DHT, NO - Peroxynitrite and Baldness?

[wookster]

If DHT stuimulates hair to produce nitric oxide but due to that nitric oxide somehow being transformed into peroxynitrite in male pattern baldness prone individuals, baldness becomes inevitable due to oxidative stress and a vicious nitric oxide - peroxytnitrite cycle?

http://www.ncbi.nlm.nih.gov/entrez/quer ... uery_hl=31



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quote:

Remarkably, basal NO level was enhanced threefold by stimulating dermal papilla cells with 5alpha-dihydrotestosterone (DHT) but not with testosterone.


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Could overstimulation and exitation by DHT - not growth inhibition, be the cause of balding?

http://molecular.biosciences.wsu.edu/Fa ... ll_cfs.htm



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quote:

It can be seen that these arrows form a series of loops that can potentially continue to stimulate each other. An example of this would be that nitric oxide can increase peroxynitrite which can stimulate oxidative stress which can stimulate NF- k B which can increase the production of iNOS which can, in turn increase nitric oxide. This loop alone constitutes a potential vicious cycle


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[docj077]

Another reason why taking arginine supplements makes absolutely no sense when it comes to hair loss. Arginine also increases IGF-1 due to increasing growth hormone release.

 

[Old Baldy]

Guys, I think they're talking about iNOS not cNOS? Look at Figure 1 in the 2nd link Wookster provided.

Peter H. Proctor View profile
More options Jan 16 2000, 4:00 am

Newsgroups: alt.baldspot
From: pproc...@proctorgamble.com (Peter H. Proctor)
Date: 2000/01/16
Subject: Re: Dr P: increased NO = bad for hair?
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In article <85susv> ahtavass...@my-deja.com writes:
>From: ahtavass...@my-deja.com
>Subject: Dr P: increased NO = bad for hair?
>Date: Sun, 16 Jan 2000 17:24:58 GMT
>Increased arginine intake
>-> more systemic NO
>-> more NO reacting with other chems
>-> more free radicals
>-> more hair loss
>What do u think?


It is not this simple. There are two systems for producing NO in your
body. One of these, cNOS, produces NO as a messenger substance for things like blood pressure control, penile erections, and hair growth. The other system, i ( or inducible ) NOS, makes NO as part of the immuologocal response along with superoxide. NO itself seems to be fairly benign at biological concentrations, but in the presence of superoxide it produces the very toxic agent peroxinitrite, as well as some other reactive agents.

Thus, it is iNOS which causes tissue damage, either directly or by
participating in the inflammatory cascade. See my other posts on the IL-1 thread today for more details on this.


Decreased activity of cNOS is a main inducer of iNOS. So you feed cNOS with arginine to keep iNOS shut down. Other tricks for minimizing tissue damage include preventing production of peroxinitritrite by either destroying superoxide with an SODase or with a competitive inhibitor of the NO + superoxide reaction such as TEMPO.


Peter H. Proctor, PhD, MD

 

[Bryan]

There's a very obvious question to be asked here, but nobody has asked it: WHAT KIND of human hair follicles did they use in this study?? :wink: Did they use balding scalp hair follicles which are known to be sensitive to DHT, or did they use occipital scalp hair follicles which are fairly neutral to DHT, or did they use body hair, which is actually stimulated by DHT? Dr. Proctor has been talking for years about the importance of nitric oxide as a growth-stimulating chemical messenger for hair follicles, so it would be fascinating to know just what kind of hair they tested, and found to exhibit a DHT-stimulated increase in NO production. How come nobody thought to wonder about that? :freaked:

The answer is that they used occipital scalp follicles, which I find somewhat puzzling. I've been meaning for a long time to email those researchers (they include one of their email addresses in that study) and ask him/her if they also did a similar test on balding frontal scalps, and on body hair follicles. It would be fascinating to know if DHT-stimulated NO production is another item in the list of differences between balding and non-balding hair follicles, or if ALL hair follicles exhibit that response to the same degree.

Bryan

 

[Johnny24601]

re:

Good stuff. What sort of things would increase NO in one's body?

 

[wookster]

An interesting quote about NO and peroxynitrite:

http://www.hairsite4.com/dc/dcboard.php ... &mode=full

( male pattern baldness Out-Thinks Minoxidil )

We all notice that male pattern baldness 'figures out' Minoxidil after a while and starts to counteract its positive effects. One reason for this could be that a chemical reaction is produced to block the conversion of Minoxidil to Minoxidil Sulfate. This reason has been noticed in many studies that showed minoxidil ineffective in follicles that did not have Phenol-Sulfating phenol sulfotransferase 1. If true, that would explain why minoxidil only grows hair on certain places of the scalp and not others. Minoxidil also increases NO, and male pattern baldness matches the increase with Superoxide. The reaction produces Peroxynitrite which puts stress on the mitochondria (minoxidil speeds this up creating a "resistance" of sorts and the detrimental reaction between NO & SO occurs at a rate 6 times greater than that which current treatments containing Cu/Zn are able to inhibit it(i.e. copper & zinc... foliigen/tricomin/zix). In other words by a paradoxical twist of biological and chemical
fate, the more you supplement NO (i.e. through minoxidil) the more there is to react in a detrimental fashion with the Superoxide to form Peroxynitrite which then actually further inhibits your attempts to achieve beneficial vasodilation amongst other things, which you want from minoxidil.) Peroxynitrite, which itself seems to be responsible for depleting NO bioavailability, and subsequently hindering vasodilation, and causing ultimate endothelial dysfunction. The toxicity of Peroxynitrite is mediated through mitochondrial dysfunction which leads to the mitochondria releasing cytochrome C.

 

[Old Baldy]

Interesting Wookster.

Good point Bryan.

 

[Bryan]

( male pattern baldness Out-Thinks Minoxidil )

We all notice that male pattern baldness 'figures out' Minoxidil after a while and starts to counteract its positive effects.

If the "offset of growth" theory of minoxidil is correct, then the perceived gradual loss of positive effects from minoxidil doesn't have anything to do with male pattern baldness supposedly "figuring out" the minoxidil. It simply has to do with the steady advance of male pattern baldness eventually overtaking the minoxidil.

Minoxidil also increases NO, and male pattern baldness matches the increase with Superoxide. The reaction produces Peroxynitrite which puts stress on the mitochondria...In other words by a paradoxical twist of biological and chemical fate, the more you supplement NO (i.e. through minoxidil) the more there is to react in a detrimental fashion with the Superoxide to form Peroxynitrite which then actually further inhibits your attempts to achieve beneficial vasodilation amongst other things, which you want from minoxidil.)

I personally asked Dr. Proctor about that several years ago on alt.baldspot, and he said that minoxidil does NOT increase the production of peroxynitrite. He said that minoxidil is merely a nitric oxide mimetic. I remember being greatly relieved when he told me that.

Bryan

 

[Old Baldy]

Thanks for the info. Bryan!

 

[squeegee]

POW!

 

[squeegee]

:freaked2: