PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “THIOGLYCOLLIC ACID”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 451 records · Page 25Linked to original sources
PubMed2000

Speciation of dimethylarsinic acid and monomethylarsonic acid by solid-phase microextraction-gas chromatography-ion trap mass spectrometry.

A solid-phase microextraction (SPME) method has been developed to determine two methylated arsenic species in human urine samples by GC-MS. The direct extraction of the methyl arsenic compounds by SPME after thioglycol methylate derivatization was studied. Direct extraction with SPME was suitable for the determination of trace levels of dimethylarsinic acid (DMA) and monomethylarsonic acid (MMA) in urine samples. Four different commercial SPME fibers were tested for the extraction of methyl arsenic compounds, and the best results were obtained using the polydimethylsiloxane coating. The extraction and desorption time profiles of DMA and MMA were determined. The detection limits for DMA and MMA using the SPME-GC-MS method were 0.12 and 0.29 ng/ml, respectively. The method is linear in the 1 to 200 ng/ml range.

Arsenicals↗
PubMed1999

Thermococcus waiotapuensis sp. nov., an extremely thermophilic archaeon isolated from a freshwater hot spring.

An extremely thermophilic, sulfur-dependent archaeon, strain WT1, was isolated from a freshwater hot spring in the Lake Taupo area of North Island, New Zealand. The cells are flagellated, strictly anaerobic cocci that grow optimally at 85 degrees C and 5.4 g NaCl l(-1). The strain grows heterotrophically on complex proteinaceous substrates or on appropriate salts plus amino acid mixtures and is also able to utilize maltose, starch, and pyruvate. Elemental sulfur could be replaced by cystine or thioglycollate. The range of temperatures allowing growth is from 60 to 90 degrees C; the pH supporting growth ranges from 5 to 8 (optimum, pH 7). Strain WT1 grew in a defined medium containing amino acids as the sole carbon and energy sources. The required amino acids were: Arg, His, Ile, Leu, Phe, Ser, Thr, Trp, Tyr, and Val. Strain WT1 showed sensitivity to rifampicin. DNA G+C content was 50.4 mol%. Phylogenetic analysis of the sequence encoding the 16S rRNA gene indicated that this isolate is a member of the Thermococcales. DNA/DNA hybridization studies revealed no similarity to several species of Thermococcus and Pyrococcus, with the exception of Thermococcus zilligii. Based on the reported results, we propose strain WT1 as a new species to be named Thermococcus waiotapuensis sp. nov.

Bacterial Typing Techniques↗
PubMed1990

In vitro survival of Bacteroides intermedius in five transport media, alone or in the presence of Streptococcus sanguis.

The survival rate of Bacteroides intermedius was first tested in monoculture, and Streptococcus sanguis was then added in 5 different transport media; 2 nonnutritious media, the viability-preserving medium of the University of Göteborg No. IV (VMG IV), reduced transport fluid (RTF), and 3 nutritious media, thioglycolate medium (TG), peptone yeast extract medium (PY) and PY medium with 1% glucose (PYG). All manipulations were carried out in an anaerobic chamber. After a given transport time (6 or 24 h) aliquots were spread on plates containing solid PY medium by means of an automated spiral system device, thus permitting counts after incubation. The slight variations in the counts of B. intermedius in monoculture, not exceeding 0.5 log10 in the 5 media tested, indicated its good survival capability, i.e. at least 24 h. By contrast, when S. sanguis was added, it was only possible to use nutritious media such as PY or TG for 6 h. In the glocose-containing media (PYG, TG), the multiplication of rapidly glucose-fermenting microorganisms such as streptococci influenced the B. intermedius survival rate. Therefore, the transport time for oral microbiological samples needs to be reduced as much as possible. The use of excessively rich media (particularly media containing a high level of glucose) should be avoided.

Antibiosis↗
PubMed1987

Rates of utilization and fates of glucose, glutamine, pyruvate, fatty acids and ketone bodies by mouse macrophages.

The concentrations of ATP and the ATP/AMP concentration ratios were maintained in thioglycollate-elicited mouse peritoneal macrophages incubated in vitro for 90 min in the presence or absence of added substrate: rates of glycolysis, lactate formation and glutamine utilization were approximately linear with time for at least 60 min of incubation. The rate of oxygen consumption by macrophages was only increased above the basal rate (i.e. that in the absence of added substrate) by addition of succinate or pyruvate, or by addition of the uncoupling agent carboxyl cyanide m-chlorophenylhydrazone ('CCCP'); it was decreased by 75% by the addition of KCN. These findings suggest that metabolism of endogenous substrate can provide most, if not all, of the energy requirement of these cells, at least for a short period. The rates of glucose and glutamine utilization by incubated macrophages were approx. 300 and 100 nmol/min per mg of protein respectively. A large proportion of the glutamine that is utilized is converted into glutamate and aspartate, and very little (perhaps less than 10%) is oxidized. Similarly almost all of the glucose that is utilized is converted into lactate and very little is oxidized. This characteristic is similar to that of resting lymphocytes and rapidly dividing cells; in non-proliferating macrophages it may be a mechanism to provide precision in control of the rate of biosynthetic processes that utilize intermediates of these pathways, e.g. purines and pyrimidines for mRNA for the synthesis of secretory proteins and glycerol 3-phosphate for phospholipid synthesis for membrane recycling. No utilization of acetoacetate or 3-hydroxybutyrate by macrophages was detected. In contrast, both butyrate and oleate were oxidized. The rate of [14C]oleate conversion into 14CO2 (1.3 nmol/h per mg of protein) could account for most of the oxygen consumption by incubated macrophages, suggesting that long-chain fatty acids might provide an important fuel in situ. This may be one explanation for the secretion of lipoprotein lipase by these cells, to provide fatty acids for oxidation from the degradation of local triacylglycerol.

Adenine Nucleotides↗
PubMed1990

Lactic acidosis increases tumor necrosis factor secretion and transcription in vitro.

Lactic acid has been shown to affect numerous biologic processes. We investigated the role of lactic acidosis as a signal for the production of TNF by macrophages in vitro. Male F344 rats were administered thioglycolate media intraperitoneally. Macrophages were recovered 7 days later, cultured for 24 hr in complete media (CM), or CM with L-lactic acid (5, 10, or 15 mM), or with endotoxin (LPS) (10 micrograms/ml). TNF levels were measured in the supernatants. Female C57BL/6 mice were similarly treated, and macrophages were harvested and cultured in CM or CM containing lactic acid (15 mM), or LPS (10 micrograms/ml). RNA was extracted after 24 hr, separated by electrophoresis, and transferred to nitrocellulose. Human 32P-cDNA TNF and actin probes were used to determine relative TNF gene expression. Gel densitometry was used to calculate the TNF expression index (EI) in lactic acid and LPS treated cells as described. pH levels of the supernatant indicated that increasing concentrations of lactic acid caused increasing acidosis. Trypan blue exclusion demonstrated that lactic acidosis did not reduce cell viability. LPS significantly increased secretion of TNF relative to control (P less than 0.001). Each concentration of lactic acid significantly increased TNF secretion (P less than 0.05), but not in a dose-dependent manner. TNF gene transcription was elevated in macrophages cultured with lactic acid and LPS relative to control (EI = 1.13 and 1.18, respectively). This suggests that lactic acid concentration can regulate TNF secretion at the level of transcription, and is consistent with the hypothesis that local levels of lactic acid (lactic acidosis) may be a regulator of cytokine secretion.

Acidosis, Lactic↗
PubMed1968

Sporicidal action of auto-oxidized ascorbic acid for Clostridium.

Neutralized ascorbic acid (AA), buffered or unbuffered and autoclaved or filter-sterilized, was sporicidal for Clostridium. A 0.2% concentration of AA was generally employed, and spore counts were made in a soft-agar modification of Wynne's medium in Prickett tubes. Spores of Clostridium botulinum 115B were less susceptible than those of C. sporogenes PA 3679, whereas C. bifermentans spores were by far the most sensitive. At 75 C, spores of PA 3679 were killed at a rate of about 9% at 0 min (warm-up) to 99+% at 100 min. The lower the temperature, the longer the time needed for a given lethality. The percentage of killing increased with increasing concentrations of AA, and the rate of killing was lower at a higher concentration of spores. At least two mechanisms were operative: a major mechanism involving a product(s) of AA auto-oxidation, and a minor mechanism involving copper-ascorbate toxicity. AA reduced in natural gas was not sporicidal after 18.5 hr at 25 C, whereas 92% of the spores were killed by oxidized AA. Although H(2)O(2) per se was sporicidal, catalase did not reverse lethality of fresh or oxidized AA. Dehydroascorbate was as sporicidal as any AA preparation. Added copper (0.00001%) increased the rate of lethality of freshly prepared AA from 66 to 83% but was not effective with thoroughly oxidized AA. Ethylenediaminetetraacetic acid, NH(4) (+), and phosphate partially reversed AA toxicity, deionized water had no effect, and complex media, as well as thioglycolate, eliminated AA lethality. Since the percentage of killing was affected by spore concentration, AA did not seem to stimulate "lethal germination."

Ascorbic Acid↗
PubMed1996

The effects of low-, medium-, and high-fat diets on 2-deoxy-D-glucose- and mercaptoacetate-induced feeding.

The present study examined the feeding responses stimulated by low suprathreshold and optimal doses of 2-DG and MA in three groups of rats maintained and tested on low (4.3%), medium (13.5%), or high (66.4%) fat diets. Results show that diet alters the response to 2-DG and MA. Rats on the low-fat diet significantly increased food intake after both the low and high doses of 2-DG. Rats on the medium- and high-fat diet significantly increased food intake after both the low and high doses of 2-DG. Rats on the medium- and high-fat diets significantly increased food intake only after the high dose of 2-DG. After administration of the low and high doses of MA, rats on the high-fat diet ate significantly more. However, rats on the low- and medium-fat diets significantly increased food intake only after the high dose of MA. These results suggest that diet-induced dependence of rats on fat or carbohydrate metabolism alters the sensitivity of systems controlling food intake in response to deficits in the availability of these specific metabolic fuels.

Animals↗
PubMed2004

Fatty acid oxidation and control of food intake.

Fatty acid oxidation is thought to play a role in the control of food intake, and a low postprandial oxidation of ingested fat may contribute to the overeating on a high-fat diet. Evidence for a role of fatty acid oxidation in control of food intake is mainly derived from the stimulation of feeding in response to administration of the acyl-CoA-dehydrogenase inhibitor mercaptoacetate (MA) and other inhibitors of fatty acid oxidation in different species (rat, mouse, man). Denervation studies suggest that this "lipoprivic feeding" is related to changes in hepatic fatty acid oxidation. In contrast to the strong case for a feeding stimulatory effect of an inhibition of fatty acid oxidation, the evidence for a feeding suppressive effect of a stimulation of fatty acid oxidation is inconsistent and comparatively weak. Ingestion of medium-chain fatty acids (MCFA) and peripheral administration of substances known to increase fatty acid oxidation, such as the fatty acid synthase inhibitor C75 and beta3-adrenergic agonists, decrease feeding. Yet, these substances also reduce the rats' usual preference for saccharin solution, indicating that the feeding suppressive effect is not only due to a stimulation of fatty acid oxidation. A possible approach to answer the question of whether a stimulation of hepatic fatty acid oxidation enhances satiety is to selectively increase expression and activity of the enzyme CPT 1alpha in the liver. CPT 1alpha transfers long-chain fatty acids in the cytosol from CoA to carnitine, which is the precondition for the entry of long-chain fatty acids into mitochondria and the rate-controlling step in mitochondrial fatty acid oxidation. The generation of rats with inducible, liver-specific overexpression of CPT 1alpha should permit to critically examine the putative contribution of hepatic fatty acid oxidation to the control of food intake.

3-Hydroxybutyric Acid↗
PubMed2003

Do metabolic signals stimulate intake in rat pups?

During early postnatal life, rat pups make a transition from suckling to food intake independent of the dam. Accompanying this transition is the requirement for pups to independently modulate their ingestive behavior. In adult animals, one set of signals known to modulate intake is generated by administration of agents that interfere with metabolism of glucose or fats (such as mercaptoacetate [MA] or 2-deoxyglucose [2-DG]). However, demonstrations of the effects of such agents in young rats have been less robust. Recent work in our lab has focused on examining the effects of MA and methyl palmoxirate (MP) on independent ingestion in pre- and periweaning rats. In rat pups between the ages of 12 and 15 days, latencies to initiate intake independent of the dam are typically longer relative to older or younger pups. However, the latency with which 12- and 15-day-old pups initiate independent ingestion is reduced following administration of MA. Further, MA produces physiological changes consistent with a change in the oxidation of fatty acids in 12- and 15-day-old pups, and similar physiological changes are produced during moderate periods of food deprivation in pups at the same ages. Thus, signals related to changes in the oxidation of fatty acids normally produced by moderate food deprivation in periweaning rats may provide a fundamental signal involved in the onset and modulation of intake independent of the dam.

Aging↗
PubMed2003

Efficacy of some neutralizers in suspension tests determining the activity of disinfectants.

The ability of six mixtures to neutralize glutaraldehyde, o-phthalaldehyde and peracetic acid was tested using four reference strains: Pseudomonas aeruginosa CIP A22, Escherichia coli CIP 54127, Staphylococcus aureus CIP 53154, and Enterococcus faecium CIP 5855. Glutaraldehyde was the hardest to neutralize, and peracetic acid the easiest. The most effective mixture was Tween 80 with sodium bisulphate, sodium thioglycolate, lecithin and cysteine, and the least effective was Tween 80, lecithin and histidine. The efficacy of the neutralizers may indicate a propensity loss of activity from interfering substances when disinfectants are used in practice.

Colony Count, Microbial↗
PubMed1999

Effects of macrophage inhibitory factor-A3 (MIF-A3) on cytokine secretion and phagolysosome fusion in murine macrophages.

Macrophage inhibitory factor-A3 (MIF-A3) is a fraction derived from Mycobacterium avium serovar 2 (Mav2) that consists of a small amine containing compound (peptide), trehalose and two or three short chain fatty acids. MIF-A3 has been shown to inhibit candidacidal activity of murine thioglycolate-elicited peritoneal-derived macrophages and bovine peripheral blood monocytes, and scavenge reactive oxygen intermediates. In this study, MIF-A3 was evaluated for its effect on secretion of IL-1beta, IL-6, IL-10, TNFalpha and GM-CSF in C57BL/6 murine thioglycolate-elicited peritoneal-derived macrophages, with and without pre-incubation with affinity purified goat anti-MIF-A3 IgG, using ELISA cytokine kit analysis. Results of this study suggest that anti-MIF-A3 IgG does not enhance clearance of Mav2, alter phagocytosis or alter phagosome-lysosome interactions as determined by electron microscopy in Mav2 infected macrophages. MIF-A3 does induce secretion of IL-6, but does not induce secretion of TNFalpha, IL-1beta, and GM-CSF. TNFalpha has been previously shown to reduce growth, while IL-6 has been shown to enhance growth of M. avium. Since IL-6 appears to enhance growth of M. avium and MIF-A3 induces IL-6 secretion, MIF-A3 may be responsible for enhanced intracellular growth in M. avium infections and be a factor in the pathogenesis of M. avium infections.

Animals↗
PubMed1972

Regulation of the enzymes converting L-mandelate into benzoate in bacterium N.C.I.B. 8250.

l-Mandelate is oxidized to benzoate by the enzymes l-mandelate dehydrogenase, phenylglyoxylate carboxy-lyase and benzaldehyde dehydrogenase I. Conditions have been established for measuring these three enzymes as well as benzyl alcohol dehydrogenase, benzaldehyde dehydrogenase II and catechol 1,2-oxygenase in a single cell-free extract prepared from bacterium N.C.I.B. 8250. The kinetics of induction of all these enzymes have been measured under a variety of conditions. l-Mandelate dehydrogenase, phenylglyoxylate carboxy-lyase and benzaldehyde dehydrogenase I appear to be co-ordinately regulated because (a) their differential rates of synthesis are proportional to one another under various conditions of induction and repression, (b) they are specifically and gratuitously induced by thiophenoxyacetate and a number of other compounds, and (c) mutant strains have been isolated that lack all three enzymes. Phenylglyoxylate is the primary inducer of the regulon as mutant strains lacking phenylglyoxylate carboxy-lyase form the other two enzymes in the presence of l-mandelate or phenylglyoxylate, whereas in mutant strains devoid of l-mandelate dehydrogenase activity only phenylglyoxylate induces phenylglyoxylate carboxy-lyase and benzaldehyde dehydrogenase I.

Alcaligenes↗
PubMed2001

Influence of ketone body and the inhibition of fatty acid oxidation on the food intake of the chick.

1. Fatty acid oxidation is known to be involved in the control of food intake in mammals. The effect of fatty acid oxidation on food intake in chickens was studied using a ketone body (beta-hydroxybutyrate (beta-HB)) and mercaptoacetate (MA) (an inhibitor of fatty acid oxidation). 2. Central and peripheral injection of beta-HB decreased food intake in a dose-dependent manner, while low doses of MA had no effect. Higher doses of MA inhibited feeding but also caused mortality. 3. These results indicate that ketone bodies act as an inhibitory signal for food intake in both the central and peripheral nervous systems but that inhibition of fatty acid oxidation may not be associated with feeding behaviour in chicks.

3-Hydroxybutyric Acid↗
PubMed1976

The nutritional requirements of methicillin-dependent and -resistant strains of Pediococcus cerevisiae.

A new methicillin-dependent and -resistant substrain (called MRD) of Pediococcus cerevisiae was developed by serial passages followed by replica-plating. Other methicillin-resistant, but not -dependent, substrains were isolated after treatment of the same parent strain with a mutagen. A methicillin-independent partial revertant, still resistant to the drug, was isolated from the original methicillin-dependent and -resistant substrain (CRD) developed several years ago. The requirements of some of these strains for acetate, vitamins and amino acids were compared. All except the parent methicillin-sensitive strain required pantothenate for growth, but no other consistent differences were found. The parent, but not strain CRD, grew without lysine added to the medium, though 19 other amino acids were needed by each strain. Both of these strains fermented glucose to lactate (mainly the L-isomer) in the absence or presence of methicillin.

Acetates↗
PubMed1971

Distribution and correlation of events during thermal inactivation of Bacillus megaterium spores.

Aqueous suspensions of Bacillus megaterium QM B1551 spores were heated at temperatures from 75 to 85 C. The rapid initial viability loss, followed by a more gradual, almost exponential decline, was not due to mixed populations with discrete heat resistances. The slight "tailing" below 0.01% survival was not the result of heat adaptation. Loss of viability was more rapid than loss of dipicolinic acid (DPA) and germinability and, although these events could not be correlated by use of simple kinetic plots, they had similar activation energies (80 to 90 kcal/mole). Probability (probit) plots of per cent survival as a function of logarithmic time yielded not the single line expected, if the heat resistances of individuals in the population were log-normally distributed, but two straight lines intersecting at a survival level of 1 to 6%. Probit-intersects occurred at times ranging from 8 min for spores heated at 85 C, to 310 min at 75 C. Probit-intersects for DPA release and loss in germinability occurred at the same time as for survival, but at much higher levels of retention. There appeared to be two subpopulations, both log-normally distributed but with different mechanisms of kill. Ninety-four to 99% of the spores died via injury to the cell-division process but retained germinability; the remaining smaller subpopulation (1 to 6%) was nonviable because of loss of the ability to germinate.

Bacillus megaterium↗