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Acetate-glucose relationship in growing pigs.

Twelve crossbred barrows from four litters (average initial body weight of 21 kg) were used to examine the relationship between acetate and glucose metabolism in pigs. The treatments were the addition of acetate in the form of triacetin to the basal diet at 0, 5 and 10% of the metabolizable energy intake. In the immediate postprandial period, the administered acetate decreased the venous plasma glucose concentration linearly (P less than .05) and increased linearly the venous plasma concentrations of lactate (P less than .01) and ketone bodies (P less than .001). There was a linear increase in the glycogen content of the liver (P less than .001), heart (P less than .001) and femoral muscle (P less than .01), as the level of acetate intake was increased. In the remote postprandial period (12 h after the last meal), glucose, which was considered to have been derived from hepatic glycogen storage, became the dominant blood metabolite in place of the acetate administered with the diet. This led to the reduction in hepatic production of endogenous acetate, arterial acetate concentration and in acetate utilization in the hind limb. Hepatic urea production was also decreased. Thus, there was a reciprocal change in acetate and glucose metabolism.

Acetates↗

Roles of acetate and its interactions with glucose and lactate in cow mammary tissue.

Slices from mammary glands from six lactating Holstein cows were incubated in Krebs-Ringer bicarbonate-based media in the presence of varying concentrations of acetate, glucose, and lactate. Conversions of acetate to carbon dioxide, fatty acids, citrate, glyceride-glycerol, and lactose were determined. Specific effects of beta-hydroxybutyrate and stearate availability also were evaluated. Utilization of acetate for all functions usually followed Michaelis-Menten kinetics with apparent affinities in the physiological concentration range of acetate. Availability of glucose had a large "permissive" effect on acetate to conversion to fatty acids. However, acetate metabolism was independent of the availability of lactate. Conversion of acetate to glyceride-glycerol was significant. This indicates the possibility of bidirectional glycolytic flux, which could limit glucose conversion to fatty acids. Addition of stearate caused general increases of acetate metabolism. Conversion of acetate to fatty acids, carbon dioxide, and citrate was elevated in the absence of beta-hydroxybutyrate. The latter observation indicates beta-hydroxybutyrate may not be a required initiator of fatty acid synthesis in mammary tissue.

Acetates↗

Effect of neutralized and native vinegar on blood glucose and acetate responses to a mixed meal in healthy subjects.

OBJECTIVE: To investigate the influence of sodium acetate and acetic acid from vinegar on blood glucose and acetate response to a mixed meal in healthy subjects. DESIGN: Five healthy subjects consumed in random order six test meals consisting of 100 g of sliced lettuce dressed with olive oil (Blank), olive oil plus 1 g acetic acid in the form of vinegar (AcOH), or olive oil plus sodium acetate in the form of vinegar neutralized to pH 6.0 with sodium bicarbonate (AcNa). On three occasions test meals were followed by a challenge consisting of 50 g carbohydrate portions of white bread (Bread). Glucose and acetate concentrations were measured in arterialized capillary blood before and until 95 min after the meals. Ultrasonography was performed in four other subjects to measure gastric emptying times after AcOH + Bread and AcNa + Bread. RESULTS: Blood acetate response over 95 min was markedly reduced after AcOH and AcOH+Bread meals compared to AcNa and AcNa + Bread. Similarly, the glucose response was depressed by 31.4% (P = 0.0228) after AcOH+Bread with respect to AcNa + Bread and Blank + Bread. No difference was observed between gastric emptying times after AcOH + Bread and AcNa + Bread. CONCLUSIONS: The results suggest that oral acetic acid and acetate might have a different effect on acetataemia and that a limited dose of vinegar, in the form of salad dressing, is sufficient to influence significantly the glycaemic response to a mixed meal in normal subjects by a mechanism related to acidity but not to gastric emptying.

Acetates↗

Main and interaction effects of acetic acid, furfural, and p-hydroxybenzoic acid on growth and ethanol productivity of yeasts.

The influence of the factors acetic acid, furfural, and p-hydroxybenzoic acid on the ethanol yield (YEtOH) of Saccharomyces cerevisiae, bakers' yeast, S. cerevisiae ATCC 96581, and Candida shehatae NJ 23 was investigated using a 2(3)-full factorial design with 3 centrepoints. The results indicated that acetic acid inhibited the fermentation by C. shehatae NJ 23 markedly more than by bakers' yeast, whereas no significant difference in tolerance towards the compounds was detected between the S. cerevisiae strains. Furfural (2 g L-1) and the lignin derived compound p-hydroxybenzoic acid (2 g L-1) did not affect any of the yeasts at the cell mass concentration used. The results indicated that the linear model was not adequate to describe the experimental data (the p-values of curvatures were 0.048 for NJ 23 and 0.091 for bakers' yeast). Based on the results from the 2(3)-full factorial experiment, an extended experiment was designed based on a central composite design to investigate the influence of the factors on the specific growth rate (mu), biomass yield (Yx), volumetric ethanol productivity (QEtOH), and YEtOH. Bakers' yeast was chosen in the extended experiment due to its better tolerance towards acetic acid, which makes it a more interesting organism for use in industrial fermentations of lignocellulosic hydrolysates. The inoculum size was reduced in the extended experiment to reduce any increase in inhibitor tolerance that might be due to a large cell inoculum. By dividing the experiment in blocks containing fermentations performed with the same inoculum preparation on the same day, much of the anticipated systematic variation between the experiments was separated from the experimental error. The results of the fitted model can be summarised as follows: mu was decreased by furfural (0-3 g L-1). Furfural and acetic acid (0-10 g L-1) also interacted negatively on mu. Furfural concentrations up to 2 g L-1 stimulated Yx in the absence of acetic acid whereas higher concentrations decreased Yx. The two compounds interacted negatively on Yx and YEtOH. Acetic acid concentrations up to 9 g L-1 stimulated QEtOH, whereas furfural (0-3 g L-1) decreased QEtOH. Acetic acid in concentrations up to 10 g L-1 stimulated YEtOH in the absence of furfural, and furfural (0-2 g L-1) slightly increased YEtOH in the absence of acetic acid whereas higher concentrations caused inhibition. Acetic acid and furfural interacted negatively on YEtOH.

Acetic Acid↗

Teprenone promotes the healing of acetic acid-induced chronic gastric ulcers in rats by inhibiting neutrophil infiltration and lipid peroxidation in ulcerated gastric tissues.

Teprenone, an anti-ulcer drug, has been reported to promote the healing of acetic acid-induced chronic gastric ulcers in rats by stimulating gastric mucus synthesis and secretion. Recently, it has been implicated that neutrophil infiltration and lipid peroxidation in ulcerated gastric tissues have an inhibitory effect on the healing of acetic acid-induced chronic gastric ulcers in rats. Therefore, we attempted to clarify whether teprenone exerts a healing-promoting effect on acetic acid-induced chronic gastric ulcers through its inhibitory effect on neutrophil infiltration and lipid peroxidation in ulcerated gastric tissues. In rats with chronic gastric ulcers made by applying acetic acid to the stomach, gastric ulcer healing started later than 3 days after the acetic acid application. Gastric mucosal myeloperoxidase (MPO) activity, an index of tissue neutrophil infiltration, and lipid peroxide content were higher in the ulcerated region than in the intact region on the 8th, 15th, and 22nd day after the acetic acid application. Gastric mucosal non-protein SH content was lower in the ulcerated region than in the intact region on the 8th, 15th, and 22nd day after the acetic acid application, and gastric mucosal adherent mucus content was lower in the ulcerated region than in the intact region on the 8th and 15th day. Daily oral administration of teprenone (100 mg kg(-1)x 2) for 7 or 14 days, starting on the 8th day after the application of acetic acid to the stomach, enhanced the reduction of the ulcer area with attenuation of all these biochemical changes found in the ulcerated region. The teprenone administration caused a decrease in MPO activity and an increase in adherent mucus content in the gastric mucosa of the intact region. These results suggest that the healing-promoting effect of teprenone on acetic acid-induced chronic gastric ulcers in rats could be due not only to stimulation of gastric mucus secretion but also to inhibition of neutrophil infiltration and enhanced lipid peroxidation in the ulcerated gastric tissue.

Acetic Acid↗

Acetate stimulates secretion in the rabbit mandibular gland.

In isolated perfused rabbit mandibular glands undergoing stimulation with 0.8 microM acetylcholine, replacement of HCO3- with acetate (25 mM) increased fluid secretion by more than 100%. Other short-chain fatty acids, except for propionate, had a similar effect. We focused our further studies on acetate, and in order to find out the cause of its stimulatory effect we investigated whether acetate itself was transported. In the absence of any other transportable anions 25 mM acetate supported secretion at the same rate as 25 mM HCO3- or 25 mM Cl-, i.e. 20% of the control rate. In solutions containing acetate as the only major anion (146 mM), fluid secretion was maintained at about 50% of the control rate. Amiloride (1 mM) inhibited this secretion by about 90%. In glands perfused with acetate/Cl- solutions, when the stimulatory effect was normally observed, amiloride (1 mM) inhibited secretion by 50-60% and SITS (0.1 mM) had no effect. Probenecid reversibly inhibited 75% of secretion in these glands, but it also inhibited 92% of secretion in glands perfused without any acetate. Interestingly, the acetate effect was abolished in glands stimulated with a higher concentration of acetylcholine (80 microM). Results of this study suggest that acetate can be transported by salivary endpieces and that this transport involves an amiloride-sensitive Na+-H+ antiport. We postulate that acetate may in addition have some regulatory or modifier role in salivary secretion.

Acetates↗

Acetate assimilation and the synthesis of alanine, aspartate and glutamate in Methanobacterium thermoautotrophicum.

Cultures of the autotrophic bacterium Methanobacterium thermoautotrophicum were shown to assimilate acetate when grown on CO2 and H2 in the presence of acetate. At 1 mM acetate 10% of the cell carbon came from acetate, the rest from CO2. At higher concentrations the percentage increased to reach a maximum of 65% at acetate concentrations higher than 20 mM. The data suggest that acetate may be an important carbon source under physiological conditions. The incorporation of acetate into alanine, aspartate and glutamate was studied in more detail. The cells were grown on CO2 and H2 in the presence of 1 mM U-14C-acetate. The three amino acids were isolated from the labelled cells by a simplified procedure. Alanine, aspartate and glutamate were found to have the same specific radioactivity. Degradation studies showed that C1 of alanine, C1 and C4 of aspartate, and C1 and C5 of glutamate were exclusively derived from CO2, whereas C2 and C3 of alanine and aspartate, and C3 and C4 of glutamate were partially derived from acetate. These findings and the presence of pyruvate synthase, phosphoenolpyruvate carboxylase and alpha-ketoglutarate synthase in M. thermoautotrophicum indicate that CO2 is assimilated into the three amino acids via acetyl CoA carboxylation to pyruvate, phosphoenolpyruvate carboxylation to oxaloacetate, and succinyl CoA carboxylation to alpha-ketoglutarate.

Acetates↗

Interaction effects of lactic acid and acetic acid at different temperatures on ethanol production by Saccharomyces cerevisiae in corn mash.

The combined effects of lactic acid and acetic acid on ethanol production by S. cerevisiae in corn mash, as influenced by temperature, were examined. Duplicate full factorial experiments (three lactic acid concentrations x three acetic acid concentrations) were performed to evaluate the interaction between lactic and acetic acids on the ethanol production of yeast at each of the three temperatures, 30, 34, and 37 degrees C. Corn mash at 30% dry solids adjusted to pH 4 after lactic and acetic acid addition was used as the substrate. Ethanol production rates and final ethanol concentrations decreased (P<0.001) progressively as the concentration of combined lactic and acetic acids in the corn mash increased and the temperature was raised from 30 to 37 degrees C. At 30 degrees C, essentially no ethanol was produced after 96 h when 0.5% w/v acetic acid was present in the mash (with 0.5, 2, and 4% w/v lactic acid). At 34 and 37 degrees C, the final concentrations of ethanol produced by the yeast were noticeably reduced by the presence of 0.3% w/v acetic acid and >or=2% w/v lactic acid. It can be concluded that, as in previous studies with defined media, lactic acid and acetic acid act synergistically to reduce ethanol production by yeast in corn mash. In addition, the inhibitory effects of combined lactic and acetic acid in corn mash were more apparent at elevated temperatures.

Acetic Acid↗

Bacterial response to acetate challenge: a comparison of tolerance among species.

Although acetate formation and tolerance are important criteria for various aspects of biotechnological process development, available studies on acetate tolerance in different species are disparate. We evaluate the response of eight bacterial strains, including two variants of Escherichia coli, two variants of Staphylococcus capitis, and one each of Acetobacter aceti, Gluconobacter suboxydans, Lactobacillus acetotolerans, and L. bulgaricus, to acetate challenges under identical conditions. Our findings were: (1) wild-type organisms of species that are considered tolerant of acetate perform only slightly better than E. coli in unadapted shaker cultures; (2) the ability to tolerate acetate is strongly dependent on the carbon source, and is, especially for E. coli, much greater on glycerol than on glucose; (3) respiration is not as important to acetate tolerance in E. coli and S. capitis as has been reported for the acetic acid bacteria; (4) S. capitis was the least affected by acetate under all conditions and grew at up to 44 g/l acetate without any preconditioning; and (5) qualitative high-throughput screening of growth characteristics can be achieved with relatively inexpensive multiwell plate readers.

Acetates↗

Correlation of increased acetate binding with alkylating agent resistance in Walker and Yoshida tumor cells.

The utilization of acetate is fundamental to numerous cellular processes. At the level of chromatin, histone acetylation is thought to regulate transcription, and acetate is a major source of cellular energy as it is the substrate for the citric acid cycle. The present work investigates the incorporation of [1-14C]sodium acetate in alkylating agent sensitive (WS) and resistant (WR) Walker 256 carcinosarcoma cells. WR bound the labeled acetate four to six times faster than WS cells, as determined by incorporation of [1-14C]sodium acetate into trichloroacetic acid precipitable material. This difference was consistently observed in both nuclear and cytoplasmic fractions of the cells and in cells permeabilized prior to incubation with radioactive acetate. WS and WR cells did not differ from each other in content of either reduced or acetylated CoA. Since adding exogenous CoA-SH to cell lysates did not alter acetate binding or reduce the differences between WS and WR, increased acetylation in WR cells was independent of CoA levels. Using [1-14C]acetyl CoA to label lysolecithin-permeabilized WS and WR cells revealed no difference between the sensitive and resistant lines, in contrast to the 5-fold greater binding of [1-14C]sodium acetate in permeabilized WR cells. This suggests that WR cells formed acetyl CoA more rapidly than did the WS cells from acetate plus endogenous CoA. Chlorambucil treatment (24 hr) did not affect acetylation of nuclear proteins in log phase cells. Finally, 3-fold greater acetylation in a line of Yoshida sarcoma cells that is resistant to alkylating agents, compared to the sensitive line, supported the generality of the phenomenon.

Acetates↗

Aspects of the spasmogenic effects of acetate esters on ileal smooth muscle.

Acetate esters, such as aspirin methylester, aspirin and resorcinol monoacetate, induced contractions of guinea-pig ileum. Their actions were selectively antagonized by atropine, but were not affected by ganglion blocking agents, conduction blockers, aging with cooling, anoxia or antihistaminics. On the other hand, N-acetates, such as acetanilide and p-acetaminophenol, and no contractile action on the ileum. These acetate esters thus seemed to have a cholinergic action, and not a direct action on muscle or other known specific receptors for endogenous active substances. The contractions induced by the acetate esters were selectively potentiated by low concentrations of choline, whereas those induced by acetylcholine, nicotine, 5-hydroxytryptamine and histamine were not. However, N-acetates did not induce the contractions even in the presence of choline. Organophosphorus cholinesterase inhibitors, such as diisopropyl fluorophosphate and paraoxon, selectively and irreversibly inhibited the actions of aspirin and N,O-diacetyl-p-aminophenol with or without choline. From these results, it is concluded that the acetate esters with or without choline act through the cholinergic system. However, their actions cannot be explained in terms of known mechanisms, such as acetylcholine release, cholinesterase inhibition or a direct muscarinic action. Therefore, the acetate esters, including phenyl acetate which was supposed to be a releaser of acetylcholine, seem to have a hitherto undescribed type of cholinergic action whose mechanism is unknown. It seems that organophosphate-sensitive esterase(s) in the preparation may be essential for initiation of the actions of the acetate esters with or without choline, but the mechanism of the effect of choline is unknown.

Acetates↗

Effects of acetate on the immune system of mice.

The effects of acetate on antibody production and cell-mediated immunity in mice were investigated. Polyclonal antibody responses could be enhanced in vivo by single intraperitoneal administration of acetate (5 mg/mouse) in C57BL/6 mice but not in DBA/2 mice. No enhancement of antibody production by acetate was also induced in athymic C57BL/6 nude mice and carrageenan-pretreated, macrophage-depleted mice. The inoculation of acetate-nonresponder BDF1 mice with T-cells and peritoneal adherent cells derived from acetate-treated C57BL/6 mice resulted in an enhanced antibody response. These results suggest that acetate increases polyclonal antibody responses in vivo by activating indirectly T-cells and macrophages. Acetate administration increased delayed hypersensitivity to pircryl chloride in C57BL/6 mice but not in DBA/2 mice. Allogeneic mixed lymphocyte reaction (MLR) of T-lymphocytes derived from the spleen of acetate-treated C57BL/6 mice was also enhanced. The natural killer (NK) activity and antibody-dependent cell-mediated cytotoxicity (ADCC) were also increased in C57BL/6 mice that were administered acetate. The possible mechanism of the immunopotentiating effect of this chemical is discussed.

Acetates↗

Effects of cadmium acetate and sodium selenite on mucociliary functions and adenosine triphosphate content in mouse trachea organ cultures.

The effects of cadmium acetate and sodium selenite in mouse trachea organ culture have been studied separately and in combination. Ciliary activity, morphology, rate of total protein and glycoconjugate (i.e. glycoprotein and proteoglycan) synthesis/secretion and ATP content were investigated. Exposure to 10 microM cadmium acetate or 2000 microM sodium selenite resulted in a complete cessation of ciliary activity within 5 h. With cadmium acetate also a swelling of epithelial cells was observed. Sodium selenite (250-2000 microM) delayed by 2-3 h the inhibitory effect of cadmium acetate (5-20 microM) on ciliary activity. The rate of protein synthesis, as determined by incorporation of [3H]proline, was reduced by 13% and 44% at exposure for 4 h at 37 degrees C to 250 microM and 500 microM sodium selenite respectively, the effect being partly abolished by cadmium acetate. With 5 microM and 10 microM cadmium acetate the rate of glycoconjugate synthesis, as measured by incorporation of [3H]glucosamine, increased by 50% and 69%, respectively, after incubation for 4 h. This increase was partly reduced by sodium selenite. Neither cadmium acetate nor sodium selenite had any effect on the rate of total protein or glycoconjugate secretion. The ATP content in trachea rings was reduced by 48% and 54% after incubation for 4 h with 250 microM and 500 microM sodium selenite, respectively. No significant effect of cadmium acetate was found on ATP content. An antagonistic effect of sodium selenite and cadmium acetate in mouse trachea organ culture is suggested from the present experiments.

Acetates↗

Effects of tibolone and continuous combined conjugated equine estrogen/medroxyprogesterone acetate on the endometrium and vaginal bleeding: results of the OPAL study.

OBJECTIVES: The primary objective of the Osteoporosis Prevention and Arterial effects of tiboLone study was to compare the effect of tibolone and placebo on the progression of the common carotid artery intima-medial thickness; the common carotid artery intima-medial thickness and bone data will be presented elsewhere. A secondary objective was to assess the effects of tibolone (2.5 mg), continuous combined conjugated equine estrogen/medroxyprogesterone acetate [0.625/2.5 mg], and placebo on the endometrium and vaginal bleeding; these results are the subject of this report. STUDY DESIGN: This 3-year, three-arm, international, randomized, double-blind, parallel group, placebo-controlled clinical trial enrolled 866 postmenopausal women (aged 45-79 years). The endometrium was assessed by annual transvaginal ultrasound scans and end-of-study biopsies (United States/United Kingdom centers only). Vaginal bleeding was recorded in daily diaries. RESULTS: Endometrial thickness measured by transvaginal ultrasound scan increased slightly during the first year with tibolone and conjugated equine estrogen/medroxyprogesterone acetate, without any further progression. After 3 years, there were no significant differences between the tibolone, conjugated equine estrogen/medroxyprogesterone acetate, and placebo groups in the incidence of proliferation (1.4%, 4.8%, and 0%, respectively), endometrial hyperplasia (0% in all groups), or cancer (1, 0, and 1 case, respectively). During the first 3 months, bleeding/spotting rates were greater with conjugated equine estrogen/medroxyprogesterone acetate (48%) than with tibolone (18%; P < .001) or placebo (3%; P < .001). During 3 years of treatment, the incidence of bleeding/spotting was 66%, 48%, and 23% for conjugated equine estrogen/medroxyprogesterone acetate, tibolone, and placebo, respectively. The mean number of bleeding/spotting days was greater in the conjugated equine estrogen/medroxyprogesterone acetate than the tibolone or placebo groups (61, 28, and 7 days, respectively; P = .023 vs tibolone; P < .0001 vs placebo). The mean number of bleeding/spotting episodes was also greater in the conjugated equine estrogen/medroxyprogesterone acetate group (13 episodes) compared with the tibolone group (six episodes; P < .001) and placebo group (four episodes; P < .001). Vaginal bleeding was more commonly reported as an adverse event with conjugated equine estrogen/medroxyprogesterone acetate than tibolone (26.4% vs 10.8%, P < .0001) and as the reason for premature discontinuation (9% vs 2%, P = .001). CONCLUSION: Compared with conjugated equine estrogen/medroxyprogesterone acetate, tibolone has a better tolerability profile with respect to vaginal bleeding but with a similar endometrial safety. These results reinforce the endometrial safety profile of tibolone.

Aged↗

Involvement of nuclear factor kappaB in up-regulation of aldose reductase gene expression by 12-O-tetradecanoylphorbol-13-acetate in HeLa cells.

To elucidate the molecular mechanisms underlying the up-regulation of aldose reductase observed in many cancer cells, we investigated the signal transduction pathways mediating induction of aldose reductase gene expression by 12-O-tetradecanoylphorbol-13-acetate, a potent tumor promoter. A maximum of four-fold induction in aldose reductase mRNA was demonstrated in HeLa cells treated with 12-O-tetradecanoylphorbol-13-acetate. The increased level of aldose reductase transcript was accompanied by the elevated level of enzyme activity, and completely abolished in the presence of actinomycin D. Inhibitors of protein kinase C, bisindolylmaleimide I and calphostin C, as well as inhibitors of tyrosine kinase, genistein and tyrphostin A23, significantly attenuated 12-O-tetradecanoylphorbol-13-acetate-induced increase in aldose reductase mRNA. Blockade of the p38 mitogen-activated protein kinase pathway by SB203580 also suppressed 12-O-tetradecanoylphorbol-13-acetate-induced aldose reductase expression. The promoter activity of aldose reductase gene was significantly augmented in the cells treated with 12-O-tetradecanoylphorbol-13-acetate, but attenuated in the presence of bisindolylmaleimide I, tyrphostin A23 or SB203580. Pyrrolidinedithiocarbamate, a nuclear factor kappaB inhibitor, dose-dependently suppressed 12-O-tetradecanoylphorbol-13-acetate-induced increase in aldose reductase mRNA. 12-O-tetradecanoylphorbol-13-acetate augmented the DNA binding activity of nuclear factor kappaB and nuclear factor kappaB-dependent gene transcription, and these effects were attenuated by bisindolylmaleimide I or tyrphostin A23, but not by SB203580. Taken together, activation of protein kinase C and tyrosine kinase by 12-O-tetradecanoylphorbol-13-acetate elicits increased promoter activity of aldose reductase gene via nuclear factor kappaB. A p38 mitogen-activated protein kinase pathway, distinct from the tyrosine kinase pathway, may also take part in 12-O-tetradecanoylphorbol-13-acetate-induced increase in aldose reductase gene expression.

Aldehyde Reductase↗

Acid stress adaptation protects Saccharomyces cerevisiae from acetic acid-induced programmed cell death.

In this work evidence is presented that acid stress adaptation protects Saccharomyces cerevisiae from acetic acid-mediated programmed cell death. Exponential-phase yeast cells, non-adapted or adapted to acid stress by 30 min incubation in rich medium set at pH 3.0 with HCl, have been exposed to increasing concentrations of acetic acid and time course changes of cell viability have been assessed. Adapted cells, in contrast to non-adapted cells, when exposed to 80 mM acetic acid for 200 min did not display loss of cell viability associated to morphological alterations typical of apoptosis. Thus, 80 mM acetic acid death-inducing conditions were selected to further characterize the early molecular events leading to such active cell death process. Catalase was specifically activated during acid stress adaptation and protection against acetic acid-induced death was associated with maintenance of its activity during treatment with 80 mM acetic acid. On the other hand, intracellular superoxide dismutase activity was found present at comparable levels both in adapted and in dying yeast cells, excepting in non-adapted cells which displayed a maximum activity value after 15 min acetic acid exposure, corresponding to more than 80% cell viability. This study gives first experimental evidence that H2O2, rather than superoxide, detoxification may have a major role in preventing yeast cell death in response to acetic acid. The results, as a whole, suggest that commitment of S. cerevisiae to a programmed cell death process in response to acetic acid is mediated through a ROS-dependent apoptotic pathway.

Acetic Acid↗

Anecortave acetate (15 milligrams) versus photodynamic therapy for treatment of subfoveal neovascularization in age-related macular degeneration.

PURPOSE: To compare 1-year safety and efficacy of anecortave acetate 15 mg with photodynamic therapy (PDT) with verteporfin in patients eligible for initial PDT treatment. DESIGN: Prospective, masked, randomized, multicenter, parallel group, active control, noninferiority clinical trial. PARTICIPANTS: Five hundred thirty patients with predominantly classic subfoveal choroidal neovascularization secondary to age-related macular degeneration were randomized to treatment with either anecortave acetate 15 mg or PDT. METHODS: In the anecortave acetate group, the drug was administered under the Tenon's capsule as a periocular posterior juxtascleral depot (PJD) at the beginning of the study and at month 6. Before the first administration of anecortave acetate, patients in this treatment group received a sham PDT treatment, and sham PDT treatments were repeated every 3 months if there was evidence of leakage on fluorescein angiography (FA). Patients assigned to PDT received up to 4 PDT treatments at 3-month intervals, as needed based upon FA, and a sham PJD procedure at the beginning of the study and at month 6. Best-corrected visual acuity was determined at baseline and all follow-up visits. Safety data were regularly reviewed by an independent safety committee. MAIN OUTCOME MEASURE: Percent responders (patients losing <3 lines of vision) at month 12. RESULTS: Percent responders in the anecortave acetate and PDT groups were 45% and 49%, respectively (not statistically different, P = 0.43). The confidence interval (CI) for the difference ranged from -13.2% favoring PDT to +5.6% favoring anecortave acetate. The month 12 clinical outcome for anecortave acetate was improved in patients for whom reflux was controlled and who were treated within the 6-month treatment window (57% vs. 49%; 95% CI, -4.3% favoring PDT to +21.7% favoring anecortave acetate). No serious adverse events related to the study drug were reported in either treatment group. CONCLUSIONS: The safety and efficacy outcomes in this study demonstrate that the benefits of anecortave acetate for the treatment of choroidal neovascularization outweigh the risks associated with either the drug or the PJD administration procedure.

Aged↗

Dynamics and influencing factors of heterotrophic bacterial utilization of acetate in constructed wetlands treating woodwaste leachate.

14C-acetate was used as a tracer of substrates for heterotrophic bacteria to investigate the dynamics and influencing factors of bacterial activity in surface flow wetlands treating woodwaste leachate. Epiphytic assimilation and mineralization of acetate increased considerably over three weeks of microbial colonization. No significant longitudinal variation in acetate uptake was found. The temporal variation of bacterial activity was neither correlated to water temperature nor acetic acid concentration. Mineralization percentage varied significantly with acetate uptake rate. Acetate uptake rates of bacterioplankton (408+/-258 microg L(-1) h(-1)), epiphyton (67.7+/-41.7 mg m(-2) h(-1)) and sedimentary bacteria (26.7+/-25.6 microg g(-1) h(-1)) were influenced by the concentrations of organic substrates and inorganic nutrients. Sedimentary bacteria contributed to the majority (55-73%) of the total heterotrophic acetate uptake, while epiphytic bacteria played only a minor role (1-3%). The acetate mineralization percentage of sediment (16%) was much lower than that of water (55%) and epiphyton (64%). Addition of ammonium nitrate fertilizer increased acetate uptake rates significantly, especially for sediment. No remarkable changes in mineralization percentage and the relative importance of water, sediment and epiphyton were found due to fertilization.

Acetates↗