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PubMed2003

The lateral spread of epileptiform discharges in rat neocortical slices: effect of focal phencyclidine application.

In vitro and in vivo brain slice techniques were used to examine phencyclidine (PCP) effects on the lateral propagation of epileptiform field potentials (EFP) across adjacent areas of rat frontal neocortex. Epileptiform activity was induced by perfusing slices with Mg 2+-free artificial cerebrospinal fluid. Simultaneous field potential recordings of EFP were obtained from four microelectrodes placed 2-3 mm apart across coronal slices in the third layer. PCP, applied focally between recording sites, blocked rapid propagation across treated areas and resulted in the emergence of spatially separate, independent pacemakers. The characteristics of paroxysmal depolarization shifts did not change significantly by the blockade of lateral propagation of EFP. The same asynchronized pattern of EFP conduction was observed after local application of the N-methyl-D-aspartate (NMDA)-receptor antagonist DL-2-amino-5-phosphono-valeric acid. Local administration of haloperidol as well as NMDA before PCP application reversibly prevented appearance of multiple pacemakers. Focal application of dopamine produced an abnormal pattern of lateral conduction of EFP in 50 % of tested slices. Pacemaker failure as an indicator of functional impairment of cortical integration is the proposed mechanism for developing of schizophrenia-like psychosis associated with epilepsy. Abbreviations. APV: DL-2-amino-5-phosphono-valeric acid EEG:electroencephalogram EFP:epileptiform field potentials NMDA:N-methyl-D-aspartate PCP:phencyclidine SLPE:Schizophrenialike psychosis associated with epilepsy

Animals↗

PubMed1990

GABA(B)-related activity involved in synaptic processing of somatosensory information in S1 cortex of the anaesthetized cat.

1. The possible role of GABA(B) receptor mechanisms in information processing in primary somatosensory (S1) cortex was assessed by use of extracellular recording combined with microiontophoretic methods from 161 neurones in anaesthetized, paralysed cats. 2. Baclofen-induced suppressions of cell responses were reversible and stereoselective, the (+)-isomer being inactive and the (-)-isomer having two to three times the apparent potency of gamma-aminobutyric acid (GABA). The responses measured were threshold to natural stimulation of receptive fields (RFs), responsiveness to thalamic electrical stimulation, change in RF size and magnitude of firing elicited by iontophoretic glutamate. 3. The action of GABA always was mimicked by muscimol or 4,5,6,7-tetrahydroisoxazolo[5,4-c]pyridin-3-ol (THIP) but not always by (-)-baclofen; in certain cases (-)-baclofen enhanced neuronal responses while the opposite occurred with GABA or with the other GABA(A) agonists. The elevation of response thresholds by (-)-baclofen was relatively stronger in peripheral than in central subregions of cutaneous RFs, by contrast with the action of muscimol which was relatively non-selective as to the area in which it was effective. 4. Glutamate-induced and thalamically-evoked cortical responses as well as spontaneous activity were differentially sensitive to the suppressant effects of muscimol and (-)-baclofen. 5. Bicuculline methiodide reversibly blocked THIP- and muscimol-induced suppressions of tactile- (air puffer)-induced S1 responses but spared those produced by (-)-baclofen. Phaclofen and delta-amino-n-valeric acid were essentially inactive as blockers of (-)-baclofen-induced effects and in fact often acted as (-)-baclofen-like agonists, phaclofen being considerably weaker than delta-amino-n-valeric acid in this respect. 6. The range of suppressant effects produced by GABA as well as by muscimol and THIP, considered in conjunction with the actions of bicuculline methiodide, suggest that the effects observed by ejected GABA are likely to be due principally to GABA(A) processes, those mediated by GABA(B) receptors largely being masked. However, GABA(B) mechanisms are extant and do appear to be active, probably presynaptically and probably at sites distal to the soma.

Anesthesia↗

PubMed1970

Effects of omega-amino acids and related compounds on staphylococcal infections in mice: a combined prophylactic-therapeutic procedure.

By a short-term combined prophylactic-therapeutic procedure, the following compounds were found to be active against staphylococcal infections in Swiss mice: gamma-aminobutyric acid, gamma-amino-beta-hydroxybutyric acid (GABOB), delta-amino-valeric acid (DAVA), epsilon-aminocaproic acid (EACA), trans-4-aminomethylcyclohexanecarboxylic acid (trans-AMCHA), taurine, and cysteic acid. Many of these compounds had displayed limited or no activity by a previously used prophylactic procedure. Although DAVA and GABOB were the most potent of the straight-chain omega-amino acids, trans-AMCHA displayed the greatest antistaphylococcic activity of the omega-amino acids thus far investigated. Homocarnosine (gamma-aminobutyrl histidine, which also was active by the prophylactic procedure) equalled trans-AMCHA in activity. Taurine was similar in potency to DAVA, and the activity of cysteic acid approximated that of EACA.

Alanine↗

PubMed1978

Hemoglobin A1C separation by isoelectric focusing.

A modified type of isolectric focusing has been applied successfully to the separation of hemoglobin A1C (HbA1C) from HbA in normal and diabetic cell lysates. It consists of transforming a linear pH gradient into a nonlinear one, by the addition of an amphoteric substance ("separator" or "pH gradient modifier") with an isoelectric point (pI) close to the pI's of the two hemoglobins. Among the "modifiers" tested, histidine, proline, threonine, beta-alanine, 6-amino caproic acid, and 5-amino valeric acid are not useful in the hemoglobin pI range (pH 6.9--7.0). The dipeptide histidyl-glycine (pI = 6.8; pI-pK1 = 1) is very efficient in flattening the pH gradient, in the hemoglobin region. even when added in low concentrations (10--100 mM), thus affording full resolution of the two hemoglobin species.

Alanine↗

PubMed2003

Psychophysical evaluation of responses to pleasant and mal-odour stimulation in human subjects; adaptation, dose response and gender differences.

A psychophysical detection test was used to measure the response of human subjects to 'good' and 'bad' smells. Different intensities and frequencies of odour stimulation were delivered by an olfactometer and the responses to a group of malodours (valeric acid, skatol, butyric acid) and pleasant smells (amyl acetate, cis-3-hexenol, linalool) were compared. A mathematical model, a power equation, was used to fit the three-dimensional data plots (dose vs. stimulus frequency vs. response). The model was able to distinguish between malodours and pleasant odours on the basis of the values of parameters describing dose-response and adaptation/habituation. We show that the olfactory system adapts/habituates more rapidly to malodours than to pleasant smells, but is much more sensitive to changes in stimulation by malodours than pleasant odours. The degree of adaptation is inversely proportional to stimulus strength. The response profile for women was different to that of men for certain odours, in particular valeric acid, skatol and cis-3-hexenol. The difference lay in their sensitivity and the slope and range of the dose response. Thus, we have shown for the first time that the olfactory system adapts more readily to 'bad' smells than 'good' smells, and that it has a broader range of adaptation for bad smells. As a consequence, the olfactory system is specially responsive to changes in potential olfactory warning signals.

Adaptation, Physiological↗

PubMed2005

Removal of volatile fatty acids with immobilized Rhodococcus sp. B261.

The removal of aqueous volatile fatty acids (VFA) in wastewater and spoiled waste-foods by immobilized Rhodococcus sp. B261 was investigated. The n-valeric acid (0.5%) was completely removed within 25 h under the following conditions; solution pH, 8.0; air flow rate, 0.2 l/min; superficial velocity, 0.96 h(-1); temperature, 37 degrees C. Under the optimized conditions, the acetic (8525 ppm), propionic (7310 ppm) and n-butyric (4360 ppm) except n-valeric (2572 ppm) acids from the wastewater were completely removed by immobilized Rhodococcus sp. B261 in 24 h. The acetic (7810 ppm), propionic (8942 ppm) and butyric (5730 ppm) acids from the solution of spoiled waste-foods were effectively removed by immobilized Rhodococcus sp. B261 from 48 h within 60 h but n-valeric acid (3625 ppm) took 72 h.

Acetic Acid↗

PubMed1999

Sensitivities of antennal olfactory neurons of the malaria mosquito, Anopheles gambiae, to carboxylic acids.

Single sensillum recordings on the antennae of female Anopheles gambiae s.s. mosquitoes revealed neurons sensitive to aliphatic carboxylic acids within (a) subtype(s) sensilla trichodea. The aliphatic acids, acetic acid, propionic acid, butyric acid, iso-butyric acid and iso-valeric acid evoked an inhibition reaction in one of the cell types recorded from. A different cell type was excited in response to the former aliphatic acids, but showed a broader range of sensitivity, as acids with a longer carbon chain length, like caproic acid, elicited excitations as well. In addition, occasionally 1-octen-3-ol elicited an excitation reaction. This article focuses on the carboxylic acid inhibited cell type and its temporal pattern of response to different doses of the compounds. Furthermore, in order to compare the stimulatory effectiveness of the compounds on a per molecule basis, corrections were made for differences in volatility by determining the absolute number of molecules in the stimulus puff.

Journal Article↗

PubMed2026

Excess iodine induces lipid metabolic disorders by the gut microbiota SCFAs/H2S-p-AMPKα/PPARγ/SREBP-1c pathway in female rats.

With the development of living standards, the problem of excess iodine has long been overlooked. This study aimed to investigate the detrimental effects of long-term excess iodine exposure on lipid metabolism in female Sprague-Dawley rats from the gut-liver axis perspective, and to elucidate the underlying molecular mechanisms by which the gut microbiota and its metabolites mediate iodine-induced lipid metabolic disorders. The results indicated that abnormal iodine nutrition has a negative effect on the health of rats. Specifically, excess iodine not only causes thyroid disorders but also leads to liver lipid metabolism disorders, including elevated serum and hepatic total cholesterol/triglyceride levels and lipid accumulation in the liver. Further investigation revealed that excess iodine causes liver lipid metabolism disorders by altering the gut microbiota, which resulted in an increase in the relative abundance of Desulfovibrio and Lachnospiraceae NK4A136_group, and a decrease in the relative abundance of Akkermansia and Blautia in excess iodine groups. A decrease in the relative abundance of Blautia and an increase in Lachnospiraceae NK4A136_group were strongly correlated with reductions in short-chain fatty acids (acetic, propionic, and valeric acids), whereas an increase in Desulfovibrio was strongly correlated with an increase in H2S. Additionally, acetic acid was negatively correlated with H2S in serum and liver. Excess iodine reduced hepatic p-AMPKα expression while upregulating key regulators of lipid metabolism, including SREBP-1c, PPARγ and ACC1. These changes may represent one of the key mechanisms by which excess iodine induces lipid metabolism disorders through the microbiota-metabolite axis. Overall, these findings suggest that excess iodine influences lipid metabolism through the gut-liver axis. The results of this study provide scientific references and guidance for the appropriate intake of iodine and offer novel insights for early nutritional interventions targeting lipid metabolism disorders.

Journal Article↗

PubMed2001

Reversal of methylation-mediated repression with short-chain fatty acids: evidence for an additional mechanism to histone deacetylation.

We have constructed a stable cell line, human embryonal kidney 293M+, containing a lacZ reporter gene controlled by an in vitro methylated hormone-responsive enhancer. Methylation of the enhancer-promoter abolishes lacZ expression controlled by ponasterone A (an analogue of ecdysone). Ponasterone A-induced expression is restored by the short-chain fatty acids valeric > butyric > propionic > acetic acid, but not by the histone deacetylase inhibitors trichostatin A and suberoylanilide hydroxamic acid (SAHA). lacZ expression is restored to levels approaching that from an unmethylated counterpart. Incubation with short-chain fatty acids alone does not promote demethylation of the lacZ promoter, however, some demethylation (30%) is observed when transcription is triggered by addition of ponasterone A. Similar levels of hyperacetylated histones H3 and H4 were observed in cells treated with short-chain fatty acids, trichostatin A or SAHA. In vivo DNase I footprinting indicates a more open chromatin structure at the promoter region for butyric acid-treated cells. A synergistic effect in reversing the methylation-mediated repression of the lacZ gene is obtained by combined treatments with the normally ineffective compounds trichostatin A and the short-chain fatty acid caproic acid. Our results suggest the existence of an alternative silencing mechanism to histone deacetylation in executing methylation-directed gene silencing.

Animals↗

PubMed1989

Particles and molecules in endodontic leakage.

It is assumed that above a critical level, microleakage causes periapical disease and jeopardizes periapical tissue repair. The purpose of this investigation was first to find out to what degree obturation prevents leakage of bacteria-sized particles or large protein molecules, and second if leakage of the commonly used dye methylene blue is comparable with that of a small bacterial metabolic product of similar molecular size. Sections, 9 mm long, obtained from 46 extracted human incisor roots had their root canals prepared in a standardized manner and obturated in four experimental ways using gutta-percha. The root sections were mounted in the middle of tubes that were closed at both ends with rubber membrane stoppers, which permitted sampling from the apical reservoir. The coronal reservoir was filled with a solution of 1 mg/ml latex beads, 4 micrograms/ml endotoxin, 0.5 per cent butyric acid, 0.1 per cent valeric acid and 0.1 per cent methylene blue water. After 1 and 2 weeks, samples were taken from the apical reservoir and tested for the presence of latex beads by phase-contrast microscopy, for endotoxin with a limulus lysate test, for butyric acid with gas-chromatography and for methylene blue with spectrophotometric analysis. Leakage of bacteria-sized particles and large-sized protein molecules could be prevented only when both sealer and pressure were used in obturating root canals with gutta-percha. Leakage of butyric acid proved to be comparable with leakage of methylene blue; microleakage of these small molecules could not be prevented in this study whatever method of filling was used.

Dental Leakage↗

PubMed1993

Endometrial bacterial flora detected in patients with uterine endometrial cancer.

Certain bacteria produce some carcinogens such as N-nitro compounds, n-butyric acid and n-valeric acid. From this point of view, the examination of intrauterine bacterial flora in patients with uterine endometrial cancer may provide important information. Twenty patients with the diagnosis of uterine endometrial cancer and 20 patients without complications other than myoma uteri were enrolled in the study. Enterobacteriaceae, Streptococcus agalactiae and anaerobic bacteria were mainly detected. The products of these bacteria might be considered to contribute to the initiation of endometrial carcinogenesis. Mixed abnormal flora between aerobic and anaerobic bacteria were detected in all patients with uterine endometrial cancer. It is suggested that uterine endometrial cancer provides favorable conditions for bacterial growth. Mixed abnormal bacterial flora also might influence the onset and growth of uterine endometrial cancer.

Aged↗

PubMed1982

Hyperlipoproteinemia, atherosclerosis and gemfibrozil.

Elevated levels of serum cholesterol have long been associated with an increased risk of both the occurrence and the progression of coronary atherosclerosis. The use of dietary therapy to reduce elevated lipid labels has received widespread attention, but like other therapy requiring behavioral modification has met with only partial success in most patients. Little wonder that drugs which lower lipids have been utilized to supplement the effect of diet in hyperlipidemia subjects. Currently available hypolipidemic agents are far from ideal in their effectiveness and lack of side effects, so the search for more potent, safer drugs has been intense. This paper reports on the use of one such agent, gemfibrozil; and its comparison with clofibrate and placebo. Gemfibrozil (CL719, 2,2-dimethyle-5-(2,5 xylyloxy) valeric acid is a substituted phenoxy alkyl acid which has been shown to decrease lipids in hyperlipidemia subjects. A short term study using 1200 mg of gemfibrozil daily demonstrated reduction in total serum cholesterol, triglyceride and apo B levels, and a concomitant rise in HDL cholesterol levels. A long term study of the effect so gemfibrozil showed that the drug had a more pronounced effect on triglyceride then cholesterol, that it had few side effects and the effect was sustained. A recent study from New Zealand demonstrated that gemfibrozil, compared to placebo, lowered plasma cholesterol, triglyceride and VLDL levels and raised HDL levels.

Adult↗

PubMed1978

[Gas chromatography analysis of volatile monocarboxylic aliphatic acids (C2 to C6) of 15 strains of Veillonella of oral origin].

A qualitative and quantitative study has been carried out on 15 strains of the Veillonella genus, isolated in the oral cavity. Following two methods of preparation of samples for injection in a chromatograph GL, we have identified among the volatil monocarboxylic aliphatic acids from C2 to C6 the glucose fermentation products of these different strains. With the same methods, we studied in parallel these products from strains A.T.C.C. 10790-17444 (Veillonella parvula) and 17445-17446 and 17447 (Veillonella alcalescens). The results, despite the diversity of origin of all these strains, based on physiological and biochemical characteristics, confirm that volatil monocarboxylic aliphatic acids are characteristic of a genus specificity and not of a species. The presence of acetic acid, proprionic acid and iso-valeric acid was shown

Chromatography, Gas↗

PubMed1989

Preparation of fecal samples for assay of volatile fatty acids by gas-liquid chromatography and high-performance liquid chromatography.

We describe a procedure for preparing fecal samples for determination of volatile fatty acids (VFAs) by gas-liquid chromatography (GLC) and "high-performance" liquid chromatography (HPLC). The simple, one-step procedure involves only ultrafiltration through a membrane with a molecular-mass cutoff of 3000 Da. As revealed by the GLC chromatograms, ultrafiltration appears to be as effective as steam distillation in sample clean-up. It also enables higher, more reproducible analytical recoveries of long-chain VFAs. The VFA content of the filtrate can also be measured by HPLC. Use of the ion-exclusion mechanism completely resolves isobutyric acid and butyric acid on a cation-exchange column. The mean (+/- SD) percentage distribution values of VFAs (measured by GLC) from five healthy subjects were 56.0 +/- 3.5 (acetic acid), 17.0 +/- 5.3 (propionic acid), 2.9 +/- 1.5 (isobutyric acid), 18.8 +/- 5.8 (butyric acid), 2.3 +/- 1.2 (isovaleric acid), and 2.9 +/- 0.8 (valeric acid).

Acetates↗

PubMedDate not supplied

[Topography, physicochemical and kinetic properties of the branched amino acid transaminases of the gastric and pancreatic mucosa].

About 40% of transaminase of branched amino acids were shown to be localized in mitochondrial matrix of pancreatic gland. The transaminases from pancreas and gastric mucosa had pH optima around pH 8.6. The enzymatic activity was increased with an increase in temperature to 50 degrees. In presence of 10 microM concentration of alpha-ketoglutarate Km volume of these two enzymes from postmitochondrial fraction of gastric mucosa and of pancreas were equal to 9.7 . 10(-4)M and 9.0 . 10(-4)M for leucine, 1.1.10(-4) M and 4.10(-3) M for valine, 6.4.10(-4) M and 8.5.10(-4) for isoleucine, respectively. The reaction or transamination proceeded via formation of a substituted form of the enzyme. The transaminase activity was inhibited by capronic acid (I506.8.10(-4) M), valeric acid (I508.10(-4)M), butyric acid (I50 5.8.10(-3) M) and propionic acid (I50 2.10(-2) M).

Amino Acids, Branched-Chain↗

PubMedDate not supplied

SEC-MALS characterization of microbial polyhydroxyalkanoates.

Characterization of poly-3-hydroxybutyric acid (PHB) and poly-3-hydroxybutyric-co-valeric acid (PHBV, 13% valerate) in chloroform was performed using size exclusion chromatography coupled to a multi-angle light scattering detector (SEC-MALS). Absolute molar mass averages, molar mass distribution, and the radius of gyration were determined. Three sample preparation methods were examined: dissolution in chloroform (1) at room temperature, (2) at 60 degrees C, and (3) after thermal pretreatment of samples (annealing at 180 degrees C with subsequent quenching in liquid nitrogen). Dissolution at 60 degrees C and dissolution of thermally pretreated samples gave molecularly dissolved PHB and PHBV. At 60 degrees C using acid free chloroform, there was no indication of degradation for up to 120 min dissolution time, whereas thermal degradation of polymers did take place during annealing at 180 degrees C. The degradation rate constants for number and weight average degree of polymerization at 180 degrees C were slightly higher for PHB (5.19 x 10(-5) min(-1), 4.95 x 10(-5) min(-1)) than for PHBV (4.99 x 10(-5) min(-1), 4.54 x 10(-5) min(-1)). The dependence of the radii of gyration on molar mass showed that both polymers form random coils in chloroform. The relationship between the absolute molar masses and relative SEC results was determined. DSC and NMR characterization also gave evidence of the progress of degradation.

Biodegradation, Environmental↗

PubMed1977

Specific and sensitive method for the determination of gamma-aminobutyric acid using gas chromatography with electron-capture or mass fragmentographic detection.

A gas chromatographic method for the determination of gamma-aminobutyric acid (GABA) in brain tissue is described. After microwave fixation, the brains were dissected and homogenized in 0.1 N formic acid; delta-amino-n-valeric acid (AVA), a homologue of GABA, was then added as an internal standard. After centrifugation, aliquots of the supernatant were treated with cation-exchange paper to adsorb the amino acids. The eluates of this paper were dried and the residues subjected to reaction with trifluoroacetic anhydride and hexafluoroisopropanol. After removal of the derivatization reagents by evaporation, the residues were dissolved in ethyl acetate and an aliquot was analysed by gas chromatography with electron-capture or mass fragmentographic detection. Quantitation can be carried out by either peak-height or peak-area measurements. The specificity of this method has been demonstrated with brain tissue by simultaneous mass fragmentographic analysis. The sensitivity is comparable to that of mass fragmentographic methods and is in the femtomole range. The method is simple and readily automated.

Aminobutyrates↗

PubMed1997

Neuroprotection by the metabolic antioxidant alpha-lipoic acid.

Reactive oxygen species are thought to be involved in a number of types of acute and chronic pathologic conditions in the brain and neural tissue. The metabolic antioxidant alpha-lipoate (thioctic acid, 1, 2-dithiolane-3-pentanoic acid; 1, 2-dithiolane-3 valeric acid; and 6, 8-dithiooctanoic acid) is a low molecular weight substance that is absorbed from the diet and crosses the blood-brain barrier. alpha-Lipoate is taken up and reduced in cells and tissues to dihydrolipoate, which is also exported to the extracellular medium; hence, protection is afforded to both intracellular and extracellular environments. Both alpha-lipoate and especially dihydrolipoate have been shown to be potent antioxidants, to regenerate through redox cycling other antioxidants like vitamin C and vitamin E, and to raise intracellular glutathione levels. Thus, it would seem an ideal substance in the treatment of oxidative brain and neural disorders involving free radical processes. Examination of current research reveals protective effects of these compounds in cerebral ischemia-reperfusion, excitotoxic amino acid brain injury, mitochondrial dysfunction, diabetes and diabetic neuropathy, inborn errors of metabolism, and other causes of acute or chronic damage to brain or neural tissue. Very few neuropharmacological intervention strategies are currently available for the treatment of stroke and numerous other brain disorders involving free radical injury. We propose that the various metabolic antioxidant properties of alpha-lipoate relate to its possible therapeutic roles in a variety of brain and neuronal tissue pathologies: thiols are central to antioxidant defense in brain and other tissues. The most important thiol antioxidant, glutathione, cannot be directly administered, whereas alpha-lipoic acid can. In vitro, animal, and preliminary human studies indicate that alpha-lipoate may be effective in numerous neurodegenerative disorders.

Animals↗