351 replies to this topic

[abolitionist]

Do a search on www.pubmed.com for "mitoQ"

looks very promising!!!

Sean

www.abolitionist-society.com

[kevin]

It sure does Sean.. you might want to check out its discussion on Google Group sci.life-extension:

http://groups.google...8&q=mitoq&meta=

as well as http://www.imminst.o...187

quite a cool little molecule..

[nootropi]

Well is it safe? What are the results of animal studies?

[abolitionist]

I'm no expert on it, but it doesn't look like it's gone very far in terms of human or animal testing yet, let's hope it's the perfect substance to protect mtDNA

This is what really got my wheels spinning;

1: J Biol Chem. 2001 Feb 16;276(7):4588-96. Epub 2000 Nov 22. Related Articles, Links

Selective targeting of a redox-active ubiquinone to mitochondria within cells: antioxidant and antiapoptotic properties.

Kelso GF, Porteous CM, Coulter CV, Hughes G, Porteous WK, Ledgerwood EC, Smith RA, Murphy MP.

Departments of Chemistry and Biochemistry, University of Otago, Box 56, Dunedin, New Zealand.

With the recognition of the central role of mitochondria in apoptosis, there is a need to develop specific tools to manipulate mitochondrial function within cells. Here we report on the development of a novel antioxidant that selectively blocks mitochondrial oxidative damage, enabling the roles of mitochondrial oxidative stress in different types of cell death to be inferred. This antioxidant, named mitoQ, is a ubiquinone derivative targeted to mitochondria by covalent attachment to a lipophilic triphenylphosphonium cation through an aliphatic carbon chain. Due to the large mitochondrial membrane potential, the cation was accumulated within mitochondria inside cells, where the ubiquinone moiety inserted into the lipid bilayer and was reduced by the respiratory chain. The ubiquinol derivative thus formed was an effective antioxidant that prevented lipid peroxidation and protected mitochondria from oxidative damage. After detoxifying a reactive oxygen species, the ubiquinol moiety was regenerated by the respiratory chain enabling its antioxidant activity to be recycled. In cell culture studies, the mitochondrially localized antioxidant protected mammalian cells from hydrogen peroxide-induced apoptosis but not from apoptosis induced by staurosporine or tumor necrosis factor-alpha. This was compared with untargeted ubiquinone analogs, which were ineffective in preventing apoptosis. These results suggest that mitochondrial oxidative stress may be a critical step in apoptosis induced by hydrogen peroxide but not for apoptosis induced by staurosporine or tumor necrosis factor-alpha. We have shown that selectively manipulating mitochondrial antioxidant status with targeted and recyclable antioxidants is a feasible approach to investigate the role of mitochondrial oxidative damage in apoptotic cell death. This approach will have further applications in investigating mitochondrial dysfunction in a range of experimental models.

PMID: 11092892 [PubMed - indexed for MEDLINE]

[abolitionist]

This page contains what may be the full text from a mitoQ study involving animals;

http://www.pubmedcen...gi?artid=154358

and here is a fellow claiming that he can sell it (hopefully for research purposes only);

http://www.animalkit...8488&forum=26

you're not going to like the price though [:o]

[abolitionist]

"After detoxifying a reactive oxygen species, the ubiquinol moiety was regenerated by the respiratory chain enabling its antioxidant activity to be recycled."

still get's me all excited [lol] [thumb]

[nootropi]

Swell; but what are the dose sizes for humans? Per dose/per day?

I will order some if the prices are reasonable per dose. Does anybody have any experience ordering products from Team L.I.F.E. Research?

[abolitionist]

Swell; but what are the dose sizes for humans?  Per dose/per day?

I will order some if the prices are reasonable per dose.  Does anybody have any experience ordering products from Team L.I.F.E. Research?

So far, I haven't seen any studies with humans nor dosage recommendations. I would imagine that the dose would be much smaller than say R-ALA, but this is just speculation based on the observation that mitoQ accumulates almost entirely in the mitochondria.

I present this information as an FYI only, and personally don't think it would be safe to experiment with mitoQ yet. However, if you are willing to take the risk, please consider working with a researcher and documenting your results [thumb]

[nootropi]

Thanks for your concern and bearing with what may seem like rude remarks towards you; like I said, I have a big mouth...

[abolitionist]

it's all good, I can tell you're very passionate about this stuff...

[mtriogd]

Dosing range is 5-20mcg/KG ED

[brooklynjuice]

BTW I can get this as well. Is there a source need for this product? Im not here to pimp proucts and I do not wish to cross that line. Just wondering in anyone is searching for a domestic source...

[ryan1113]

Sure, very interested. Where do you get it from?

Just so everyone knows, MitoQ is actually mitochondrial-targeted idebenone, and not CoQ10.

Idebenone has been revealed to substantially increase production of superoxide by up to 20-fold
recently, raising questions as to whether the net effect may be negative. Of course,
since most superoxide is produced in the mitochondria, MitoQ would theoretically be especially effective at
raising superoxide levels.

Mito-VitE and MitoPBN are two others.

The most promising research chemical for reducing oxidative stress on the horizon is probably STAZN. There will probably be a mitochondria-targeted form of it eventually.

See the following info someone recently posted to usenet:

http://tinyurl.com/44hov

[nootropi]

Sure, very interested. Where do you get it from?

Just so everyone knows, MitoQ is actually mitochondrial-targeted idebenone, and not CoQ10.

Idebenone has been revealed to substantially increase production of superoxide by up to 20-fold
recently, raising questions as to whether the net effect may be negative. Of course,
since most superoxide is produced in the mitochondria, MitoQ would theoretically be especially effective at
raising superoxide levels.

Mito-VitE and MitoPBN are two others.

The most promising research chemical for reducing oxidative stress on the horizon is probably STAZN. There will probably be a mitochondria-targeted form of it eventually.

See the following info someone recently posted to usenet:

http://tinyurl.com/44hov

This twenyfold increase you speak of is NOT consistently emulated in vitro. Add to that the exact opposite has been proven in vivo. There was a small labratory whom reported these results and you guys are running around with it like its the sacred truth...

[AORsupport]

Sure, very interested. Where do you get it from?

Just so everyone knows, MitoQ is actually mitochondrial-targeted idebenone, and not CoQ10.

The phrasing here initially led me to believe that you were saying that MitoQ was the same as idebenone and was mitochondrially-targeted, which is of course not what you intended. Just to be sure that people don't misunderstand this, MitoQ is an analog of idebenone, produced by covalently bonding on triphenylphosphonium through an aliphatic carbon chain, to yield 10-(6'-ubiquinonyl)decyltriphenylphosphonium (MitoQ) (idebenone is 2,3-dimethoxy-5-methyl-6-(10-hydroxydecyl)-1,4-benzoquinone).

Idebenone has been revealed to substantially increase production of superoxide by up to 20-fold
recently, raising questions as to whether the net effect may be negative. 

Yes, an important concern as I've noted here in recent months. It's not totally clear that MitoQ would have the same potential problems as idebenone (and I am not aware of any studies to specifically address this issue, as opposed to the quenching of existing free radicals, at which MitoQ undeniably excels), although one would expect them on a mechanistic basis.

Of course, since most superoxide is produced in the mitochondria, MitoQ would theoretically be especially effective at
raising superoxide levels.

... and, to make things worse, this is exactly the place where superoxide (or hydroperoxyl (HO2•)) production is widely acknowledged to play its key role in aging. Thanks for drawing our attention to this.

The most promising research chemical for reducing oxidative stress on the horizon is probably STAZN.  There will probably be a mitochondria-targeted form of it eventually.

See the following info someone recently posted to usenet:

http://tinyurl.com/44hov

These results are interesting; however, whether they are relevant to normal, essentially healthy organisms is a question unanswered by this research.

To your health!

AOR

[zoolander]

any news on the availability?

this recently

J Biomed Biotechnol. 2006;2006(3):31372.

    Mitochondrial oxidative damage in aging and Alzheimer's disease: implications for mitochondrially targeted antioxidant therapeutics.

        * Reddy PH.

    The overall aim of this article is to review current therapeutic strategies for treating AD, with a focus on mitochondrially targeted antioxidant treatments. Recent advances in molecular, cellular, and animal model studies of AD have revealed that amyloid precursor protein derivatives, including amyloid beta (A beta) monomers and oligomers, are likely key factors in tau hyperphosphorylation, mitochondrial oxidative damage, inflammatory changes, and synaptic failure in the brain tissue of AD patients. Several therapeutic strategies have been developed to treat AD, including anti-inflammatory, antioxidant, and antiamyloid approaches. Among these, mitochondrial antioxidant therapy has been found to be the most efficacious in reducing pathological changes and in not producing adverse effects; thus, mitochondrial antioxidant therapy is promising as a treatment for AD patients. However, a major limitation in applying mitochondrial antioxidants to AD treatment has been the inability of researchers to enhance antioxidant levels in mitochondria. Recently, however, there has been a breakthrough. Researchers have recently been able to promote the entry of certain antioxidants-including MitoQ, MitoVitE, MitoPBN, MitoPeroxidase, and amino acid and peptide-based SS tetrapeptides-into mitochondria, several hundred-fold more than do natural antioxidants. Once in the mitochondria, they rapidly neutralize free radicals and decrease mitochondrial toxicity. Thus, mitochondrially targeted antioxidants are promising candidates for treating AD patients.

    PMID: 17047303 [PubMed - in process]

see attached free access paper

Attached Files

•  mitochondrial_oxidative_damage_in_Alzheimers_and_aging.pdf   649.22KB   160 downloads

[goku]

Wow...

So, yeah, any reliable/potential suppliers out there?

[Gerald W. Gaston]

Potential use of MitQ for IBS:

http://blogs.biomedc...-bowel-disease/

[niner]

Potential use of MitQ for IBS:

http://blogs.biomedc...-bowel-disease/

Wow, this is a really nice result. They got a very nice knock-down of disease in a rodent model. Inflammatory bowel disease (IBD, not IBS, which is a much milder condition) is a pretty horrible condition and the current treatment is tons of corticosteroids that have a lot of nasty side effects of their own. An exciting aspect of this is that rather than waiting a decade for MitoQ to become available, you could just take C60 instead, which would probably work better anyway.

[Gerald W. Gaston]

Thanks niner, Until you mentioned it, I was under the impression IBS was synonymous for IBD.. Now that I have looked it up and see that Ulcerative Coloitis (UC) and Crohn's Disease (CD) fall under IBD. I know that's not the case. And I guess I should have known given my past experience. At one point in my life my doctor at the time, after a lot of testing and probing, called an issue I had IBS (seemed to be a common catch-all diagnosis at the time). He prescribed dicyclomine and some other meds. Ultimately I fixed it by reducing stress, changing my diet, and the big kicker - going up a pant size.

What I was going through was nothing compared to one of my co-workers with CD who is often hospitalized with it..

http://www.webmd.com.../ibd-versus-ibs

[PWAIN]

Is there somewhere to get this stuff??

[Boris_Badenoff]

MitoQ is now sold online (not cheap) in capsule or cream at http://www.mitoq.com. Anyone know of an alternative bulk source? There was a new study this week showing MitoQ reverses MS (Multiple Sclerosis) in rats.

Edited by Boris_Badenoff, 28 December 2013 - 02:06 PM.

[niner]

Wow, it finally made it to market! I would have been very excited about this a few years ago, but now we have C60-oo that I think works in a similar manner, only better. The MitoQ paper didn't actually reverse MS. It acted as an anti-inflammatory antioxidant, which subverted the method that they used to experimentally induce "an MS-like disease". I suspect C60 would have acted similarly. It would be interesting to combine MitoQ with C60-oo to see if they have any synergy.

[mitomutant]

Wow, it finally made it to market! I would have been very excited about this a few years ago, but now we have C60-oo that I think works in a similar manner, only better. The MitoQ paper didn't actually reverse MS. It acted as an anti-inflammatory antioxidant, which subverted the method that they used to experimentally induce "an MS-like disease". I suspect C60 would have acted similarly. It would be interesting to combine MitoQ with C60-oo to see if they have any synergy.

MitoQ was once the hope of people - me included - with mitochondrial diseases. Too bad it has ended-up as a skin care product. Nevertheless, I have just ordered a bottle. It will be interesting too see its effects on my faulty mitos. I will report any significant effect.

[Boris_Badenoff]

So C60-oo seems to be favored? What purity and source have Longecity testers found to be safe and effective?

[niner]

MitoQ was once the hope of people - me included - with mitochondrial diseases. Too bad it has ended-up as a skin care product. Nevertheless, I have just ordered a bottle. It will be interesting too see its effects on my faulty mitos. I will report any significant effect.

Thanks for trying it, mm. I'm looking forward to hearing about it. If you combine it with c60, I think that synergy is at least plausible. They both place electronically active molecules in the mitochondrial membrane, but the two structures are very different. I suppose anti-synergy is also a possibility...

[hav]

Just read through the mito paper and it seems like what they are doing is proposing a high performance delivery mechanism for lipophilic molecules. They picked two of them, Vitamin E and CoQ10, only because they were popular lipophilic anti-oxidants in 2003. The paper mentions "conjugation to a triphenylphosphonium cation" but doesn't detail the process. I assume its more complicated than stirring VitE and/or CoQ10 in olive oil for 2 weeks.

From what they say, similar cations could be conjugated out of any lipophilic antioxidant. Like resveratrol or c60. My sense is that the major limitation of using simple olive oil stirring is the amount per unit volume of antioxidant possible to adduct that way. My suspicion is that C60 works so well in olive oil only because its such a powerful antioxidant that relatively little is required. A similar amount of resveratrol dissolved in olive oil doesn't seem as exciting a prospect but it hasn't been formally studied yet for comparative effect. But it does make me wonder if a "MitoC60" would be potent enough to give a little capsule the equivalent effect of many milliliters of c60/evoo.

Howard

Edited by hav, 29 December 2013 - 04:58 PM.