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PubMed1996

Phenylalanine utilization for protein synthesis in beta-phenylpyruvic acid treated Escherichia coli cells.

The possibility of coupling along the supply routes of phenylalanine from its uptake by the cell, through the charging of specific tRNAs, has been postulated. The experimental approach to testing this hypothesis has been to study the competition between endogenously synthesized and exogenously supplied amino acids, from which preferences for their incorporation into cellular proteins can be deduced. The results indicate that manipulation of the endogenous phenylalanine pool size, achieved by addition of its immediate precursor, beta-phenylpyruvate, does not cause the predicted changes in the incorporation of exogenous labelled phenylalanine into proteins. The evidence favours exogenous phenylalanine being preferentially delivered to the sites of protein synthesis.

Amino Acids↗
PubMed1984

Increased urinary excretion of aromatic amino acid catabolites by Microtus montanus chronically infected with Trypanosoma brucei gambiense.

Microtus montanus infected with Trypanosoma brucei gambiense for 16 and 21 days excreted significantly greater quantities of several aromatic amino acid catabolites when compared to uninfected control animals. Very large quantities of three aromatic alpha-keto acids (alpha-oxocarboxylic acids), phenylpyruvic acid, 4- hydroxyphenylpyruvic acid and indole-3-pyruvic acid, were excreted by infected animals. Increased excretion of indole-3-lactic acid and indole-3-acetic acid was also detected. Gas chromatographic-mass spectral analysis of the trimethylsilyl derivatives of phenylpyruvic acid, 4- hydroxyphenylpyruvic acid and indole-3-pyruvic acid confirms the identity of the aromatic alpha-keto acids elevated during infection. The marked alpha-keto aciduria indicates that a large disturbance exists in aromatic amino acid metabolism in this chronic animal model of African trypanosomiasis. The disturbance may contribute to the pathogenesis of the disease. The increased catabolite concentrations may also prove to be useful diagnostically and prognostically.

Amino Acids↗
PubMed1984

Novel formation of alpha-amino acids from alpha-oxo acids and ammonia in an aqueous medium.

In the course of a study of possible mechanisms for chemical evolution in the primeval sea, we found the novel formation of alpha-amino acids and N-acylamino acids from alpha-oxo acids and ammonia in an aqueous medium. Glyoxylic acid reacted with ammonia to form N-oxalylglycine, which gave glycine in a 5-39% yield after hydrolysis with 6N HC1. Pyruvic acid and ammonia reacted to give N-acetylalanine, which formed alanine in a 3-7% overall yield upon hydrolysis. The pH optima in these reactions were between pH 3 and 4. These reactions were further extended to the formation of other amino acids. Glutamic acid, phenylalanine and alanine were formed from alpha-ketoglutaric acid, phenylpyruvic acid and oxaloacetic acid, respectively, under similar conditions. N-Succinylglutamic acid was obtained as an intermediate in glutamic acid synthesis. Phenylacetylphenylalanineamide was also isolated as an intermediate in phenylalanine synthesis. Alanine, rather than aspartic acid, was produced from oxaloacetic acid. These reactions provide a novel route for the prebiotic synthesis of amino acids. A mechanism for the reactions will be proposed.

Amino Acids↗
PubMed1985

Effects of various compounds on histidine decarboxylase activity: active site mapping.

The effect of about one hundred compounds on the activity of histidine decarboxylase partially purified from whole bodies of fetal rats was determined. Most of them at their 10 mM concentration had little effect on the enzyme activity; but 12 compounds inhibited the enzyme to a greater extent than 30%. Among these, except for alpha-methylhistidine that has been known to be a strong and specific inhibitor, DOPA, homocysteine, cysteine, methionine and urocanic acid were the best inhibitors; beta-phenyllactic acid, phenylpyruvic acid and carnosine were less strong inhibitors; valine, oxaloacetic acid and N tau-methylimidazole acetic acid were weak inhibitors. Histamine had no inhibitory action. Thus, the substrate binding site of histidine decarboxylase is very rigid and specific for L-histidine.

Amino Acids↗
PubMed1983

A novel way for the formation of alpha-amino acids and their derivatives in an aqueous medium.

In the course of a study of possible mechanism for chemical evolution in the primeval sea, we observed the formation of alpha-amino acids and N-acylamino acids from alpha-oxo acids and ammonia in an aqueous medium. Glyoxylic acid reacted with ammonia to form N-oxalylglycine, which gave glycine in a 5-39% yield after hydrolysis with 6N HCl. Similarly when glyoxylic acid was treated with methylamine it yielded N-oxalylsarcosine, which could be hydrolyzed to sarcosine with 17-25% overall yield upon hydrolysis. Pyruvic acid and ammonia reacted to give N-acetylalanine, which formed alanine in a 3-7% overall yield upon hydrolysis. The pH optima in these reactions were pH 3-4. These reactions were further extended to the formation of other amino acids. Glutamic acid, phenylalanine and serine were formed from alpha-ketoglutaric acid, phenylpyruvic acid and hydroxypyruvic acid, respectively, under similar conditions. N-Succinylglutamic acid was obtained as an intermediate for glutamic acid synthesis. Phenylacetylphenylalanineamide was also isolated as an intermediate for phenylalanine synthesis. Alanine, rather than aspartic acid, was produced from oxaloacetic acid. These reactions provide a novel route for the prebiotic synthesis of amino acids. A mechanism for the reactions is proposed.

Amino Acids↗
PubMed2005

Impaired glutamatergic synaptic transmission in the PKU brain.

This paper reviews recent results of our investigation of the mechanisms whereby hyperphenylalaninemia may cause brain dysfunction in classical phenylketonuria (PKU). Acute applications of L-Phe in rat and mouse hippocampal and cerebrocortical cultured neurons, at a range of concentrations found in PKU brain, significantly and reversibly depressed glutamatergic synaptic transmission by a combination of pre- and postsynaptic actions: (1) competition for the glycine-binding site of the N-methyl-D-aspartate (NMDA) receptors; (2) attenuation of neurotransmitter release; (3) competition for the glutamate-binding site of (RS)-amino-3-hydroxy-5-methyl-4-isoxazolepropioinic acid and kainate (AMPA/kainate) receptors. Unlike L-Phe, its non-tyrosine metabolites, phenylacetic acid, phenylpyruvic acid, and phenyllactic acid, did not produce antiglutamatergic effects. L-Phe did not affect inhibitory gamma-aminobutyric (GABA)-ergic transmission. Consistent with this specific pattern of effects caused by L-Phe in neuronal cultures, the expression of NMDA receptor NR2A and AMPA receptor Glu1 and Glu2/3 subunits in brain of hyperphenylalaninemic PKU mice (Pah(enu2) strain) was significantly increased, whereas expression of the NMDA receptor NR2B subunit was decreased. There was no change in GABA alpha1 subunit expression. Considering the important role of glutamatergic synaptic transmission in normal brain development and function, these L-Phe-induced changes in glutamatergic synaptic transmission in PKU brain may be a critical element of the neurological symptoms of PKU.

Animals↗
PubMed2000

Effect of phenylalanine and its metabolites on the proliferation and viability of neuronal and astroglial cells: possible relevance in maternal phenylketonuria.

Phenylketonuria is a genetic defect that, without strict dietary control, results in the accumulation of phenylalanine (Phe) in body fluids. If a low-Phe diet is not maintained during pregnancy, the offspring of phenylketonuric women are born with mental retardation and microcephaly. Primary cultures of rat cerebellar granule cells, rat cortical astrocytes, human fetal astrocytes, and human neuroblastoma (SY5Y) cells and human astrocytoma (1321N1) cells were used to test the hypothesis that the microencephaly may be a result of neuronal cell death and reduced astrocyte proliferation. Exposure to Phe or to six Phe metabolites [phenylacetic acid (PAA), phenyllactic acid, hydroxyphenylacetic acid, phenylpyruvic acid, phenylethylamine (PEA), and mandelic acid] did not result in astroglial or neuronal cell cytotoxicity. Treatment of 1321N1 cells, human fetal astrocytes, or rat astrocytes with 5 mM Phe for 24 h decreased DNA synthesis 19 +/- 4, 30 +/- 4, and 60 +/- 6%, respectively. This effect was concentration dependent, and flow cytometry revealed that Phe treatment resulted in the accumulation of cells in the G(0)/G(1) phase of the cell cycle. In addition, in 1321N1 cells, exposure to 5 mM PAA, and in rat astrocytes, exposure to 0.5 mM PEA inhibited cell proliferation 42 +/- 4 and 55 +/- 4%, respectively. These metabolites also resulted in the accumulation of cells in the G(0)/G(1) phase of the cell cycle. In human fetal astrocytes, 0.5 mM PEA and 0.5 mM PAA resulted in a 41 +/- 12 and 52 +/- 11% reduction proliferation, respectively.

Astrocytes↗
PubMed1978

Inability of accumulated metabolic byproducts of uremia to alter the extent of warfarin binding in charcoal treated plasma.

The addition to charcoal treated normal and charcoal treated uremic plasma of four metabolites which accumulate during uremia--uric acid, beta -phenylpyruvic acid, guanidinosuccinic acid, and p-hydroxyphenylacetic acid--failed to produce a warfarin binding defect. Charcoal treatment corrected the warfarin binding defect in uremic plasma, however it diminished the extent of warfarin binding to normal plasma. These observations rule out the possibility that uric acid, beta -phenylpyruvic acid, guanidinosuccinic acid, or p-hydroxyphenylacetic acid contribute to the warfarin binding defect in uremia, and suggest that free fatty acids have no role in the warfarin binding defect.

Blood Proteins↗