Phenylalanine
Common Names: L-Phenylalanine; D,L-Phenylalanine, DLPA; PhenylethylaminePlease read the disclaimer concerning the intent
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References
Anonymous. Phenylalanine fails to help chronic back pain patients. Family Pract News 1987;17(3):37.
Boulton AA. Phenylethylaminergic modulation of catecholaminergic neurotransmission.
Prog Neuropsychopharmacol Biol Psychiatry. 1991;15(2):139-156. (Review)
Bucci LR. Nutrition Applied to Injury Rehabilitation and Sports Medicine. CRC Press, 43-44, 1994.
Budd K. Use of D-phenylalanine, an enkephalinase inhibitor, in the treatment of intractable pain.
Adv Pain Res Ther 1983;5:305-308.
Fischer E, Heller B, Nachon M, Spatz H. Therapy of depression by phenylalanine. Preliminary note.
Arzneimittelforschung. 1975 Jan;25(1):132.
Abstract: To 23 subjects with endogenous depression after a previous unsuccessful treatment with common antidepressive drugs (imipramine-like or MAO inhibitors) dl- or d-phenylalanine was given in dialy oral doses of 50 or 100 mg during 15 days. A complete euthymia was obtained in 17 subjects between one and 13 days of treatment. No important adverse reaction was observed.
Haavik J. L-DOPA is a substrate for tyrosine hydroxylase. J Neurochem 1997 Oct;69(4):1720-1728.
Abstract: In the presence of thiols, tyrosine hydroxylase (TH) oxidizes L-dihydroxyphenylalanine (L-DOPA) with a specific activity of up to 140 nmol min(-1) mg(-1) at 37 degrees C and pH 7.0, which is approximately 12-50% of its TH activity under similar experimental conditions. Using assay conditions that are optimal for measuring TH activity, the specific DOPA oxidase activity of human TH is similar to that of mushroom tyrosinase, but the two enzymes are clearly different in terms of substrate specificities, cofactor dependencies, and selectivity with respect to the effects of metal chelators and other inhibitors. In the presence of an excess of dithiothreitol, 2-mercaptoethanol, cysteine, or reduced glutathione, the reaction products of the two enzymes are identical and have been identified tentatively as thioether derivatives of DOPA. Theoretically, the oxidation of L-DOPA by TH may contribute to the formation of neuromelanin (pheomelanin) in catecholaminergic neurons and in the metabolism of DOPA to reactive intermediates that can react with free thiol groups in cellular proteins. The DOPA oxidase activity of TH can lead to errors in the estimation of in vivo or in vitro TH activity, and currently used assay protocols may have to be modified to avoid interference from this activity.
Heller B, Fischer E, Martin R. Therapeutic action of D-phenylalanine in Parkinsons disease.
Arzneimittelforschung. 1976 Apr;26(4):577-579.
Lehmann WD, Theobald N, Fischer R, Heinrich HC. Stereospecificity of phenylalanine plasma kinetics and hydroxylation in man following oral application of a stable isotope-labelled pseudo-racemic mixture of L- and D-phenylalanine.
Clin Chim Acta. 1983 Mar 14;128(2-3):181-198.
Abstract: L-[15N]Phenylalanine and D-[2H5]phenylalanine have been administered orally to two healthy adult volunteers as a pseudo-racemic mixture at a dose of 25 mg/kg each. After oral application, the plasma kinetics of phenylalanine and tyrosine have been followed by the combined use of high pressure liquid chromatography and field desorption mass spectrometry. Additional incubation with D-amino acid oxidase was used to determine the enantiomeric composition of the differently labelled species of phenylalanine and tyrosine. D-Phenylalanine plasma levels show a faster rise to higher maximum values compared to L-phenylalanine (D/L ratio at maximum 3.19, 3.26). L-Phenylalanine is efficiently hydroxylated to L-tyrosine. In contrast, conversion of D-phenylalanine to the L-form with subsequent hydroxylation to L-tyrosine was observed. From the plasma kinetics it is estimated that about 1/3 of the applied dose of 25 mg/kg of D-phenylalanine is converted to the L-isomer. Of the administered dose of L-phenylalanine only very small amounts are excreted into urine as such (0.25%, 0.8%), whereas a substantial amount of the D-phenylalanine dose is found in urine (27.4%, 38.0%).
Marz, Russell. Medical Nutrition From Marz. Second Edition. Portland, OR. 1997.
Sabelli HC, Fawcett J, Gusovsky F, Javaid JI, Wynn P, Edwards J, Jeffriess H, Kravitz H. Clinical studies on the phenylethylamine hypothesis of affective disorder: urine and blood phenylacetic acid and phenylalanine dietary supplements.
J Clin Psychiatry 1986 Feb;47(2):66-70.
Abstract: To test the hypothesis that 2-phenylethylamine (PEA) modulates affect, plasma levels and urinary excretion of its main metabolite, phenylacetic acid (PAA), were studied in depressed and manic subjects, and the mood-elevating effects of its precursor, L-phenylalanine, were studied in depressed subjects. Mean total plasma PAA concentrations were 491.83 +/- 232.84 ng/ml in 12 healthy volunteers and 300.33 +/- 197.44 ng/ml in 23 drug-free patients with major depression. The 24-hour urinary PAA excretion was also measured in 48 healthy volunteers (141.1 +/- 10.2 mg PAA/24 hr) and in 144 patients with major depression (78.2 +/- 41.0 mg PAA/24 hr). The results suggest that low plasma and urinary PAA may be state markers for depression and are compatible with the PEA hypothesis. In further support, phenylalanine elevated mood in 31 of 40 depressives.
Sabelli HC, Javaid JI. Phenylethylamine modulation of affect: therapeutic and diagnostic implications.
J Neuropsychiatry Clin Neurosci. 1995 Winter;7(1):6-14. (Review)
Abstract: A review of the literature indicates that brain phenylethylamine (PEA) may be a neuromodulator of aminergic synapses and that it promotes energy, elevates mood, and favors aggression. Phenylacetic acid, the main metabolite of PEA, is decreased in the biological fluids of depressed subjects and schizophrenic subjects and is increased in schizoaffective subjects. The administration of PEA or of its precursor L-phenylalanine improves mood in depressed patients treated with a selective monoamine oxidase B inhibitor. The authors speculate that studies of PEA metabolism may have diagnostic value and that PEA administration may be therapeutic in selected depressed patients.
Sabelli HC. Rapid treatment of depression with selegiline-phenylalanine combination.
J Clin Psychiatry. 1991 Mar;52(3):137.
Schulpis CH, Antoniou C, Michas T, Strarigos J. Phenylalanine plus ultraviolet light: preliminary report of a promising treatment for childhood vitiligo.
Pediatr Dermatol 1989;6:332-335.
Siddiqui AH, Stolk LM, Bhaggoe R, Hu R, Schutgens RB, Westerhof W. L-phenylalanine and UVA irradiation in the treatment of
vitiligo. Dermatology 1994;188(3):215-218.
Werbach MR. Foundations of Nutritional Medicine. Tarzana, CA: Third Line Press, 1997. (Review).