-limiting step in the hydrolysis of resorufin acetate and of PNP acetate is hydrolysis of the common acetyl-enzyme, as shown by the observation of bursts of chromophoric product and very similar values of kcat. In the presence of NAD+ or NADH, however, the deacylation step with resorufin acetate is greatly accelerated until acylation seems to become rate-limiting, because no burst is seen under these conditions. Millimolar concentrations of Mg2+ activate the hydrolyis of resorufin acetate both in the presence and absence of cofactors. With both Mg2+ and cofactor the kcat for hydrolysis of resorufin acetate is 30-35 s-1; this is three orders of magnitude higher than the kcat for aldehyde oxidation in the presence of Mg2+, showing that the enzyme's potential catalytic efficency is very much hampered by the slowness with which NADH dissociates from its binding site. The pH profile for the hydrolysis of resorufin acetate in the presence of NAD+ or NADH fits well to a theoretical ionization curve of pKa approx. 8.2; it is suggested that this might belong to the enzyme's putative catalytic residue (Cys-302).

Aldehyde Dehydrogenase↗
PubMed2001

Mode-of-action-based dosimeters for interspecies extrapolation of vinyl acetate inhalation risk.

Vinyl acetate is used in the manufacture of many polymers. The Clean Air Act Amendments of 1990 require that an inhalation risk assessment be conducted to assess risks to human health from ambient exposures. Vinyl acetate is a nasal carcinogen in rats and induces olfactory degeneration in rats and mice. Because of the many unique aspects of the rodent nasal cavity compared to that of humans, conventional means for extrapolating dosimetry between species are not appropriate. Physiologically based pharmacokinetic (PBPK) and pharmacodynamic (PD) modeling can address many of these unique aspects. A PBPK/PD model has been developed for vinyl acetate, but the choice of appropriate dosimeter(s) to use for interspecies extrapolation depends on a hypothesis regarding mode of action. This article summarizes the key studies that formulate a mode of action hypothesis for vinyl acetate. Dose-response relationships for vinyl acetate-induced nonneoplastic and neoplastic responses are highly nonlinear, suggesting complex kinetic processes. Carboxylesterase-dependent metabolism of vinyl acetate forms acetic acid, a potent cytotoxicant, and acetaldehyde, a weak clastogen. Cell death, proposed to be the result of intracellular acidification, results in restorative cell proliferation. In conjunction with sufficient genetic damage, induced by spontaneous mutation and acetaldehyde-induced DNA-protein cross-links (DPX), olfactory degeneration progresses to a state of elevated proliferation and eventually, at high vinyl acetate concentrations, to neoplastic transformation. Thus, reduction in intracellular pH (pHi) is proposed as the dosimeter most closely linked to the earliest stages of vinyl acetate toxicity. Consequently, risk assessments that are based on protection of nasal epithelium from intracellular acidification will be protective of all subsequent pathological responses related to vinyl acetate exposure. Proposing a reasonable mode of action is an important step in any risk assessment and is critical to the choice of dosimeter(s) to be used for interspecies dosimetry extrapolation.

Animals↗
PubMed2002

Final report on the safety assessment of ethoxyethanol and ethoxyethanol acetate.

Ethoxyethanol is an ether alcohol described as a solvent and viscosity-decreasing agent for use in cosmetics. Ethoxyethanol Acetate is the ester of Ethoxyethanol and acetic acid described as a solvent for use in cosmetics. Although these ingredients have been used in the past, neither ingredient is in current use. Ethoxyethanol is produced by reacting ethylene oxide with ethyl alcohol. Ethoxyethanol Acetate is produced via an esterification of Ethoxyethanol and acetic acid, acetic acid anhydride, or acetic chloride. Ethoxyethanol is metabolized to ethoxyacetaldehyde, which is further metabolized to ethoxyacetic acid, which is also a metabolite of Ethoxyethanol Acetate. Low to moderate acute inhalation toxicity is seen in animals studies. Acute oral toxicity studies in several species reported kidney damage, including extreme tubular degeneration. Kidney damage was also seen in acute dermal toxicity studies in rats and rabbits. Minor liver and kidney damage was also seen in short-term studies of rats injected subcutaneously with Ethoxyethanol, but was absent in dogs dosed intravenously. Mixed toxicity results were also seen in subchronic tests in mice and rats. Ethoxyethanol and Ethoxyethanol Acetate were mild to moderate eye irritants in rabbits; mild skin irritants in rabbits, and nonsensitizing in guinea pigs. Most genotoxicity tests were negative, but chromosome aberrations and sister-chromatid exchanges were among the positive results seen. Numerous reproductive and developmental toxicity studies, across several species, involving various routes of administration, indicate that Ethoxyethanol and Ethoxyethanol Acetate are reproductive toxicants and teratogens. Mild anemia was reported in individuals exposed occupationally to Ethoxyethanol, which resolved when the chemical was not used. Reproductive effects have been noted in males exposed occupationally to Ethoxyethanol. Although there are insufficient data to determine the potential carcinogenic effects of Ethoxyethanol or Ethoxyethanol Acetate, there is evidence that these chemicals are absorbed across human skin and that they are reproductive and developmental toxicants via dermal exposure. Therefore, these ingredients are unsafe for use in cosmetic formulations.

Abnormalities, Drug-Induced↗
PubMed2002

Vinyl acetate-induced intracellular acidification: implications for risk assessment.

Cancerbioassays have demonstrated the carcinogenic activity of vinyl acetate in rodents. Tumors appear only at the site of contact and mechanistic data suggest that the carcinogenic mechanism involves carboxylesterase-mediated metabolism of vinyl acetate to acetic acid. It has been hypothesized that intracellular formation of acetate causes a reduction of intracellular pH (pH(i)) at noncytotoxic levels, but that prolonged exposure to reduced pH(i) is cytotoxic and/or mitogenic and drives proliferative responses. Coupled with exposure to metabolically formed acetaldehyde at high administered concentrations, nonlinear dose-response curves for epithelial tumors are produced. Freshly isolated rat hepatocytes were used as a model system to test the concept that exposure of cells to vinyl acetate causes a reduction in pH(i). Quantitative fluorescence imaging ratio microscopy showed that exposure of hepatocytes to vinyl acetate concentrations ranging from 10 to 1000 microM caused rapid and sustained reductions of approximately 0.03 to 0.65 pH units. Cellular acidification was rapidly reversed to control pH(i) upon removal of vinyl acetate. There was minimal accumulation of protons during the exposure period, as suggested by minor differences in pH(i) of cells with or without prior exposure to vinyl acetate. The effect of vinyl acetate on pH(i) was attenuated by prior exposure to the carboxylesterase inhibitor bis(p-nitrophenyl)phosphate. These results support the concept that intracellular acidification is a sentinel pharmacodynamic response of cells to vinyl acetate exposure and that pH(i) is an appropriate metric dose for use in quantitative risk assessments of cancer and noncancer human health risk assessment.

Animals↗
PubMed1986

Fermentative Metabolism of Chlamydomonas reinhardii: III. Photoassimilation of Acetate.

The anaerobic photodissimilation of acetate by Chlamydomonas reinhardii F-60 adapted to a hydrogen metabolism was studied utilizing manometric and isotopic techniques. The rate of photoanaerobic (N(2)) acetate uptake was approximately 20 mumoles per milligram chlorophyll per hour or one-half that of the photoaerobic (air) rate. Under N(2), cells produced 1.7 moles H(2) and 0.8 mole CO(2) per mole of acetate consumed. Gas production and acetate uptake were inhibited by monofluoroacetic acid (MFA), 3-(3',4'-dichlorophenyl)-1,1-dimethylurea (DCMU) and by H(2). Acetate uptake was inhibited about 50% by 5% H(2) (95% N(2)). H(2) in the presence of MFA or DCMU stimulated acetate uptake and the result was interpreted to indicate a transition from oxidative to reductive metabolism. Carbon-14 from both [1-(14)C]- and [2-(14)C]acetate was incorporated under N(2) or H(2) into CO(2), lipids, and carbohydrates. The methyl carbon of acetate accumulated principally (75-80%) in the lipid and carbohydrate fractions, whereas the carboxyl carbon contributed isotope primarily to CO(2) (56%) in N(2). The presence of H(2) caused a decrease in carbon lost from the cell as CO(2) and a greater proportion of the acetate was incorporated into lipid. The results support the occurrence of anaerobic and light-dependent citric acid and glyoxylate cycles which affect the conversion of acetate to CO(2) and H(2) prior to its conversion to cellular material.

Journal Article↗
PubMed1999

Anaerobic conversion of carbon dioxide to methane, acetate and propionate on washed rice roots.

Washed excised roots of rice (Oryza sativa) produced H(2), CH(4), acetate, propionate and butyrate when incubated under anoxic conditions. Acetate production was most pronounced with a maximum rate (mean+/-standard error; four different root preparations) of 3.4+/-0.6 µmol h(-1) g-dry weight(-1) roots, compared to 0.45+/-0.13, 0.06+/-0.03, and 0.04+/-0.01 µmol h(-1) g-dw(-1) for propionate, butyrate and CH(4)1 kPa after one day of incubation. Then it decreased and reached more or less constant concentrations of about 50-80 Pa after about 7-8 days. Hydrogen partial pressures were always high enough to allow exergonic methanogenesis (DeltaG=-67 to -98 kJ mol(-1) CH(4)) and exergonic homoacetogenesis (DeltaG=-18 to -48 kJ mol(-1) acetate) from H(2) plus CO(2). Radioactive bicarbonate/CO(2) was incorporated into CH(4), acetate and propionate. The specific radioactivities of the products indicated that CH(4) was exclusively produced from H(2)/CO(2) confirming a previous study. The contribution of CO(2) to the production of acetate and propionate was 32-39% and 42-61%, respectively, assuming that each carbon atom was equally labeled. Propionate also became radioactively labeled, when the roots were incubated with either [1-(14)C]acetate or [2-(14)C]acetate accounting for 60-76% of total propionate production. Reductive formation of propionate was thermodynamically favorable both from H(2) plus acetate plus CO(2) (DeltaG=-15 to -38 kJ mol(-1) propionate) and from H(2) plus CO(2) (DeltaG=-34 to -85 kJ mol(-1) propionate). A substantial fraction of propionate was apparently reductively formed from acetate and/or CO(2). In conclusion, our results demonstrate an intensive anaerobic dark metabolism of CO(2) on washed rice roots with reduction of CO(2) contributing significantly to the production of acetate, propionate and CH(4). The CO(2) reduction seemed to be driven by decay and fermentation of root material.

Journal Article↗
PubMed2000

Turnover of glucose and acetate coupled to reduction of nitrate, ferric iron and sulfate and to methanogenesis in anoxic rice field soil.

Turnover of glucose and acetate in the presence of active reduction of nitrate, ferric iron and sulfate was investigated in anoxic rice field soil by using [U-(14)C]glucose and [2-(14)C]acetate. The turnover of glucose was not much affected by addition of ferrihydrite or sulfate, but was partially inhibited (60%) by addition of nitrate. Nitrate addition also strongly reduced acetate production from glucose while ferrihydrite and sulfate addition did not. These results demonstrate that ferric iron and sulfate reducers did not outcompete fermenting bacteria for glucose at endogenous concentrations. Nitrate reducers may have done so, but glucose fermentation may also have been inhibited by accumulation of toxic denitrification intermediates (nitrite, NO, N(2)O). Addition of nitrate resulted in complete inhibition of CH(4) production from [U-(14)C]glucose and [2-(14)C]acetate. However, addition of ferrihydrite or sulfate decreased the production of (14)CH(4) from [U-(14)C]glucose by only 70 and 65%, respectively. None of the electron acceptors significantly increased the production of (14)CO(2) from [U-(14)C]glucose, but all increased the production of (14)CO(2) from [2-(14)C]acetate. Uptake of acetate was faster in the presence of either nitrate, ferrihydrite or sulfate than in the unamended control. Addition of ferrihydrite and sulfate reduced (14)CH(4) production from [2-(14)C]acetate by 83 and 92%, respectively. Chloroform completely inhibited the methanogenic consumption of acetate. It also inhibited the oxidation of acetate, completely in the presence of sulfate, but not in the presence of nitrate or ferrihydrite. Our results show that, besides the possible toxic effect of products of nitrate reduction (NO, NO(2)(-) and N(2)O) on methanogens, nitrate reducers, ferric iron reducers and sulfate reducers were active enough to outcompete methanogens for acetate and channeling the flow of electrons away from CH(4) towards CO(2) production.

Journal Article↗
PubMed1982

Acetic Acid Production by Clostridium thermoaceticum in pH-Controlled Batch Fermentations at Acidic pH.

Four strains of the homofermentative, obligately anaerobic thermophile Clostridium thermoaceticum were compared in pH-controlled batch fermentation for their tolerance to acetic acid, efficiency of converting glucose to acetic acid and cell mass, and growth rate. At pH 6 (and pH 7) and initial acetic acid concentrations of less than 10 g/liter, the four strains had mass doubling times of 5 to 7 h and conversion efficiencies to acetic acid and cell mass of about 90% (70 to 110%) and 10%, respectively. At pH 6 and initial acetic acid concentrations of greater than 10 g/liter, only two of the strains grew, the mass doubling time increased to 18 h, and the conversion efficiencies to acetic acid and cell mass remained unchanged. Both of these strains had been selected for their ability to grow in the presence of acetate at neutral pH. The highest acetic acid concentrations reached were about 15 and 20 g/liter at pH 6 and 7, respectively. C. thermoaceticum is apparently more sensitive to free acetic acid than to either acetate ion or pH. It was also shown that, at pH 6 and 7, the redox potential must be at least as low as -300 and -360 mV, respectively, for growth to occur.

Journal Article↗