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Re: Tryptophan/ serotonin, tyrosine/dopamine... RAY » tealady

Posted by raybakes on October 17, 2004, at 7:41:55

In reply to Tryptophan/ serotonin, tyrosine/dopamine... RAY, posted by tealady on October 16, 2004, at 4:59:25

Hi Jan, wrote a bit about testosterone in an anxiety thread - did you manage to make any sense of it?

> II'm probably completely off course here, that the problem may be caused by competition for the same enzyme cofactors ...

Think that could be a possibility! Have to look out for some research..
>
> Dopamine is produced from tyrosine by the action of tyrosine hydroxylase (TH), which uses tetrahydrobiopterin (BH4) as a cofactor. BH4 is also a cofactor for tryptophan and serotonin synthesis, and also for the enzyme nitrous oxide synthetase
>
> or possibly its P5P B6 which I THINK is needed by somehow by tyrosine hydroxylase ?(not sure here)

dopa decarboxylase to dopamine needs p5p...


, and low adrenal function meaning it can take up to 21 days(heard that from a doc) to resynthesize enough tyrosine hydroxylase..not sure of this but I think it fits in somewhere with the competiton theory too.

Haven't heard this, but did find an abstract that says vitamin d can stimulate tyrosine hydroxylase gene expression.

Just looked up on pubmed and found this though...

Prevalence and clinical associations of 10 defined autoantibodies in autoimmune polyendocrine syndrome type I.

Department of Medical Sciences, University Hospital, SE-751 85 Uppsala, Sweden.

The prevalence of autoantibodies against nine intracellular enzyme autoantigens, namely 21-hydroxylase, side-chain cleavage enzyme (SCC), 17 alpha-hydroxylase, glutamic acid decarboxylase 65, aromatic L-amino acid decarboxylase, tyrosine phosphatase-like protein IA-2, tryptophan hydroxylase (TPH), tyrosine hydroxylase, cytochrome P450 1A2, and against the extracellular calcium-sensing receptor, was assessed in 90 patients with autoimmune polyendocrine syndrome type I. A multivariate logistic regression analysis was performed for the presence of autoantibodies as independent predictors for different disease manifestations. Reactivities against 21-hydroxylase and SCC were associated with Addison's disease with odds ratios (ORs) of 7.8 and 6.8, respectively. Hypogonadism was exclusively associated with autoantibodies against SCC with an OR of 12.5. Autoantibodies against tyrosine phosphatase-like protein IA-2 were associated with insulin-dependent diabetes mellitus with an OR of 14.9, but with low sensitivity. Reactivities against TPH and, surprisingly, glutamic acid decarboxylase 65, were associated with intestinal dysfunction, with ORs of 3.9 and 6.7, respectively. TPH reactivity was the best predictor for autoimmune hepatitis, with an OR of 27.0. Hypoparathyroidism was not associated with reactivity against any of the autoantigens tested. No reactivity against the calcium-sensing receptor was found. Analysis of autoantibodies in autoimmune polyendocrine syndrome type I patients is a useful tool for establishing autoimmune manifestations of the disease as well as providing diagnosis in patients with suspected disease.

>
> The competiton means making too much of one(say serotonin) will deplete the ability to make the other (say dopamine)..and depletion will eventually cause oversensitivity of the related receptorsI guess.
>
> hmm guess I must be low on serotonin looking at this

I sometimes wonder if balancing the immune system, increasing energy and, blood flow and oxygen, would bring a lot of the body's neurotansmitters into balance? Just seems to be so much juggling and interaction - surely god can't be so mean!!

Thanks for the pathways - bit complicated! Mentioned in a reply to Larry about dopamine and noradrenaline degrading to toxic quinones when monoamine oxidase degrades them - methylation via the enzyme COMT can protect the brain from these quinones (think they are dopachrome, adrenochrome). Another abstract talked about biopterin and it's precursor, protection tyrosine hyroxylase.

The role of adrenochrome in stimulating the oxidation of catecholamines.

Bindoli A, Scutari G, Rigobello MP.

Centro Studio Biomembrane, CNR, Padova, Italy. labbind@civ.bio.unipd.it

Adrenochrome, a stable oxidation product formed after oxidation of adrenaline, strongly stimulates oxygen uptake occurring during the autoxidation of adrenaline, other catecholamines and ascorbate. Oxygen consumed is converted to hydrogen peroxide suggesting the occurrence of a redox cycling process. The reduction of adrenochrome operated by adrenaline is accelerated by the exclusion of oxygen indicating that the oxidation of adrenaline occurs directly and superoxide anion does not necessarily mediate it. Oxygen consumption, observed in the catecholamine/adrenochrome and ascorbate/adrenochrome systems, is due to the autoxidation of leucoadrenochrome that, at variance with adrenaline, easily autoxidizes also at physiological pH. Therefore, in these systems, leucoadrenochrome appears to be the major determinant of the production of superoxide anion.


Ray


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