Post by beebs on Aug 6, 2011 8:04:11 GMT -5
A good find!! I read some time ago, about rubbing hydrogen peroxide on joints helps with chems soups (nitric oxide, uric acid etc) pain... Not sure of the relevance of this with the study below. Interesting, the mention of hydrogen on Molecular hydrogen protects chondrocytes from oxidative stress and indirectly alters gene expressions through reducing peroxynitrite derived from nitric oxide. Am not a biochemist, so, don't ask questions, ;D read up on it.
There may be some studies out there concerning alleviating chondrocytes trauma post floxing/other meds using patches such as GTN helping dilating small vessels (or other prods using some type of hydrogen) for pain etc.. worth looking into.
There are some posts already on NO-ONOO, and look at Dr Pall's theory. It all ties in nicely.
Molecular hydrogen protects chondrocytes from oxidative stress and indirectly alters gene expressions through reducing peroxynitrite derived from nitric oxide
Teruyasu Hanaoka, Naomi Kamimura, Takashi Yokota, Shinro Takai and Shigeo Ohta
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Medical Gas Research 2011, 1:18 doi:10.1186/2045-9912-1-18
Published: 4 August 2011
Abstract (provisional)
Background
Molecular hydrogen (H2) functions as an extensive protector against oxidative stress, inflammation and allergic reaction in various biological models and clinical tests; however, its essential mechanisms remain unknown. H2 directly reacts with the strong reactive nitrogen species peroxynitrite (ONOO-) as well as hydroxyl radicals ( * OH), but not with nitric oxide radical (NO * ). We hypothesized that one of the H2 functions is caused by reducing cellular ONOO-, which is generated by the rapid reaction of NO * with superoxides ( * O2-). To verify this hypothesis, we examined whether H2 could restore cytotoxicity and transcriptional alterations induced by ONOO- derived from NO * in chondrocytes.
Methods
We treated cultured chondrocytes from porcine hindlimb cartilage or from rat meniscus fibrecartilage with a donor of NO * , S-nitroso-N-acetylpenicillamine (SNAP) in the presence or absence of H2. Chondrocyte viability was determined using a LIVE/DEAD Viability/Cytotoxicity Kit. Gene expressions of the matrix proteins of cartilage and the matrix metalloproteinases were analyzed by reverse transcriptase-coupled real-time PCR method.
Results
SNAP treatment increased the levels of nitrated proteins. H2 decreased the levels of the nitrated proteins, and suppressed chondrocyte death. It is known that the matrix proteins of cartilage (including aggrecan and type II collagen) and matrix metalloproteinases (such as MMP3 and MMP13) are down- and up-regulated by ONOO-, respectively. H2 restoratively increased the gene expressions of aggrecan and type II collagen in the presence of H2. Conversely, the gene expressions of MMP3 and MMP13 were restoratively down-regulated with H2. Thus, H2 acted to restore transcriptional alterations induced by ONOO-.
Conclusions
These results imply that one of the functions of H2 exhibits cytoprotective effects and transcriptional alterations through reducing ONOO-. Moreover, novel pharmacological strategies aimed at selective removal of ONOO- may represent a powerful method for preventive and therapeutic use of H2 for joint diseases.
The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production. www.medicalgasresearch.com/content/1/1/18/abstract