Vitamin D: increases glutathione, induces glioma apoptosis

[liveonearth]

New data shows that vitamin D has more biochemical actions that anticipated:
--inhibits the synthesis of inducible nitric oxide synthase
--increases intracellular glutathione levels-->helps remove mercury & other toxins from your body
--could be used to Tx neurodegenerative and neuroimmune diseases
--induces glioma cell death-->good for management of brain tumors?

According to Dr. Cannel, founder of the Vitamin D Council, in an interview:
--vitamin D is not a vitamin, but rather the only known substrate for a powerful repair and maintenance steroid hormone that is involved in numerous functions of your body and organs
--like all steroid hormones vit D regulates your body by turning your genes on or off
--you have about 2,000 genes that are directly influenced by vitamin D

SOURCES
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T3K-45BCJ53-7&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=36fe7df09fbacd4b33fe816072a1793d
http://articles.mercola.com/sites/articles/archive/2008/12/04/how-sunshine-and-vitamin-d-can-help-you-eliminate-mercury.aspx

Comments

Re: Vitamin D

[liveonearth.livejournal.com]

Thanks for the comment, though I do not believe that you are a microbiologist. The receptor is not on the gene, it is on the membrane. The only chronic disease I find repeatedly mentioned in the lecture is chronic fatigue syndrome. The speaker has nothing to say about vitamin D supplementation.

The point of the speaker as far as I can tell is that when we know the genetics of an organism, we still know very little about the way the organism works. This is true because the regulation of genes is far more complex than the genetics themselves. The same gene may be activated or deactivated by many different things and we know that these vary by species. As organisms we are also comprised of a great many other organisms, which have their own genetics and triggers.

Here's a section from the lecture:

The other reason that this has escaped study by science is that the VDR stands for Vitamin D Receptor. It is activated by a substance which we know as Vitamin D, which is a transcriptional activator, a secosteroid. Vitamin D is not a nutrient. There is a very complex control system by which 7-dehydro-cholesterol is synthesized into 1,25-dihydroxyvitamin-D, which then activates transcription by the VDR nuclear receptor. There are multiple feedback pathways, there is transcription of degrading enzymes, there is trans-repression of an enhancing enzyme, and then, via the PXR (the Pregnane-X Receptor), other enzymes are affected and finally this primary CYP27B1 second hydroxylation enzyme is activated by PKA P300/CBP pathway—very complex mechanism, which you would expect. It's at the heart of innate immunity. A paper we published this year goes into the control system in some detail. And this is the interesting thing. Here's in-silico technology. We've taken the X-ray structure of the VDR, actually a number of VDRs from different groups, and we've docked the various types of Vitamin D, the various hydroxlations, into that receptor. Only one of them has the 1-alpha-hydroxylation here, which is capable of activating transcription. But all of the others overlay the same region in the receptor. In other words, they are antagonists for that transcription process. If we take the VDR agonist which we have found, which is a drug called olmesartan, we see here olmesartan in the human VDR. This is a molecular dynamics emulation using a large computer array computing real-time atomic force interactions, and, of course, like all proteins, everything is in motion, there's total motion all the time. And here we have a rat VDR with the same drug in it. Now what's particularly interesting is the orientation of the tetrazoles and the functioning of the drug is different in the two VDRs. If you look at that tetrazole orientation and the other one, they're different—there are 7 hydrogen bonds there, and there are only 5 hydrogen bonds in the VDR of a rat. So the drug itself doesn't behave in the same way in the VDR of the rat versus the VDR of the man.