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At least 181 records · Page 10Linked to original sources
PubMed1977

Effects of t-AMCHA and EACA on the plasma kallikrein system.

Varied amounts of t-AMCHA or EACA added to non-contact fresh dog plasma generates kininogenase and TAME esterase activities. These phenomena may be abolished by prior addition of lima bean trypsin inhibitor. t-AMCHA or EACA had no effect on partially purified kallikrein, but had a significant inhibitory influence on plasma kininase. The generation of prekallikrein activator with t-AMCHA was ascertained by gel filtration on a Sephadex G-100 column. The blood kinin level increased about 50% one hr after administration of t-AMCHA. It is suggested from these results that t-AMCHA may initiate the true activation of the kallikrein system by activating the Hageman factor.

Aminocaproates↗
PubMed1983

Use of gamma-aminobutyric acid (GABA)-transaminase inhibitors and a GABA uptake inhibitor to investigate the influence of GABA neurons on dopamine-containing amacrine cells of the rat retina.

The effects of inhibiting gamma-aminobutyric acid-transaminase (GABA-T) with aminooxyacetic acid or with gabaculine and inhibiting GABA uptake with nipecotic acid on dopamine (DA) synthesis in the retina of light-exposed rats were studied. 3,4-Dihydroxyphenylalanine (Dopa) accumulation after the inhibition of L-aromatic amino acid decarboxylase with NSD-1015 was used as an index of DA synthesis. The GABA-T inhibitors significantly increased GABA levels in the retina but had no effect on retinal Dopa accumulation in the light. Dopa accumulation was significantly inhibited at a high dosage by nipecotic acid alone and by low dosages of nipecotic acid in rats pretreated with either aminooxyacetic acid or gabaculine. The dosages of nipecotic acid which inhibited Dopa accumulation in the light also inhibited [3H]GABA uptake in the retina. The inhibitory effects of gabaculine and nipecotic acid on Dopa accumulation appeared to occur at least partially via GABA receptors because their action was significantly reversed by the GABA antagonist bicuculline methiodide. These experiments thus suggest that endogenous GABA can suppress the light-evoked increase in DA synthesis in the rat retina and support previous studies which concluded that an inhibitory GABA input may at least partially regulate the activity of the DA neurons in the retina of rats.

4-Aminobutyrate Transaminase↗
PubMed1980

[Anti-inflammatory effect of aluminum or aurin tricarboxylic acid].

The anti-inflammatory effect of aurin tricarboxylic acid is studied in rats after parenteral injection of 20 and 50 mg/kg. Aurin tricarboxylic acid reduces: the carrageenan-induced oedemas in paws, the carragenan-induced pleural effusion, the carragen-induced granulation tissue growth and the Freund adjuvant-induced arthritis. As non steroïdal antiinflammatory drugs, the aurin tricarboxylic acid inhibits (ED50 = 0.34.10-2 M) the human erythrocyte delta aminolevulinic acid dehydratase, a zinc dependent enzyme. A possible interaction between zinc-enzymes and non steroïdal antiinflammatory compounds is suggested.

Animals↗
PubMedDate not supplied

Phenylpropanoid constituents of essential oils.

While the major constituents of essential oils are generally mono- and sesquiterpenes, in certain plant families or genera phenylpropanoid compounds are also found in the essential oil, sometimes as the main component. A survey is given of the distribution of these substances, as well as of their structural properties and biochemical origin. In particular, cinnamic acid not only occurs in some cases as a constituent of essential oils, but together with p-hydroxycinnamic acid is the most important metabolic intermediate in the pathways leading to the volatile phenylpropanoids found in these essential oils. These compounds are mostly phenolics, and often occur as their non-volatile glycosides. However, after enzymatic cleavage, which happens frequently during catabolic or postmortal processes, the resulting aglycones, which are not normally components of the essential oil, act as the carriers of flavors and fragrances. These compounds too are included in the survey.

Chemical Phenomena↗
PubMed1988

Effects of inhibition of ornithine aminotransferase or of general aminotransferases on urea and citrulline synthesis and on the levels of acetylglutamate in isolated rat hepatocytes.

Canaline and gabaculine, inhibitors of gamma-aminotransferases and thus of ornithine aminotransferase (E.C. 2.6.1.13), decreased the flow through ornithine carbamoyl transferase (E.C. 2.1.3.3) in isolated rat hepatocytes incubated with 10 mM NH4Cl and ornithine. The levels of acetylglutamate, an essential activator of carbamoyl phosphate synthetase (ammonia) (E.C. 6.3.4.16), were also decreased, suggesting that the inhibitors had also caused a decrease in the rate of carbamoyl phosphate synthesis. Under these conditions, ornithine appears to be a precursor of acetylglutamate, via ornithine aminotransferase, possibly as a consequence of glutamate synthesis. The influence of aminooxyacetate, an aminotransferase inhibitor, has also been examined.

Aminobutyrates↗
PubMed1978

Fractionation of aurintricarboxylic acid and effects of its components on nuclear swelling and nucleic acid synthesis.

Crude aurintricarboxylic acid synthesized by the conventional method was fractionated into 8 components (A1-A8) by silica gel thin layer chromatography. Some of the components were isolated and their effects were tested on nuclear swelling and on in vitro RNA synthesis and DNA synthesis using isolated polymerases. Only two components with low RF (A7 and A8) induced strong nuclear swelling. The other components were almost inactive. Formaurin-dicarboxylic acid, a contaminating polyanion of crude aurintricarboxylic acid, was synthesized separately. It was as effective as the two active components in nuclear swelling and inhibited RNA and DNA polymerases on naked DNA template. However, it stimulated RNA synthesis on chromatin template probably by dissociating histones from DNA. Unfractionated aurintricarboxylic acid showed the same effects at higher concentrations. A preliminary analysis indicated one of the inactive components (A4) is genuine aurintricarboxylic acid. The results suggest that the observed activity of crude aurintricarboxylic acid is due to some contaminating substances, one of which is formaurindicarboxylic acid.

Animals↗
PubMed1985

A highly active chemotactic peptide analog incorporating the unusual residue 1-aminocyclohexanecarboxylic acid at position 2.

Analogs of chemotactic peptides (Formyl-Met-X-Phe-OMe) containing the stereochemically constrained residues alpha-aminoisobutyric acid (Aib), 1-aminocyclopentanecarboxylic acid (Acc5) and 1-aminocyclohexanecarboxylic acid (Acc6) at position 2 are compared with the parent sequence (X = Leu) for their ability to induce lysozyme release in rabbit neutrophils. The Acc6 analog is about 78 times more active than the parent peptide, For-Met-Leu-Phe-OH, whereas Aib and Acc5 analogs are approximately 3 and 2 times, respectively, less active than the parent peptide. NMR and model building studies clearly favour a Met-Acc6 beta-turn solution conformation in the Acc6 analog, suggesting that the neutrophil receptor is capable of recognizing a folded peptide structure. The significant differences in the activities of the Acc5 and Acc6 analogs suggest an important role for the residue 2 sidechain in receptor interactions.

Amino Acids↗