Phenylacetic acid production in dominant and non-dominant vervet monkeys.

Free and conjugated plasma phenylacetic acid concentrations were significantly higher in dominant male vervet monkeys than in non-dominant males living in stable social groups. These findings may be connected with an earlier observation that plasma from aggressive human psychopaths contains higher concentrations of phenylacetic acid than non-aggressive controls; whether they reflect an increased production of phenylethylamine is still unknown.

Homovanillic acid in caudate and pre-frontal cortex following neuroleptics.

Homovanillic acid (HVA) was measured in rat caudate and pre-frontal cortex 3 h following a single dose of a variety of neuroleptics. Thioridazine, haloperidol, fluphenazine, and metoclopramide increased HVA levels in caudate more than in pre-frontal cortex; whereas sulpiride and clozapine produced greater increases in HVA in pre-frontal cortex. These results are consistent with the proposal that rat pre-frontal cortex is relatively deficient in dopamine autoreceptors.

Characteristics of dopamine uptake and 3,4-dihydroxyphenylacetic acid (DOPAC) formation in the dopaminergic terminals of the neurointermediate lobe of the pituitary gland.

The kinetics of dopamine (DA) uptake were studied in synaptosomal preparations of the neurointermediate lobe (NIL) of the pituitary gland, a region containing the terminals of the tuberoinfundibular dopaminergic neurons. Lineweaver-Burk plots of the initial velocity of DA uptake versus the concentration of DA yielded a single straight line in the NIL. The Km values in the NIL of the rat and the steer were 2.2+/-0.5 x 10(-6) M and 2.0+/-0.1 x 10(-6) M, respectively. The uptake was predominantly into dopaminergic terminals since preincubation with desipramine did not affect the Vmax or Km of DA uptake. Observed uptake was predominantly due to transport across the neuronal membrane and not into storage granules, since reserpine caused only a small decrease in uptake. The concentration of the DA metabolite 3,4-dihydroxyphenylacetic acid (DOPAC) in the NIL was 3.6 ng/mg protein. The ratio of DA to DOPAC in the NIL (3.73) was similar to that obtained in the medial basal hypothalamus, another region innervated by the tuberoinfundibular dopaminergic neurons. The kinetics of DA uptake in the nerve terminals of the NIL are similar to those observed in the DA terminals in the median eminence. The affinity of uptake in the terminal fields of the tuberoinfundibular system is considerably lower than in terminals of the mesolimbic and nigrostriatal dopaminergic terminals.

Production of phenylacetic and hydroxyphenylacetic acids by clostridium botulinum type G.

Phenylacetic and hydroxyphenylacetic acids were present as major acids in spent growth medium from Clostridium botulinum type G. These aromatic acids were identified by gas-liquid chromatography and mass spectrometry.

The metabolism of phenylacetic acid by Aspergillus fumigatus ATCC 28282: identification of 2,6-dihydroxyphenylacetic acid.

Aspergillus fumigatus ATCC 28282 converted phenylacetic acid into a new dihydroxylated compound (2,6-dihydroxyphenylacetic acid) which was identified as 2,6-dimethoxyphenylacetic acid methyl ester. Two other new metabolites have been isolated also and identified as orthohydroxyphenylacetic acid and meta-hydroxyphenylacetic acid.

[Method for the quantitative determination of penicillin acylase activity by the formation of phenylacetic acid]. / Metod kolichestvennogo opredeleniia aktivnosti penitsillinatsilazy po obrazovaniiu feniluksusnoi kisloty

The quantitative method for determination of penicillinacylase activity is described. The method is based on detection of phenylacetic acid (PAA) formed during hydrolysis of benzylpenicillin. PAA is extracted with toluol and nitrated with potassium nitrate solution in concentrated sulphuric acid followed by reduction of nitrophenylacetic acid into aminophenylacetic acid with zinc powder. Aminophenylacetic acid interacts with p-dimethylaminobenzaldehyde in acid medium forming a coloured compound (Schiff base). The optic density of the latter was determined with spectrophotometer SF-16 at 430 nm. The method was used for determination of acylase in Yersinia species and some other bacteria.

Microbial metabolism of phenolic amines: degradation of dl-synephrine by an unidentified arthrobacter.

Microorganisms capable of degrading dl-synephrine were isolated from soil of Citrus gardens by enrichment culture, with dl-synephrine as the sole source of carbon and nitrogen. An organism which appears to be an arthrobacter, but which cannot be identified with any of the presently recognized species was predominant in these isolates. It was found to metabolize synephrine by a pathway involving p-hydroxyphenylacetaldehyde, p-hydroxyphenylacetic acid, and 3,4-dihydroxyphenylacetic acid as intermediates. Some of the enzymes of this pathway were demonstrated in cell-free extracts. An aromatic oxygenase, which could also be readily obtained in a cell-free system, was found to degrade 3,4-dihydroxyphenylacetic acid by meta cleavage.

Absorption, metabolism and distribution of (14C)-O-methyldopa and (14C)-L-dopa after oral administration to rats.

1 The absorption, tissue distribution, and metabolism of [(14)C]-O-methyldopa were compared with those of [(14)C]-L-DOPA after oral administration to rats.2 Total radioactivity in the plasma and brain of rats treated with [(14)C]-O-methyldopa was significantly higher (2 fold and 30-50 fold, respectively) than that of rats treated with [(14)C]-L-DOPA.3 Total radioactivity in the gut washings and intestinal tissue 2 h after oral administration was significantly higher in rats treated with [(14)C]-L-DOPA than in rats treated with [(14)C]-O-methyldopa. The reverse was observed in the stomach tissues.4 Peripheral metabolism of [(14)C]-O-methyldopa was much lower than that of [(14)C]-L-DOPA; the major metabolite of [(14)C]-O-methyldopa in the plasma is L-DOPA, whereas L-DOPA is mainly metabolized to phenylcarboxylic acids.

The kinetics of intramolecular distribution of 15N in uric acid after administration of (15N) glycine. A reappraisal of the significance of preferential labeling of N-(3+9) of uric acid in primary gout.

THE CONCEPT OF AN ABNORMALITY OF GLUTAMINE METABOLISM IN PRIMARY GOUT WAS FIRST PROPOSED ON THE BASIS OF ISOTOPE DATA: when [(15)N]glycine was administered to gouty subjects, there was disproportionately great enrichment of N-(3 + 9) of uric acid, which derive from the amide-N of glutamine. An unduly high concentration of (15)N in glutamine was postulated, and attributed to a hypothetical defect in catabolism of glutamine. Excess glutamine was proposed as the driving force of uric acid overproduction. WE HAVE REEXAMINED THIS PROPOSITION IN FOUR GOUTY SUBJECTS: one mild overproducer of uric acid with "idiopathic gout," one marked overproducer with high-grade but "partial" hypoxanthine-guanine phosphoribosyl-transferase deficiency, and two extraordinary overproducers with superactive phosphoribosylpyrophosphate synthetases. In the last three, the driving force of excessive purine biosynthesis is a known surplus of alpha-5-phosphoribosyl-1-pyrophosphate. Disproportionately high labeling of N-(3 + 9) was present in all four gouty subjects, most marked in the most flamboyant overproducers. The precursor glucine pool was sampled by periodic administration of benzoic acid and isolation of urinary hippuric acid. Similarly, the precursor glutamine pool was sampled by periodic administration of phenylacetic acid and isolation of the amide-N of urinary phenylacetylglutamine. The time course of (15)N enrichment of hippurate differed from that of the amide-N of glutamine. Whereas initial enrichment values of hippurate were very high, those of glutamine-amide-N were low, increasing to a maximum at about 3 h, and then declining less rapidly than those of hippurate. However, enrichment values of hippurate and of phenacetyl glutamine were normal in all of the gouty subjects studied. Thus, preferential enrichment of N-(3 + 9) in gouty overproducers given [(15)N]glycine does not necessarily reflect a specific abnormality of glutamine metabolism, but rather appears to be a kinetic phenomenon associated with accelerated purine biosynthesis per se.In addition, greater enrichment of N-9 than of N-3 on days 1 and 2 provided suggestive evidence for a second pathway for synthesis of the initial precursor of purine biosynthesis, phosphoribosylamine, perhaps utilizing ammonia rather than the amide-N of glutamine as nitrogen donor. In this limited study, the activity of this potential second pathway did not appear to be selectively increased in gout.