Determination of 2-phenylethylamine in rat brain after MAO inhibitors, and in human CSF and urine by capillary GC and chemical ionization MS.
A highly specific and sensitive method for the determination of beta-phenylethylamine (PEA) in biological material is presented. It involves prepurification of the extracts on Sep-Pak C18 cartridges, derivatization with heptafluorobutyric acid anhydride, gas chromatography on 50 m capillary columns and quantification by chemical ionization mass spectrometry. Using this method, levels of PEA in the rat brain and the effects of various monoamine oxidase (MAO) inhibitors thereon have been determined. PEA control levels were found to vary considerably: the lowest and highest values found were 0.4 and 12.5 ng/g tissue (n = 25). Within one and the same control group, the variation was somewhat smaller. The preferential or specific inhibitors of MAO A, amiflamine, cimoxatone, CGP 11305 A, moclobemide and toloxatone did not alter rat brain PEA even at high doses. In contrast, the preferential inhibitors of MAO B, deprenil, pargyline and MD 780236, as well as the nonselective agent tranylcypromine, caused strong (up to about 60-fold) increases. The threshold doses corresponded to those which caused about an 80% inhibition of MAO B as measured ex vivo. The method was also used to determine the concentration of PEA in human CSF (mean 17.3 +/- 3.3 ng/ml, range 3-45 ng/ml, n = 15) and urine (males: mean 35 +/- 5 micrograms/g creatinine, range 3.8 - 219 micrograms/g, 78 control days of a total of 12 subjects; females: mean 35 +/- 6 micrograms/g creat., range 2.7 - 266 micrograms/g, 55 control days of a total of 8 subjects).[1]References
- Determination of 2-phenylethylamine in rat brain after MAO inhibitors, and in human CSF and urine by capillary GC and chemical ionization MS. Lauber, J., Waldmeier, P.C. J. Neural Transm. (1984) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
