Excitotoxics (long) and Neuroendocrine Damage (fwd)
sgex400 at uk.ac.lon.sghms
Thu Aug 12 07:54:37 EST 1993
> In article <CBKJ91.2r9 at cunews.carleton.ca>
> wcsbeau at superior.carleton.ca (OPIRG) writes:
> > >>... aspartic acid, glutamic acid or phenyalanine blood spikes
> > >>which then cause an imbalance in brain neurotransmitters levels
> > >>are similiar to those that occur in adults. Dizzyness and
> > >>headaches after consuming food or beverages that contain high
> > >>amounts of these amino acids.
> > Both Glu and Asp have neurotransmitter functions in the mammalian
> > brain. But I hadn't heard that phenylalanine is now considered a
> > putative neurotransmitter. Could you elaborate on this? (I rather
> > doubt it could be, given that anyone with PKU would automatically
> > be missing a neurotransmitter. Which seems *highly* unlikely.
> I don't know whether F is a neurotransmitter or not, but your last
> comment doesn't make sense. F is an essential amino acid. From what I
> understand, people with PKU can't metabolize F and it builds up to
> toxic levels. This doesn't mean low levels aren't necessary, and I
> doubt it could be completely eliminated. Please correct me if I'm
> Absolutely correct. The question about the role of F in neurotransmission
though should surely relate to the pathway:
F -> Y -> DOPA -> Dopamine -> adrenalin* -> noradrenaline*
* epinephrine and norepinephrine for those of you over the pond.
As many of the enzymes invoved in this pathway are not very specific, incuding
the catabolic enzymes MAO then an excess of F could muck up the pathway in
many places. I am sure that someone has done this but I do not know who.
As for PKU this is a result of a lack of the enzyme for the F -> Y step, the
F that accumulates goes into other pathways, principally by oxidative
deamination to produce phenyl ketones hence the name. I think that one of the
early models for the biochemistry of these pathways involved feeding rats
huge amounts of F.
Hope that this all added more light than shadow
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