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PubMed2003

[Synthesis, characterization and in vitro release of poly (succinimide-co-4-aminobutanoic acid) by acid-catalyzed polycondensation of L-aspartic acid and 4-aminobutanoic acid].

For the purpose of increasing the hydrophilicity of poly aspartic acid, a series of polymer of L-aspartic acid and 4-aminobutanoic acid with different ratios (mol/mol) were prepared. The copolymers were characterized by 13CNMR, DSC and x-ray. The confirmed the structures of the polymers. In-vitro tests of release at phosphate buffer saline, enzyme solution of trypsin and papain (37.0 degrees C, pH = 7.4) were carried out. The result indicated that the polymers could be degraded in some degree, and that 4-aminobutanoic acid segments accelerated the degradation rate of the polymers. Skin irritation test and systemic acute toxicity test were carried out, which showed that the polymer was a nontoxic biomedical material.

Animals↗
PubMed1998

Growth, mortality, tissue histopathology and fatty acid compositions, eicosanoid production and response to stress, in juvenile turbot fed diets rich in gamma-linolenic acid in combination with eicosapentaenoic acid or docosahexaenoic acid.

Three diets containing either borage oil (BO) and southern hemisphere fish oil Marinol (MO), or BO and tuna orbital oil (TO), or a northern hemisphere fish oil (FO) were fed to duplicate groups of turbot (Scophthalmus maximus) of initial mean weight 1.2 g for a period of 12 weeks. The BO/MO and BO/TO diets were enriched in gamma-linolenic (18:3n-6, GLA) and eicosapentaenoic (20:5n-3, EPA) acids, and GLA and docosahexaenoic acid (22:6n-3, DHA), respectively. No differences were observed in final weights or growth rates, either between duplicate tanks or between dietary treatments. Half of the FO-fed fish sampled showed a histopathological lesion indicative of lipoid liver degeneration while the other treatments only showed a slight incidence of the same pathology. The fatty acid compositions of carcass and tissues broadly reflected the dietary input. In general, fish fed the BO/MO diet had increased levels of 18:2n-6, 18:3n-6, 20:3n-6 and 20:5n-3, but a lower level of 22:6n-3, compared to fish fed FO. In fish fed the BO/TO diet, levels of 18:2n-6, 18:3n-6, 20:3n-6 and 20:4n-6 were increased while levels of 20:5n-3 and 22:5n-3 were reduced, compared to fish fed FO. Concentrations of thromboxanes B (TXB) and leukotrienes B (LTB), derived from 20:4n-6 and 20:5n-3, were measured in plasma and stimulated blood cells. Levels of TXB2 were greatest in fish fed the BO/TO diet compared to both other treatments, while LTB4 was decreased in fish fed the BO/MO diet compared to both other treatments. In a stress test which involved anaesthesia followed by measurement of recovery times, fish fed the BO/MO diet had significantly lower recovery times compared to fish fed the FO diet.

Animals↗
PubMed2006

Characterization and crystal structure of cadmium(II) halide complexes with amino acids and their derivatives: VII. Crystal structures of aquadibromo(3-aminopropanoic acid)cadmium(II), dichloro(4-aminobutanoic acid)cadmium(II), diaquabis(aminohexanoic acid)cadmium(II) tetrachlorocadmium(II), and dibromo(azetidine-3-carboxylic acid)cadmium(II).

Seven cadmium complexes: [CdX2(Hapro)(H2O)n] (X: Cl(1), Br(2)), [CdX2(Hgaba)] (X: Cl(3), Br(4)), [Cd(Hahex)2(H2O)2][CdCl4] (5), and [CdX2(Haze-3)](H2O)n (X: Cl(6), Br(7)) have been prepared and investigated by means of IR and FT Raman spectra. The crystal and molecular structures of 2, 3, 5 and 7 were determined by a single-crystal X-ray diffraction method. In complex 2, the cadmium atom is in a distorted octahedral geometry, ligated by two carboxyl oxygen atoms of Hapro, a water molecule, and three bromine atoms; one is terminal and each of the other two is bridging two cadmium atoms to make a polymer. The structure of 3 consists of one-dimensional polymers bridged by two chlorine atoms and a carboxyl group. The carboxyl oxygen atoms of Hgaba coordinate forkedly to two cadmium atoms. The cadmium atom of [Cd(Hahex)2(H2O)2]2+ in complex 5 is in a distorted octahedral geometry, ligated by four carboxyl oxygen atoms of two molecules of Hahex and by two water molecules. [Cd(Hahex)2(H2O)2]2+ exists between two layers which are formed of infinite [CdCl4]2- chains. The carboxyl oxygen atoms of Hahex coordinate to the same cadmium atom. In complex 7, the cadmium atom is ligated by two carboxyl oxygen atoms and four bridging bromine atoms to make a polymer.

Amino Acids↗
PubMed1984

Effects of glutamic acid, kainic acid and aspartic acid on GABA release from rat retina degenerated by kainic acid.

The effects of L-glutamic acid (Glu), kainic acid (KA) and L-aspartic acid (Asp) on 14C-GABA release from the rat retina degenerated by KA were investigated. In the normal rat retina, Glu initially enhanced GABA release and subsequently inhibited it. Both KA and Asp did not have dual effects; KA enhanced GABA release, while Asp inhibited it. In the KA-degenerated retina, the stimulatory effect of Glu or KA on GABA release was markedly suppressed, while the inhibitory effects of Glu or Asp were preserved.

Animals↗
PubMed1999

Improved method for simultaneous determination of ascorbic acid and dehydroascorbic acid, isoascorbic acid and dehydroisoascorbic acid in food and biological samples.

The total vitamin C amount in different food and plasma samples was determined by a dual detection system, after HPLC separation, with direct detection of ascorbic acid and indirect fluorimetric detection of dehydroascorbic acid after a post-column O-phenyldiamine derivatisation. The two active forms of vitamin C and their D-isomers were separated within 10 min. The repeatability was determined by measurement of several fruits and vegetables and ranged from 0.3 to 1.9% (relative standard deviation) for vitamin C. The reproducibility, based on double determinations, ranged from 1.9 to 3.6% for vitamin C, depending on the matrix. The reproducibility, based on several determinations of reference materials, ranged from 2.4 to 3.7% for ascorbic acid and from 4.3 to 5.8% for dehydroascorbic acid, again depending on the matrix.

Ascorbic Acid↗
PubMed2001

X-ray studies on crystalline complexes involving amino acids and peptides. XXXVIII. Crystal structures of the complexes of L-arginine and L-histidine with glutaric acid and a comparative study of amino acid-glutaric acid complexes.

The complexes of glutaric acid with L-arginine and L-histidine (two crystal forms) exhibit different stoichiometries and ionization states. The aggregation patterns in two of the crystals are remarkably similar to those observed earlier in similar structures, while the pattern in the remaining one has not been seen earlier. The variability in the ionization state and stoichiometry observed in amino acid-dicarboxylic acid complexes appears to represent subtle differences in the response of a molecule to the presence in its neighbourhood of another type of molecule. The glutaric acid molecules (or glutarate or semiglutarate ions) in their complexes and in other crystals favour a fully extended conformation, albeit with frequent departures from it. The change in the chirality of the component molecules in the complex could lead to drastic changes in the aggregation pattern; alternatively, the effects of the change are accommodated through small adjustments in essentially the same pattern.

Amino Acids↗
PubMed1981

Sulfur amino acid metabolism in the developing rhesus monkey brain: subcellular studies of taurine, cysteinesulfinic acid decarboxylase, gamma-aminobutyric acid, and glutamic acid decarboxylase.

Taurine, cysteinesulfinic acid decarboxylase (CSAD), glutamate, gamma-aminobutyric acid (GABA), and glutamic acid decarboxylase (GAD) were measured in subcellular fractions prepared from occipital lobe of fetal and neonatal rhesus monkeys. In addition, the distribution of [35S]taurine in subcellular fractions was determined after administration to the fetus via the mother, to the neonate via administration to the mother prior to birth, and directly to the neonate at various times after birth. CSAD, glutamate, GABA, and GAD all were found to be low or unmeasurable in early fetal life and to increase during late fetal and early neonatal life to reach values found in the mother. Taurine was present in large amounts in early fetal life and decreased slowly during neonatal life, arriving at amounts found in the mother not until after 150 days of age. Significant amounts of taurine, CSAD, GABA, and GAD were associated with nerve ending components with some indication that the proportion of brain taurine found in these organelles increases during development. All subcellular pools of taurine were rapidly labeled by exogenously administered [35S]taurine. The subcellular distribution of all the components measured was compatible with the neurotransmitter or putative neurotransmitter functions of glutamate, GABA, and taurine. The large amount of these three amino acids exceeds that required for such function. The excess of glutamate and GABA may be used as a source of energy. The function of the excess of taurine is still not clear, although circumstantial evidence favors an important role in the development and maturation of the CNS.

Aging↗
PubMed1976

A comparison of gamma-aminobutyric acid and the semi-rigid analogues 4-aminotetrolic acid, 4-aminocrotonic acid and imidazole-4-acetic acid on the isolated superior cervical ganglion of the rat.

1 The rat superior cervical ganglion possesses receptors for gamma-aminobutyric acid (GABA). This can be demonstrated in vitro by recording the changes in ganglionic surface potential which occur after the addition of GABA to the bathing solution. 2 The action of three conformationally-restricted analogues of GABA namely 4-aminotetrolic acid (4-ATA), trans 4-aminocrotonic acid (4-ACA) and imidazole-4-acetic acid (IAA) have been examined for activity at this peripheral receptor. 3 All three analogues depolarized the ganglion in a manner similar to GABA. Their actions were transient and were 'occluded' by GABA; also the dose-response curve in each case was parallel to that of GABA. Molar potencies relative to GABA (= 1) were 4-ACA = 1.48, IAA = 0.100, 4-ATA = 0.0028. 4 The action of each analogue could be blocked by the GABA antagonists bicuculline and tetramethylenedisulphotetramine at doses which had relatively little effect on responses to the cholinomimetic carbachol. 5 4-ACA and IAA (1 mM) significantly reduced the ganglionic accumulation of [3H]-GABA (0.2 muM) by 88% and 58% respectively whereas 4-ATA (1 mM), caused no significant reduction in [3H]-GABA accumulation.

Aminobutyrates↗
PubMed1981

Semisynthetic cephalosporins with alpha-oximino acid side chains. The preparation and coupling of 4-acylamino-alpha-oximinobenzeneacetic acids and 1,2-dihydro-6-methyl-alpha-oximino-2-oxo-3-pyridineacetic acid to 7-aminocephalosporanic acid.

A series of 4-acylamino-alpha-oximinobenzeneacetic acids, and 1,2-dihydro-6-methyl-alpha-oximino-2-oxo-3-pyridineacetic acid were prepared and coupled to 7-aminocephalosporanic acid and its 3'-(1-methyltetrazol-5-yl)thiolo analogue. Several coupling methods and oxime protecting groups were thoroughly examined. The best coupling procedure employed dimethylchloroformiminium chloride, and the tetrahydropyranyl (THP) group was selected for oxime protection. The cephalosporins prepared were tested and compared to cefuroxime and cefotaxime. The corresponding alpha-keto acids, and O-methyl oximes were also examined.

Anilides↗
PubMedDate not supplied

[Acid-soluble CoA and free amino acid levels in the liver of pantothenic acid-deficient albino rats after separate and combined administration of panthotenic acid and cysteine].

The feeding of white rats with a synthetic diet deprived of pantothenic acid (PAA) for 10 weeks led to a decrease in the content of acid-soluble CoA (AS-CoA) and to an increase in the liver taurine and glycine concentration. One hour after pantothenate injection (30 mg/kg) to PAA-deficient animals the level of AS-CoA rose by 96%, whereas after administration of an equimolar dose of cystein by 63%. Combined administration of CoA precursors did not result in summation of the effects. In all the cases of cystein injections, substantial changes were recorded in the structure of the liver amino acid pool, which were less marked if cystein was combined with pantothenate. It is assumed that the metabolism of cystein, glycine and, probably, that of alanine may depend on the changes in the CoA pool in hepatocytes.

Acids↗
PubMed2000

13-cis retinoic acid exerts its specific activity on human sebocytes through selective intracellular isomerization to all-trans retinoic acid and binding to retinoid acid receptors.

Despite its potent biologic effect on human sebocytes, 13-cis retinoic acid exhibits low binding affinity for cellular retinoic acid binding proteins and nuclear retinoid receptors. Hence, 13-cis retinoic acid may represent a pro-drug possibly acting through all-trans isomerization. In this study, marked isomerization of 13-cis retinoic acid has been confirmed in cultured SZ95 sebocytes showing 2- to 15-fold higher levels of all-trans retinoic acid at 12-72 h, as measured by high performance liquid chromatography. In contrast, only low amounts of all-trans retinoic acid were converted intracellularly to its 13-cis isoform. 9-cis retinoic acid was not detected after either 13-cis retinoic acid or all-trans retinoic acid treatment. The rapid isomerization of 13-cis retinoic acid to high levels of all-trans retinoic acid was a sebocyte-specific event, as no significant isomerization of 13-cis retinoic acid to all-trans retinoic acid occurred in HaCaT keratinocytes. De novo mRNA expression of cytochrome P450 1A1, a major xenobiotic metabolizing enzyme, in SZ95 sebocytes was induced by all-trans retinoic acid, but not by 13-cis retinoic acid. In addition, mRNA levels of cellular retinoic acid-binding protein II, which is supposed to regulate the concentration of intracellular all-trans retinoic acid, rapidly increased under all-trans retinoic acid treatment (30 min-6 h), whereas the 13-cis retinoic acid effect was markedly weaker and delayed. Both 13-cis retinoic acid and all-trans retinoic acid suppressed mRNA expression of cytochrome P450 1A2. In parallel experiments, 13-cis retinoic acid significantly reduced SZ95 sebocyte proliferation at 10-7 M, show- ing 30-40% inhibition after 9 d. All-trans retinoic acid and 9-cis retinoic acid exhibited similar anti-proliferative effects. AGN 193109, a pan-antagonist of the retinoic acid receptors, antagonized the anti-proliferative activity of all retinoic acid isomers tested in a concentration-dependent manner with complete abolishment at ratios of 1:10 13-cis retinoic acid and 1:1 all-trans retinoic acid. Coincubation of SZ95 sebocytes with 13-cis retinoic acid and AGN 193109 did not alter the intracellular concentration of 13-cis retinoic acid and its isomerization profile. In contrast, the retinoid X receptor antagonist CD 3507 did not affect the inhibition of SZ95 sebocyte proliferation induced by retinoic acids. Our findings indicate: (i) a selective 13-cis retinoic acid isomerization to all-trans retinoic acid in the intracellular compartment of SZ95 sebocytes; (ii) a reduced all-trans retinoic acid inactivation process after 13-cis retinoic acid treatment as compared with treatment with all-trans retinoic acid; and (iii) a retinoic acid receptor-mediated inhibition of SZ95 sebocyte proliferation. These data explain the sebocyte-specific activity of 13-cis retinoic acid and support a pro-drug/drug relation between 13-cis retinoic acid and all-trans retinoic acid.

Cell Division↗
PubMed2001

Colon-specific prodrugs of 5-aminosalicylic acid: synthesis and in vitro/in vivo properties of acidic amino acid derivatives of 5-aminosalicylic acid.

5-aminosalicyl-L-aspartic acid (5-ASA-Asp) and 5-aminosalicyl-L-glutamic acid (5-ASA-Glu) were synthesized and their properties as colon-specific prodrugs of 5-aminosalicylic acid (5-ASA) were investigated employing rats as test animals. Incubation of 5-ASA-Asp and 5-ASA-Glu with the homogenates of tissue and contents of stomach or small intestine released no 5-ASA, indicating that they were stable in this condition. Incubation of 5-ASA-Asp with the cecal contents released 5-ASA 37%, whereas 5-ASA-Glu released only 8% of the dose in 16 h. Plasma concentration of 5-ASA-Asp after intravenous administration decreased rapidly and became undetectable in 60 min. No 5-ASA was detected in the blood, which indicated 5-ASA-Asp was stable in the plasma. After oral administration of 5-ASA-Asp, concentration of 5-ASA, its metabolite N-acetyl-5-ASA, and 5-ASA-Asp in the plasma, feces, and urine was determined. In the plasma, 5-ASA-Asp was not detected and the concentration of 5-ASA or N-acetyl-5-ASA was very low. About 33% of the administered dose was recovered as 5-ASA and N-acetyl-5-ASA and 43% as 5-ASA-Asp from feces, and 20% as 5-ASA and N-acetyl-5-ASA and 1% as 5-ASA-Asp from urine in 24 h. These results suggested that most of 5-ASA-Asp was delivered to the large intestine and about half of the administered dose was activated to liberate 5-ASA. After oral administration of free 5-ASA, fecal recovery was only 7% of the dose in 24 h and more than 80% was recovered from urine. Comparing 5-ASA-Asp and free 5-ASA, the amount of 5-ASA available in the large intestine was much larger, while the amount of 5-ASA in urine, which might be related to the systemic toxicity of 5-ASA, was much lower by the administration of 5-ASA-Asp than free 5-ASA.

Administration, Oral↗
PubMed1980

Stereochemistry in the formation of 9-hydroxy-10,12-octadecadienoic acid and 13-hydroxy-9,11-octadecadienoic acid from linoleic acid by fatty acid cyclooxygenase.

9-Hydroxy-10,12-octadecadienoic acid and 13-hydroxy-9,11-octadecadienoic acid are formed from linoleic acid upon incubation with the microsomal fraction of homogenates of the sheep vesicular gland (Hamberg, M. and Samuelsson, B. (1967) J. Biol. Chem. 242, 5344-5354. This communication is concerned with the stereochemical aspects of the conversion. The ratio between the 9- and 13-hydroxy isomers was 77:23. Steric analysis of the individual isomers showed that the hydroxyl group of both isomers had mainly the L configuration, i.e. 9L:9D, 79:21 and 13L:13D, 9- and 13-hydroxyoctadecadienoates which had largely lost the tritium label (6% and 7% retention of tritium relative to precursor, respectively) showing that the hydrogen which is removed from C-11 during the conversion has the L (pro-S) configuration.

Animals↗
PubMed1986

Disposition of the naturally occurring antimutagenic plant phenol, ellagic acid, and its synthetic derivatives, 3-O-decylellagic acid and 3,3'-di-O-methylellagic acid in mice.

The effect of ellagic acid and some of its more lipophilic derivatives on the mutagenicity of (+/-)-7 beta,8 alpha-dihydroxy-9 alpha,10 alpha-epoxy-7,8,9,10-tetrahydrobenz[a]pyrene was examined in Salmonella typhimurium TA100. Ellagic acid, 3,3'-di-O-methylellagic acid, 4,4'-di-O-methylellagic acid and 3-O-decylellagic acid were found to have approximately equal antimutagenic activity. The tissue distribution and elimination of ellagic acid, 3,3'-di-O-methylellagic acid and 3-O-decylellagic acid were examined in CD-1 mice. Little or no ellagic acid (less than 1 nmol/g) was found in blood, lung or liver after the oral administration by gavage of 300 mumol of ellagic acid per kg body weight of after feeding 1% of ellagic acid in the diet for 1 week. Following the i.p. administration of 120 mumol/kg of ellagic acid, the blood and lung levels of ellagic acid were 15-20 nmol/g at 30 min after the dose, and the concentrations of ellagic acid decreased to 1-3 nmol/g at 6-8 h after the dose. A portion of the administered i.p. dose precipitated in the abdominal cavity. After i.v. administration, ellagic acid was eliminated very rapidly from blood, lung and liver, and approximately 70% of the administered dose was recovered in the urine and feces as free ellagic acid and its conjugates. At 2 h after an i.v. injection of 60 mumol/kg of ellagic acid, 46% of the dose was recovered in the urine as ellagic acid and its conjugates. Of this amount, about half was excreted as free ellagic acid and half was excreted as conjugates. An additional 25% of the dose was recovered in the feces (mostly as free ellagic acid) after 7 h. The disposition of 3,3'-di-O-methylellagic acid or 3-O-decylellagic acid after i.v. administration (32 mumol/kg) was examined and compared to the disposition of the same i.v. dose of ellagic acid. The concentrations of ellagic acid, 3,3'-di-O-methylellagic acid and 3-O-decylellagic acid decreased rapidly in the blood, liver and lung, but the concentrations of 3-O-decylellagic acid in the lung throughout the experimental period (2-360 min) was on average 20- to 40-fold higher than the corresponding average concentrations of ellagic acid or 3,3'-di-O-methylellagic acid.

7,8-Dihydro-7,8-dihydroxybenzo(a)pyrene 9,10-oxide↗
PubMed2003

Arginine of retinoic acid receptor beta which coordinates with the carboxyl group of retinoic acid functions independent of the amino acid residues responsible for retinoic acid receptor subtype ligand specificity.

The biological actions of retinoic acid (RA) are mediated by retinoic acid receptors (RARalpha, RARbeta, and RARgamma) and retinoid X receptors (RXRalpha, RXRbeta, and RXRgamma). Consistent with the X-ray crystal structures of RARalpha and RARgamma, site-directed mutagenesis studies have demonstrated the importance of a conserved Arg residue (alphaArg(276), betaArg(269), and gammaArg(278)) for coordination with the carboxyl group of RA. However, mutation of Arg(269) to Ala in RARbeta causes only a 3- to 6-fold increase in the K(d) for RA and EC(50) in RA-dependent transcriptional transactivation assays while the homologous mutation in either RARalpha or RARgamma causes a 110-fold and a 45-fold increase in EC(50) value, respectively. To further investigate the nature of this difference, we prepared mutant RARs to determine the effect of conversion of betaR269A to a mutant which mimics either RARalpha ligand selectivity (betaA225S/R269A) or RARgamma ligand selectivity (betaI263M/R269A/V338A). Our results demonstrate that in RARbeta mutants that acquire either RARalpha or RARgamma ligand specificity the Arg(269) position responsible for coordination with the carboxyl group of retinoids continued to function like that of RARbeta. Furthermore, three mutant receptors (betaA225S/R269A, betaA225S/F279, and alphaF286A) were found to have a greater than wild-type affinity for the RARalpha-selective ligand Am580. Finally, a homology-based computer model of the ligand binding domain (LBD) of RARbeta and the X-ray crystal structures of the LBD of both RARalpha and RARgamma are used to describe potential mechanisms responsible for the increased affinity of some mutants for Am580 and for the difference in the effect of mutation of Arg(269) in RARbeta compared to its homologous Arg in RARalpha and RARgamma.

Alanine↗