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At least 937 records · Page 52Linked to original sources
PubMed1977

[Gas chromatographic determination of the volatile fatty acids (C1-C5) including lactic acid after conversion into their benzyl esters by phenyldiazomethane. Determination of the acids in silages (author's transl)].

A gas chromatographic method for the determination of the volatile fatty acids (C1-C5) including lactic acid is described. The acids are converted into their benzyl esters by means of phenyldiazomethane without previous purification of the reagent by distillation. The benzyl esters are well separated from the solvent as well as from one another. Silicone SE-30 is used as the stationary phase. An application of the method on silage acids is demonstrated.

Animal Feed↗
PubMed2003

Protein adsorption, fibroblast activity and antibacterial properties of poly(3-hydroxybutyric acid-co-3-hydroxyvaleric acid) grafted with chitosan and chitooligosaccharide after immobilized with hyaluronic acid.

Poly(3-hydroxybutyric acid-co-3-hydroxyvaleric acid) (PHBV) membrane was treated with ozone and grafted with acrylic acid. The resulting membranes were further grafted with chitosan (CS) or chitooligosaccharide (COS) via esterification. Afterward hyaluronic acid (HA) was immobilized onto CS- or COS-grafting membranes. The antibacterial activity of CS and COS against Staphylococus aureus, Escherichia coli, and Pseudomonas aeruginosa was preserved after HA immobilization. Among them, CS-grafted PHBV membrane showed higher antibacterial activity than COS-grafted PHBV membrane. In addition, after CS- or COS-grafting, the L929 fibroblasts attachment and protein adsorption were improved, while the cell number was decrease. After immobilizing HA, the cell proliferation was promoted, the protein adsorption was decreased, and the cell attachment was slightly lower than CS- or COS-grafting PHBV.

Absorbable Implants↗
PubMed2001

Release of salicylic acid, diclofenac acid and diclofenac acid salts from isotropic and anisotropic nonionic surfactant systems across rat skin.

Release of salicylic acid, diclofenac acid, diclofenac diethylamine and diclofenac sodium, from lyotropic structured systems, namely; neat and middle liquid crystalline phases, across mid-dorsal hairless rat skin into aqueous buffer were studied. Release results were compared with those from the isotropic systems. The donor systems composed of the surfactant polyoxyethylene (20) isohexadecyl ether, HCl buffer of pH 1 or distilled water and the specific drug. High performance liquid chromatography (HPLC) methods were used to monitor the transfer of the drugs across the skin barrier. Results indicated that the rate-determining step in the transport process was the release of the drug from the specified donor system. Further, apparent zero order release was demonstrated with all systems. Except for diclofenac sodium, drug fluxes decreased as the donor medium changed from isotropic to anisotropic. The decrease in fluxes was probably due to the added constrains on the movement of drug molecules. By changing the anisotropic donor medium from neat to middle phase, drug flux decreased in case of salicylic acid and diclofenac sodium. In the mean time, flux increased in case of the diethylamine salt and appeared nearly similar in case of diclofenac acid. Rates of drug transfer across the skin from the anisotropic donors seemed to be largely controlled by the entropy contribution to the transport process. The type and extent of drug-liquid crystal interactions probably influenced the latter.

Animals↗
PubMed1981

Mechanism of inactivation of gamma-aminobutyric acid-alpha-ketoglutaric acid aminotransferase by 4-amino-5-halopentanoic acids.

(S)-4-Amino-5-halopentanoic acids were previously shown to irreversibly inhibit pig brain gamma-aminobutyric acid--alpha-ketoglutaric acid aminotransferase, and a mechanism for the inactivation was proposed (Silverman, R. B., & Levy M. A. (1980) Biochem. Biophys. Res. Commun. 95, 250). Evidence is presented to show that these compounds are mechanism-based inactivators, and experiments are described to elucidate their mechanism of action. The enzyme must be in the pyridoxal phosphate form for inactivation to occur, the gamma proton of the inactivators is removed in a rate-determining step, and one fluoride ion is released from 4-amino-5-fluoropentanoic acid per active site labeled. The change in the optical spectrum of the enzyme during inactivation suggests that the coenzyme is converted into the pyridoxamine phosphate form. Every turnover of inactivator leads to an inactivation event, i.e., the partition ratio is zero.

4-Aminobutyrate Transaminase↗
PubMed1977

5-(Tetradecyloxy)-2-furancarboxylic acid and related hypolipidemic fatty acid-like alkyloxyarylcarboxylic acids.

5-(Tetradecyloxy)-2-furancarboxylic acid (91, RMI 14514) was found to lower blood lipids and to inhibit fatty acid synthesis with minimal effects on liver weight and liver fat content. This fatty acid-like compound represents a new class of hypolipidemic agent; it is effective in rats and monkeys. The compound resulted from discovery of hypolipidemic activity in certain beta-keto esters, postulation and confirmation of the corresponding benzoic acids as active metabolites, and systematic exploration of the structure--activity relationships.

Animals↗
PubMed1998

Retinoic acid-dependent stimulation of 2,2'-azobis(2-amidinopropane)-initiated autoxidation of linoleic acid in sodium dodecyl sulfate micelles: a novel prooxidant effect of retinoic acid.

(E)-Retinoic acid (RA) was shown to stimulate the rate of 2,2'-azobis(2-amidinopropane) (AAPH)-initiated autoxidation of linoleic acid (18:2) in sodium dodecyl sulfate (SDS) micelles. RA-dependent stimulation of 18:2 autoxidation was characterized by enhanced rates of dioxygen uptake which were linear with retinoid concentration. In contrast, 5,6-epoxy-RA, a major oxidation product of RA, failed to affect the rate of dioxygen consumption at all concentrations tested. RA was also shown to stimulate peroxyl radical-dependent oxidation of styrene to the corresponding oxirane when styrene was included in the micellar system as a molecular probe. Furthermore, unequivocal evidence of RA-dependent stimulation of 18:2 autoxidation was obtained by relative quantitation of 13-hydroxy-(9Z, 11E)-octadecadienoic acid (13-HODE) plus 9-hydroxy-(10E,12Z)-octadecadienoic acid (9-HODE) production. In addition, enhanced carbon-centered radical formation was demonstrated in the presence of RA by EPR spectroscopy using alpha-(4-pyridyl 1-oxide)-N-tert-butylnitrone (4-POBN) as a spin trap. Analysis and quantitation of RA oxidation products indicated that RA was oxidized to one primary product, 5,6-epoxy-RA, which was identified on the basis of cochromatography with synthetic standard (in a reverse-phase HPLC system), electronic absorption spectroscopy, and positive chemical ionization mass spectrometry of the corresponding methyl ester. Other minor oxidation products were also detected but not characterized. In contrast, reaction mixtures devoid of 18:2 failed to demonstrate significant retinoid oxidation. Mechanisms are proposed to account for the prooxidant effects of RA in this system.

Amidines↗
PubMed1970

Evidence for the absence of the terminal adenine nucleotide at the amino acid-acceptor end of transfer ribonucleic acid in non-lactating bovine mammary gland and its inhibitory effect on the aminoacylation of rat liver transfer ribonucleic acid.

1. tRNA isolated from non-lactating bovine mammary gland competitively inhibits the formation of aminoacyl-tRNA in the rat liver system. 2. Non-lactating bovine mammary gland tRNA and twice-pyrophosphorolysed rat liver tRNA are unable to accept amino acids in a reaction catalysed by aminoacyl-tRNA synthetases from either rat liver or bovine mammary gland. Deacylated rat liver tRNA can however be aminoacylated in the presence of either enzyme. 3. Bovine mammary gland tRNA lacks the terminal adenine nucleotide at the 3'-terminus amino acid acceptor end, which can be replaced by incubation in the presence of rat liver nucleotide-incorporating enzyme, ATP and CTP. 4. The enzymically modified bovine tRNA (tRNApCpCpA) can bind labelled amino acids to form aminoacyl-tRNA, which can then transfer its labelled amino acids to growing polypeptide chains on ribosomes. 5. Molecules of rat liver tRNA or bovine mammary gland tRNA that lack the terminal adenine nucleotide or the terminal cytosine and adenine nucleotides inhibit the aminoacylation of normal rat liver tRNA to varying degrees. tRNA molecules lacking the terminal -pCpCpA nucleotide sequence exhibit the major inhibitory effect. 6. The enzyme fraction from bovine mammary gland corresponding to that containing the nucleotide-incorporating enzyme in rat liver is unable to catalyse the incorporation of cytosine and adenine nucleotides in pyrophosphorolysed rat liver tRNA and deacylated bovine tRNA. This fraction also markedly inhibits the action of the rat liver nucleotide-incorporating enzyme.

Adenine Nucleotides↗
PubMed1974

The control of ribonucleic acid synthesis in bacteria. Fluctuations in messenger ribonucleic acid synthesis in cultures recovering from amino acid starvation.

Changes in the cell content and rate of synthesis of mRNA were studied in auxotrophs of Escherichia coli recovering from a period of amino acid deprivation. Parallel studies were carried out on bacterial strains inhibited with trimethoprim, when glycine and methionine were added to relieve an amino acid deficiency. In the latter case, protein synthesis was still severely inhibited through a lack of N-formylmethionyl-tRNA(fMet) for chain initiation, so that fewer ribosomes were attached to mRNA chains. (1) In RC(str) strains recovering from amino acid starvation, there was a transient oversynthesis of mRNA, but the amounts returned to normal after about a 15-min period of recovery. RC(rel) strains did not show this effect; any extra mRNA accumulated during the previous starvation period was rapidly lost, but no oversynthesis occurred during the resumption of growth. (2) In trimethoprim-inhibited cultures supplemented with glycine and methionine, mRNA was produced at the same rate, relative to stable RNA species, as during normal growth. The evidence implied that decreased rates of ribosome attachment had no effect on the functional or chemical lifetime of the mRNA fraction. This suggests that mRNA stability does not depend on the frequency of translation by ribosomes. (3) Changes in the mRNA contents of trimethoprim-inhibited RC(str) and RC(rel) cultures were noted soon after supplementation with glycine and methionine. These closely followed those observed in cultures recovering from simple amino acid withdrawal.

Amino Acids↗
PubMed1990

The fatty acid analogue 11-(dansylamino)undecanoic acid is a fluorescent probe for the bilirubin-binding sites of albumin and not for the high-affinity fatty acid-binding sites.

1. The fluorescent fatty acid probe 11-(dansylamino)undecanoic acid (DAUDA) binds with high affinity to bovine and human serum albumin (BSA and HSA) at three sites. 2. The Kd of the primary binding site could not be determined; however, the two secondary sites appeared to be equivalent, with an apparent Kd of 8 x 10(-7) M for both BSA and HSA. 3. The spectral characteristics of DAUDA when bound to the primary site of the two albumins were different, with HSA producing a greater fluorescence enhancement and emission maximum at a shorter wavelength (480 nm) than for BSA (495 nm). 4. Displacement studies indicated that the DAUDA-binding sites were not equivalent to the primary long-chain fatty acid-binding sites on albumin, but corresponded to the bilirubin sites. Fatty acyl-CoAs also bind to the bilirubin sites, as do medium-chain fatty acids. 5. The solubility, stability and spectral properties of DAUDA make it an excellent probe for investigating the bilirubin-binding sites of albumin, particularly HSA.

Bilirubin↗
PubMed2001

Isolation from Cussonia barteri of 1'-O-chlorogenoylchlorogenic acid and 1'-O-chlorogenoylneochlorogenic acid, a new type of quinic acid esters.

1'-O-Chlorogenoylchlorogenic acid and 1'-O-chlorogenoylneochlorogenic acid, a new type of quinic acid esters, have been isolated, in addition to six known quinic acid esters, rutin, and a mixture of saponins, from the methanol extract of Cussonia barteri Seemann (Araliaceae) leaves collected in Cameroon. Structure determination was achieved by NMR, mass, IR, and UV spectroscopy. All compounds were tested for inhibitory activity on 5-lipoxygenase and cyclooxygenase-1, for antimicrobial activity against Bacillus subtilis, Pseudomonas fluorescens, and Cladosporium cucumerinum, and for haemolytic activity.

Anti-Infective Agents↗
PubMed1980

Hydrazonopropionic acid, a new class of hypoglycemic substances. 2. Influence of 2-(phenylethylhydrazono)- and 2-(2-cyclohexyl-ethylhydrazono)-propionic acid on redox systems, acid base status and monoamino oxidase activity.

Phenylethylhydrazono-propionic acid (PEHP) and cyclohexyl-ethylhydrazono-propionic acid (CHEHP) has been shown to lower blood glucose concentrations in various laboratory animals after intraperitoneal or oral application. The present study has been conducted to investigate, if these hydrazones may induce lactic acidosis like the biguanides or may cause unwanted side reactions due to an inhibition of monoamino oxidase like the corresponding hydrazines. It was found that intramitochondrial and cytoplasmatic redox ratios were not influenced at a hypoglycemic effective dosage (145 mumol/kg body weight) of these substances in fasted guinea pigs. An effect on the acid base status was not observed. Both substances lowered the concentration of ketone bodies in fasted guinea pigs. In vitro the activity of monoamino oxidase purified from guinea pig liver was much less inhibited by the hydrazones than by one of the corresponding hydrazines (phenelzine). Furthermore CHEHP (145 mumol/kg body weight) did not influence the serum activity of various liver enzymes and the concentration of triglycerides, cholesterol and uric acid in plasma of fasted guinea pigs. It is concluded that CHEHP meets basic requirements for a potential oral antidiabetic agent.

Acetoacetates↗
PubMed1993

Requirements for indispensable amino acids in adult humans: longer-term amino acid kinetic study with support for the adequacy of the Massachusetts Institute of Technology amino acid requirement pattern.

Twenty young men received an L-amino acid diet, supplying 140 mg N.kg-1 x d-1 and patterned as in the Egg diet for 1 wk, and then for 3 wk either a pattern based on international recommendations (modified FAO diet; n = 7), our new amino acid requirement pattern (MIT diet; n = 7), or the egg pattern (Egg diet; n = 6). At the end of the initial week, at 1 and 3 wk with the three experimental diets, and after 3 d after return to the Egg diet, an 8-h continuous intravenous infusion with [1-13C]leucine (3 h fast, 5 h fed while subjects received hourly meals supplying the equivalent of one-twelfth the daily intake) was conducted. After 3 wk with the different diets, mean daily leucine balances were lower (P < 0.01) with the FAO diet (-160 mumol.kg-1 x d-1) than with the MIT diet (-15 mumol.kg-1 x d-1). Together with changes in plasma amino acid profiles [eg, methionine increased (P < 0.05) during feeding with the FAO and Egg diets but not with the MIT diet; increased proline concentrations during the fed state (P < 0.05) with the FAO diet but not with the MIT or Egg diets] we interpret these findings to indicate that the FAO diet is not capable of maintaining amino acid homeostasis, as is the case with the MIT and Egg diets.

Adult↗
PubMed2001

Dietary trans fatty acids combined with a marginal essential fatty acid status during the pre- and postnatal periods do not affect growth or brain fatty acids but may alter behavioral development in B6D2F(2) mice.

The objective of this study was to investigate whether dietary trans fatty acids (TFA) during the pre- and postnatal periods would exacerbate the effects of marginal essential fatty acid (EFA) status on growth, brain long-chain polyunsaturated fatty acids (LC-PUFA) and behavioral development in B6D2F(2) mice. Pregnant B6D2F(1) females were randomly assigned to one of the following three diets: marginal EFA plus 22% trans 18:1 (mEFA + TFA); marginal EFA (mEFA); and control (CON). The total 18:1 content in all diets was similar. The offspring were weaned and maintained on the same diets. Both the mEFA and mEFA + TFA groups had reduced growth and brain weight compared with CON, but did not differ from one another. As expected, the mEFA and mEFA + TFA groups had reduced docosahexaenoic acid [DHA; 22:6(n-3)]) and increased 22:5(n-6) concentrations in brain phosphatidylcholine (PC) and phosphatidylethanolamine (PE) compared with the CON group, but again did not differ from one another. Reversal learning in the T-water maze was significantly slower in the mEFA + TFA groups compared with the mEFA group and both were slower than the CON group. These findings illustrate that TFA combined with a marginal EFA status do not exacerbate the effects of marginal EFA status on growth or brain LC-PUFA. However, long-term effects of dietary TFA during the pre- and postnatal period on behavioral development and neural function should be investigated in future studies.

Animals↗
PubMed1993

Teichoic acid and lipoteichoic acid of Streptococcus pneumoniae possess identical chain structures. A reinvestigation of teichoid acid (C polysaccharide).

Teichoic acid (C polysaccharide) was extracted and purified from Streptococcus pneumoniae R6 with standard procedures except that lipoteichoic acid was extracted first. The dephosphorylated repeating unit was isolated after hydrolysis with 48% (by mass) HF, the bis(phosphocholine)-containing repeating unit was isolated by alkali hydrolysis, anion-exchange chromatography and phosphomonoester cleavage. On the basis of compositional analysis, fast-atom-bombardment mass spectrometry and NMR spectroscopy the following structure is proposed: [formula: see text] where AATGal is 2-acetamido-4-amino-2,4,6-trideoxy-D-galactose. The repeating units are linked to each other by phosphodiester bonds between O5 of the ribitol and O6 of the glucopyranosyl residue of adjacent units. This chain structure is identical with that previously established for pneumococcal lipoteichoic acid [Behr, T., Fischer, W., Peter-Katalinić, J. & Egge, H. (1992) Eur. J. Biochem. 207, 1063-1075]. This represents a unique situation because in other Gram-positive bacteria teichoic and lipoteichoic acids are structurally unrelated.

Carbohydrate Sequence↗
PubMed1971

Oxidation of nicotinic acid by a Bacillus species: purification and properties of nicotinic acid and 6-hydroxynicotinic acid hydroxylases.

The enzymes of a Bacillus species that hydroxylate nicotinic acid to 6-hydroxynicotinic acid and 6-hydroxynicotinic acid to 2,6-dihydroxynicotinic acid were purified and characterized. The purified enzymes contained approximately two molecules of flavine and eight molecules of iron per molecule of enzyme. The enzymes were large (molecular weight, 400,000 to 450,000) and appeared to consist of subunits.

Ammonium Sulfate↗
PubMed2005

Suppression of mammary carcinoma growth by retinoic acid: proapoptotic genes are targets for retinoic acid receptor and cellular retinoic acid-binding protein II signaling.

Retinoic acid (RA) displays pronounced anticarcinogenic activities in several types of cancer. Whereas the mechanisms that underlie this activity remain incompletely understood, tumor suppression by RA is believed to emanate primarily from its ability to regulate transcription of multiple target genes. Here, we investigated molecular events through which RA inhibits the growth of MCF-7 mammary carcinoma cells, focusing on the involvement of the two proteins that mediate transcriptional activation by RA, the nuclear hormone receptor retinoic acid receptor (RAR) and the cellular retinoic acid-binding protein (CRABP) II, in this process. RA treatment of MCF-7 cells did not affect cell cycle distribution but triggered pronounced apoptosis. Accordingly, expression array analyses revealed that RA induces the expression of several proapoptotic genes, including caspase 7 and caspase 9. Whereas caspase 7 is an indirect responder to RA signaling, caspase 9 is a novel direct target for RAR, and it harbors a functional retinoic acid response element in its second intron. In agreement with the known role of CRABP-II in enhancing the transcriptional activity of RAR, the binding protein augmented RA-induced up-regulation of caspase 9, cooperated with RA in activating both caspase 7 and 9, and amplified the ability of RA to trigger apoptosis. Surprisingly, the data indicate that CRABP-II also displays proapoptotic activities on its own. Specifically, overexpression of CRABP-II, in the absence of RA, up-regulated the expression of Apaf1 and triggered caspase 7 and caspase 9 cleavage. These observations suggest that, in addition to its known role in direct delivery of RA to RAR, CRABP-II may have an additional, RA-independent, function.

Antineoplastic Agents↗
PubMed2005

Retinol inhibits the growth of all-trans-retinoic acid-sensitive and all-trans-retinoic acid-resistant colon cancer cells through a retinoic acid receptor-independent mechanism.

Retinol (vitamin A) is thought to exert its effects through the actions of its metabolite, all-trans-retinoic acid (ATRA), on gene transcription mediated by retinoic acid receptors (RAR) and retinoic acid response elements (RARE). However, retinoic acid resistance limits the chemotherapeutic potential of ATRA. We examined the ability of retinol to inhibit the growth of ATRA-sensitive (HCT-15) and ATRA-resistant (HCT-116, SW620, and WiDR) human colon cancer cell lines. Retinol inhibited cell growth in a dose-responsive manner. Retinol was not metabolized to ATRA or any bioactive retinoid in two of the cell lines examined. HCT-116 and WiDR cells converted a small amount of retinol to ATRA; however, this amount of ATRA was unable to inhibit cell growth. To show that retinol was not inducing RARE-mediated transcription, each cell line was transfected with pRARE-chloramphenicol acetyltransferase (CAT) and treated with ATRA and retinol. Although treatment with ATRA increased CAT activity 5-fold in ATRA-sensitive cells, retinol treatment did not increase CAT activity in any cell line examined. To show that growth inhibition due to retinol was ATRA, RAR, and RARE independent, a pan-RAR antagonist was used to block RAR signaling. Retinol-induced growth inhibition was not alleviated by the RAR antagonist in any cell line, but the antagonist alleviated ATRA-induced growth inhibition of HCT-15 cells. Retinol did not induce apoptosis, differentiation or necrosis, but affected cell cycle progression. Our data show that retinol acts through a novel, RAR-independent mechanism to inhibit colon cancer cell growth.

Antineoplastic Agents↗
PubMed2001

Synthesis of anacardic acids, 6-[8(Z),11(Z)-pentadecadienyl]salicylic acid and 6-[8(Z),11(Z),14-pentadecatrienyl]salicylic acid.

11-Chloro-3-methoxy-2-undecenal was synthesized from 8-bromooctanol, and an annelation reaction with this aldehyde and ethyl acetoacetate proceeded to give the ethyl 6-(8-chlorooctyl)salicylate. Ethyl 6-(8-chlorooctyl)salicylate was converted to ethyl 6-(7-formylheptyl)-2-methoxybenzoate through the iodide after protection of the phenolic hydroxyl group. Finally, the Wittig reaction with the aldehyde and triphenylphosphonium iodides in the presence of BuLi gave the methoxybenzoates, and then treatments of these methoxybenzoates with BBr3 in CH2Cl2 and 10% NaOH in ethanol gave 6-18(Z),11(Z)-pentadecadienyllsalicylic acid (anacardic acid 3) and 6-[8(Z),11(Z),14-pentadecatrienyl]salicylic acid (anacardic acid 4) which were isolated from plants of the anacardiaceae.

Alkenes↗