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Re: dopamine oxidation » raybakes

Posted by Larry Hoover on October 17, 2004, at 14:04:51

In reply to dopamine oxidation, posted by raybakes on October 17, 2004, at 12:57:24

> Came across some more info about the oxidation of dopamine/catecholamines. The degradation to toxic quinones like dopachrome and adrenochrome by monoamine oxidase seems a problem in mental illness. Increasing the activity of the methyltransferase enzyme COMT, and maybe sulphation and glucuronidation, might be a way to reduce the production of these toxic by-products - anyone heard anything about them before?

I think there's an alternative view of what's going on, suggested by points in each of those abstracts.

> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1956581&dopt=Abstract

"This BH4/DHPR-mediated antioxidation system is as effective as other antioxidation agents such as ascorbic acid, cysteine and reduced glutathione."

I.e. keep your antioxidant supplies up (avoid oxidative stress). Make sure you take vitamin C, and selenium.

> the radical superoxide can oxidise catecholamines too, so wonder whether depletion of dopamine by autoxidation can then change receptor sensitivity too?

> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2982420&dopt=Abstract.

"Adrenaline oxidation was unaffected by the presence of exogenous linolenic acid or methylarachidonic acid, while arachidonic acid, with a Km for this reaction of 175 microM, showed a marked stimulatory effect. This activation was suppressed by superoxide dismutase, catalase and NaCN, while mannitol was without effect."

I.e. shift the omega-6:omega-3 balance to reduce arichidonate release by phospholipase A2, and ensure adequate zinc and manganese to maintain SOD function.

> and another...
>
> http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8913362

"N-acetylcysteine produced a dose-dependent decrease in dopamine-induced cell death; this correlated with a decrease in peroxide formation."

NAC spares glutathione, so again, you have antioxidant defenses implicated, rather than the dopamine, IMHO.

Ray, did you ever read any of Dr. Pall's articles on oxidative stress? Some of my old links just aren't working, and the ones on his faculty page aren't either, but here's a full-text article that gets into the meat of the issue: http://www.annalsnyas.org/cgi/content/full/933/1/323

> the toxic quinones need to be detoxified by our friend glutathione!
>
> Ray

Actually, glutathione et al keep them from forming in the first place.

Oxidative stress plays havoc with your sulphur metabolism. So, cysteine, carnitine, taurine, glutathione, SAMe....many key molecules get trashed because sulphur gets trashed before carbon. The reason many antixidants have sulphur atoms is sacrificial. Selenium substitutes for sulphur to become even more sacrificial (as in seleno-cysteine). If there isn't enough sulphur to martyr itself on our behalf, other stuff gets mucked right up, or sulphur-bearing molecules we need for other purposes get destroyed instead.

Lar

 

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