635 replies to this topic

[niner]

Here's full text of the article "Ryanodine Receptor Oxidation Causes Intracellular Calcium Leak and Muscle Weakness in Aging"
http://www.ncbi.nlm....les/PMC3690519/

C60 might either get into the cell membrane and deoxidize the ryanodine receptors to some extent, repairing the calcium leakage, and/or they could get into the mitochondrial membrane and reduce superoxide, which would also decrease the oxidation of those receptors (and many other things).

Since the ryanodine receptors along with other proteins are likely to be recycled and replaced at some point, reduced superoxide would allow new receptors to keep working better for longer before they become oxidized.

Yes, in fact, in the paper you linked, it says:

Jang et al showed that ablation of the antioxidant enzyme superoxide dismutase 1 (SOD1) increased superoxide levels in murine skeletal muscle resulting in reduced specific force and accelerated age-dependent muscle pathology.

This shows that increased superoxide causes muscle dysfunction; it stands to reason that decreased superoxide would help. I don't know of anyone old enough to suffer from noticeable sarcopenia who has taken c60-oo. I'd love to run the experiment of trying 60-oo in the extreme elderly or someone with heart failure, but I don't want to recommend it to anyone like that because I wouldn't want to be responsible if something bad happened. It might be interesting to give it to a very old rat.

If there's an interaction between the ryanodine receptor and c60-oo, I suspect it's mediated through ROS. I think there are some other candidate enzymes, like aconitase, that may have more explanatory power. With c60 use, we're seeing increased endurance, but not particularly increased force generation. That suggests, at least in the young-ish clientele that are using c60 at the moment, that the RyR isn't a big factor. In the elderly, OTOH, it might come into play.

[markymark]

I came across this one (hope it is the right place to post it here):

PLoS One. 2013 Jun 13;8(6):e66337. doi: 10.1371/journal.pone.0066337. Print 2013.
Anti-influenza activity of c60 fullerene derivatives.


Well, we'll find out, as to whether "our" C60-oo (C60-Oleic acid&X) does also possess anti PA endonuclease activity (or has any meaningful effect) in H1N1 and other influenza viruses, when the next pandemic (real or fake ;-)) is going to be announcend by the WHO. But it is interesting anyway, that C60-fullerene derivatives are being studied that way.

[smithx]

I was reading a little about shilajit, a tarry exudate of indeterminate origin which oozes from rocks in the Himalayas and elsewhere. According to Wikipedia:

An ancient Ayurvedic text, called the Charaka Samhita, states that there is no curable disease in the universe, which is not effectively cured by shilajit when it is administered at the appropriate time, in combination with suitable drugs and by adopting the prescribed method.

http://en.wikipedia....hilajit#History

Recently LEF.org has started selling a supplement containing shilajit. So I started wondering if some of that black tar could be C60, and if that might be at least partly responsible for any benefits.

According to this article, yes there is C60 in shilajit, perhaps from ancient meteorite strikes:

A unified manifestation of the macrocosmic and microcosmic actions is expressed by the co-occurrence of C₆₀-fullerene-dibenzo-α-pyrone (DBP) conjugates in meteorites, ammonites, and Shilajit. The crystal forms of mineral (aragonite) deposition in ammonites (the major marine precursors of Shilajit), are distinctly different in many respects from the inorganic mineral, aragonite. The mineral deposition in the living ammonite shells is under strict biological control and involves organo-mineral complexes received from meteorites. These constituents in ammonites are eventually transformed into Shilajit by humification. Hence, the supramolecular assemblies of complex chemical constituents of ammonites, in many respects, show striking similarities with the humic constituents (FAs, HAs and HMs) of meteorites and of Shilajit. Some selected assemblies, viz. fusoms and DCPs, of Shilajit, comprising of fullerene-DBP conjugates in their inner core, were found to confer facile water-solubility, stability and superior bioavailability (Yogahahi in Ayurveda) to a host of chemical agents that are ordinarily water-insoluble, thermolabile, autoxidizable, and/or prematurely biodegradable before reaching the target site. The potential of this superior drug delivery system is evaluated.

http://cat.inist.fr/...cpsidt=20642347

[hav]

According to this article, yes there is C60 in shilajit, perhaps from ancient meteorite strikes:

A unified manifestation of the macrocosmic and microcosmic actions is expressed by the co-occurrence of C₆₀-fullerene-dibenzo-α-pyrone (DBP) conjugates in meteorites, ammonites, and Shilajit. The crystal forms of mineral (aragonite) deposition in ammonites (the major marine precursors of Shilajit), are distinctly different in many respects from the inorganic mineral, aragonite. The mineral deposition in the living ammonite shells is under strict biological control and involves organo-mineral complexes received from meteorites. These constituents in ammonites are eventually transformed into Shilajit by humification. Hence, the supramolecular assemblies of complex chemical constituents of ammonites, in many respects, show striking similarities with the humic constituents (FAs, HAs and HMs) of meteorites and of Shilajit. Some selected assemblies, viz. fusoms and DCPs, of Shilajit, comprising of fullerene-DBP conjugates in their inner core, were found to confer facile water-solubility, stability and superior bioavailability (Yogahahi in Ayurveda) to a host of chemical agents that are ordinarily water-insoluble, thermolabile, autoxidizable, and/or prematurely biodegradable before reaching the target site. The potential of this superior drug delivery system is evaluated.

http://cat.inist.fr/...cpsidt=20642347

Sounds to me like they found that a Shilajit/c60 conjugate is water soluble at its inner core. Might constitute Hy/c60 all by itself. But I'm not sure that pure Shilajit is directly soluble in water... turpentine and milk seem to be the most mentioned solvents. Perhaps adding more c60 to Shilajit and water? This study on Shilajit alone seems to support the c60 connection finding some of the same effects attributed to c60/evoo:

Shilajit attenuates behavioral symptoms of chronic fatigue syndrome by modulating the hypothalamic-pituitary-adrenal axis and mitochondrial bioenergetics in rats

Shilajit reversed the CFS-induced increase in immobility period and decrease in climbing behavior as well as attenuated anxiety in the EPM test. Shilajit reversed CFS-induced decrease in plasma corticosterone level and loss of adrenal gland weight indicating modulation of HPA axis. Shilajit prevented CFS-induced mitochondrial dysfunction by stabilizing the complex enzyme activities and the loss of MMP. Shilajit reversed CFS-induced mitochondrial oxidative stress in terms of NO concentration and, LPO, SOD and catalase activities.

Howard

[Eray Ozkural]

This essay, well basically a science news piece, argues that anti-oxidants *in general* may be promoting cancer.

http://www.theatlant...in-myth/277947/

Do you think it was mere chance that so far we haven't seen such a case with c60 in animal studies? Or maybe the kind of anti-oxidant does make a huge difference? The piece is obviously a bit hyperbolical but it did get me think. What's your take?

[Hebbeh]

This essay, well basically a science news piece, argues that anti-oxidants *in general* may be promoting cancer.

http://www.theatlant...in-myth/277947/

Do you think it was mere chance that so far we haven't seen such a case with c60 in animal studies? Or maybe the kind of anti-oxidant does make a huge difference? The piece is obviously a bit hyperbolical but it did get me think. What's your take?

http://www.longecity...ed-supplements/

[Eray Ozkural]

Ok, I've read the discussion there, but not much is said upon whether the claims about certain vitamins (like the anti-oxidant C) promoting cancer are factually true or whether there is any substance to the claim in the article about anti-oxidants in general? Which is relevant to C60, such as this part:

In 2008, a review of all existing studies involving more than 230,000 people who did or did not receive supplemental antioxidants found that vitamins increased the risk of cancer and heart disease.

The posters there claim the article refers to 30 year old results and bases its conclusion on Pauling's obsession but it seems they haven't read the whole essay. I'm very curious about whether there is a significant risk posed by anti-oxidants in general, because I know a very large rat that's dying to lick off some C60 olive oil.

Edited by Eray Ozkural, 22 July 2013 - 12:27 AM.

[Eray Ozkural]

I just saw a discussion on slashdot about that article:

http://science.slash...min-supplements

Some interesting points raised there. I must admit that the article did alarm my BS detector, but I really need to hear someone who has some actual expertise on the matter of vitamins, that's why I've asked about it. For instance, there was a quite logical objection, such as might it be that anti-oxidants increase lifespan, which might then increase cancer probability? Another person says that the article was part of a book by someone with ties to the vaccine industry, and might be biased against vitamins.

Also interesting that Pauling lived to 93.

Please let me know what you think. I think we should have some solid arguments against this, surely we can do better than handwaving it away. Thanks in advance.

[hav]

Ok, I've read the discussion there, but not much is said upon whether the claims about certain vitamins (like the anti-oxidant C) promoting cancer are factually true or whether there is any substance to the claim in the article about anti-oxidants in general? Which is relevant to C60, such as this part:

In 2008, a review of all existing studies involving more than 230,000 people who did or did not receive supplemental antioxidants found that vitamins increased the risk of cancer and heart disease.

The posters there claim the article refers to 30 year old results and bases its conclusion on Pauling's obsession but it seems they haven't read the whole essay. I'm very curious about whether there is a significant risk posed by anti-oxidants in general, because I know a very large rat that's dying to lick off some C60 olive oil.

The essay makes no effort to do a formal statistical meta-analysis of studies and is a good example of why generalization without basis is bad. Not that I want to advocate Pauling's faith in vitamin C, but the obvious slant in the essay culminates in the final paragraph, where the author tries to use Pauling's eventual death to drive his point home but ignores the fact that Pauling actually achieved his goal of living more than another 25 years after commencing his protocol in 1966. The essay does seem to prove by bad example what should be intuitively obvious. That all antioxidants are not the same and that one size does not fit all... which probably applies to more than shoes and multivitamins.

The Baati study, by the way, proved rather convincingly that at least one anti-oxidant, C60 dissolved in olive oil, extends the life of rats, who normally die of cancer, by 90%. But just to illustrate how resistant to broad generalization anti-oxidants can be, Resveratrol dissolved in corn oil was shown in one study to inhibit tumor growth in mice but the same researchers in another study found the same anti-oxidant accelerated tumor growth in mice when dissolved in a coconut-like oil. Wasn't Pauling big on coconut oil too?

Howard

[somecallmetim]

The Baati study, by the way, proved rather convincingly that at least one anti-oxidant, C60 dissolved in olive oil, extends the life of rats, who normally die of cancer, by 90%. But just to illustrate how resistant to broad generalization anti-oxidants can be, Resveratrol dissolved in corn oil was shown in one study to inhibit tumor growth in mice but the same researchers in another study found the same anti-oxidant accelerated tumor growth in mice when dissolved in a coconut-like oil. Wasn't Pauling big on coconut oil too?

Howard

If I read the second study correctly, the mice were given either a neobee oil/ethanol mixture or resveratrol. So the resveratrol was administered to the mice by itself, not dissolved in a coconut-like oil.

[niner]

The Baati study, by the way, proved rather convincingly that at least one anti-oxidant, C60 dissolved in olive oil, extends the life of rats, who normally die of cancer, by 90%. But just to illustrate how resistant to broad generalization anti-oxidants can be, Resveratrol dissolved in corn oil was shown in one study to inhibit tumor growth in mice but the same researchers in another study found the same anti-oxidant accelerated tumor growth in mice when dissolved in a coconut-like oil. Wasn't Pauling big on coconut oil too?

If I read the second study correctly, the mice were given either a neobee oil/ethanol mixture or resveratrol. So the resveratrol was administered to the mice by itself, not dissolved in a coconut-like oil.

Neobee oil was the vehicle, so it was both the placebo and the solvent for the drug. Neobee oil is an MCT oil like coconut oil, but is not coconut oil per se.

It's worth noting that these were immunocompromised mice, injected with tumor cells. The relevance to normal humans is debatable.

Edited by niner, 24 July 2013 - 09:28 PM.

[hav]

Neobee oil was the vehicle, so it was both the placebo and the solvent for the drug. Neobee oil is an MCT oil like coconut oil, but is not coconut oil per se.

It's worth noting that these were immunocompromised mice, injected with tumor cells. The relevance to normal humans is debatable.

Just got a chance to look more closely at the oil compositions. Neobee is a brand name of MCT made from coconut and palm oils. Here's the datasheet for the M5 version. Looks like they've managed to make it 100% saturated fatty acids compared to around 91% for coconut oil. And with more shorter chained fatty acids: caprylic (c8:0) and capric (c10:0) compared to coconut with more lauric (c12:0). Probably makes neobee a better performer with regard to liver delivery and energy release, following the same path that resveratrol usually takes. The dramatic difference in results they got with regard to resveratrol's effect on tumor growth just makes me wonder if resveratrol and mct oils are a bad combination to take together. Here's a study that found that regular cooking with coconut milk might be a bad idea:

Method of cooking and risk of breast cancer in the Philippines

Boiling food in coconut milk was associated with a significantly increased risk of breast cancer (odds ratio (OR) = 2.2; 95% confidence interval (CI) 1.3-3.8). There were positive associations between boiling food in coconut milk and the risk of breast cancer currently (OR = 1.9; 95% CI 1.0-3.3), and at 12 years of age (OR = 2.9; 95% CI 1.6-5.5). A positive association between frying food and breast cancer risk was restricted to women whose household fried food at 12 years of age (OR = 1.89; 95% CI 1.1-3.4).

Granted dissolving resveratrol in alcohol and then mct oil is pretty different from frying foods in coconut oil, but I wouldn't have expected even immunocompromised mice to react that way to resveratrol.

Howard

[Turnbuckle]

The Baati study, by the way, proved rather convincingly that at least one anti-oxidant, C60 dissolved in olive oil, extends the life of rats, who normally die of cancer, by 90%.

The proof will be in the replication, and the mechanism of life extension still needs to be shown.

[free10]

Here is an interesting page from 2010, or I found it to be. It starts out about C60 and see growth and then expands into other arenas of C60

http://smarteconomy....owth-by-60.html

[mait]

Turns out that enhancing autophagy by spermidine ( C60 in EVOO may also have pro-autophagy effect according to Baati et al.,) may result in strong pro-cognitive and neural tissue specific anti- aging effect.

http://www.nature.co...ll/nn.3518.html
http://www.nature.co...ll/nn.3512.html

[niner]

C60 in EVOO may also have pro-autophagy effect according to Baati et al.

Did they talk about this in their paper? I don't remember seeing it.

[mait]

C60 in EVOO may also have pro-autophagy effect according to Baati et al.

Did they talk about this in their paper? I don't remember seeing it.

I re-checked it and You are right. This is mess-up for my part. C60 and autophagy I thought that was described by original rat study was actually from another article (read at abstract level) about underivatized nano c60 autophagy inducing effect in cancer cells. So it is not related to C60 EVOO.

Thank You for pointing it out. I cant delete my previous erroneous post so I ask from forum moderators to do it.

Edited by mait, 04 October 2013 - 01:53 PM.

[clairvoyant]

This is my latest hypothesis on the chemistry of C60OO in vivo. See the files attached.

Attached Files

•  main_file.doc   386.5KB   81 downloads
•  file_1.pdf   249.46KB   69 downloads
•  file_2.doc   82.5KB   36 downloads

[Turnbuckle]

The difference between C60 and C70

C60 is situated in the mitochondria but C70 in lysosomes for extraction. It is courtesy of Turnbuckle, provided study.
According to the book of Franco Cataldo both fullerenes are fatty soluble. According to Turnbuckle’s experiment, C70 is not soluble in olive oil. This controversy can explain the whereabouts in the cells of the two compounds and the reason why C70 does not get into the mitochondrion. It just cannot get through the lipid membranes. I would rather believe Turnbuckle.

Actually, I found that C70 was soluble, and a C60 + C70 mix went into solution much faster than C60 alone, no doubt because C70 disrupted the crystal structure. I also found that C70 had toxic effects. One paper I posted a link to claimed that C70 collected preferentially in the ER (endoplasmic reticulum), but also in the mitochondria. In the ER it could disrupt protein synthesis.

The study used a conjugate of C70 and Texas Red--

The intracellular localization was found predominately in the ER and to a lesser degree in mitochondria and lysosomes.

http://www.ncbi.nlm....les/PMC2888797/

[hav]

This is my latest hypothesis on the chemistry of C60OO in vivo. See the files attached.

I remember seeing a passing mention in the Baati paper of c60 being known to react with vitamin A in liver:

... it has been already shown that C60 reacts inside the liver cells with vitamin A following a DielseAlder like reaction both in mice and in rats [21,42]. These two routes may be sufficient for C60 elimination, nevertheless, we have to look for other possible biotransformations and elimination routes, all the more so as the fate of the addition product is not known.

Thanks for posting the Moussa paper that details the previous finding; I couldn't even find the abstract in PubMed. Both papers suggest that the in vivo reaction of c60 and retinol in the liver may result in its removal from the body but do not pursue it further. Couldn't find anything new on that issue in Pubmed. I did find this fairly old study, however, suggesting the opposite, that Retinol Palmate Oil might function as an in vivo c60 delivery agent:

Spectroscopic and thermodynamic study of charge transfer interactions of retinol palmitate with [60]- and [70]fullerenes by absorption spectrometric method.

Retinol palmitate (1), which is commonly called "Vitamin A palmitate", has been shown to form charge transfer (CT) complexes with a series of electron acceptors including [60]- and [70]fullerenes, and from the trends in CT transition energies the vertical ionization potential of 1 has been estimated to be 7.73eV. Stoichiometries of the fullerene complexes have been shown to be 1(Vitamin 1): 1([70]fullerene) and 1(Vitamin 1): 2([60]fullerene). The enthalpies and entropies of formation of these two complexes have been determined by estimating the formation constants spectrophotometrically at five different temperatures. The complexation phenomenon may be utilised to dissolve the fullerenes in the non-toxic Vitamin A oil and the solution may be used for testing the biological activity of the fullerenes in vivo.

Maybe the sunscreen controversy has made researchers stop thinking about using it, however.

Howard

Edited by hav, 13 January 2014 - 12:14 AM.

[Turnbuckle]

A Russian paper published at about the same time as Baati, overviewed effects of various C60 derivatives on apoptosis and cell proliferation, and its action as an antioxidant vs prooxidant--

It is hardly possible to exaggerate a significance of the fullerene nanoparticles functionalization type, their sizes and surface nanotopology for further promoting of either cytoprotective or cytotoxic effects. Noteworthy, the antioxidant properties of some water soluble fullerene derivatives were revealed while the fullerenes induced ROS formation might be also occurred. One of the most intriguing peculiarity of the fullerenes as pharmacophores consists in capabilities of some of them to intervene into the structure domains of functional proteins including enzymes and organelles linked receptors as well as to play a role of intercalators interacting with DNA double helix which, in turn, leads to a number of crucial consequences such as the biopolymer conformational flexibility shifts, catalytic activity changes, ligand docking affinity impacts in cell signaling pathways. Last not least, the fullerens are about to compete with several natural metabolites and effectots which is itself a valid platform for pharmacological outreach. This Review deals with an Authors’s original attempt to analyse the above mentioned points with an aim to elucidate those properties, methodological and structural, of numerous fullerene adducts that determine their apoptosis and cell proliferation modulating effects with a special respect to a target cell / tumor type.

[free10]

How about a little cancer fighting and absorbing through the skin

http://cen.acs.org/a...iological SCENE)

For those not aware of it, graphene is a single layer of C60, and graphene is about to rock the world we live in, and in just about every aspect of our realities. This reality is already beginning to roll out and will make a lot of people feel like they are living in the Twilight Zone.

[mikeinnaples]

For those not aware of it, graphene is a single layer of C60

Not quite right

[free10]

For those not aware of it, graphene is a single layer of C60

Not quite right

How about open C60

[xEva]

This is my latest hypothesis on the chemistry of C60OO in vivo. See the files attached.

clairvoyant, I finally looked at your main_file.doc. I'm sure you want some feedback. I am not a chemist, but I have a few suggestions and questions regarding your hypothesis. Here it comes, from least important to most.

Hypotheses
....proof: ....

This is probably a language issue. Far from a "proof"; "support" (for the hypothesis) is the right term.

The necessary conditions for a compound to be predominantly accumulated in mitochondrion are:

1. Not to be metabolized (at least not all of it)

2. To be attracted by the negative charge

3. To be lipid soluble (so as to pass through the cell and mitochondrial membranes)

1. Not to be metabolized = not to be broken down, which is the case for most, if not all, small molecules.
2. To be attracted by the negative charge = to be positively charged. Is C60oo positively charged?
3. Passing through the cell and mitochondrial membranes is not limited to lipid-soluble compounds.

Ubiquinone is lipid soluble and freely floats through the lipid membrane. The Complexes (enzymes) are static and embedded in IMM. Q+2(e-) + 2(H+)àQH2 and the reverse reaction. C60+2HàC60H2. This molecule is called methanofullerene.

...Proof: In vivo. Again, courtesy of Turnbuckle ... ...statins ... are known to deplete ubiquinone, as a side effect, via interference with ubiquinone synthesis. ... Upon taking C60, the respiration was resumed immediately. Thus, C60 replaced ubiquinone as lipid electron carrier in ETC. ..."

1. Your linking ubiquinone to C60oo via methanofullerene is very tenuous.
2. Turnbuckle's experience with statins and C60oo does not prove that "C60 replaced ubiquinone as lipid electron carrier in ETC".


This is the most troubling part:

Dosage and susceptibility to C60

We may suppose that younger and physically fitter individuals will have better mitochondria i.e. with higher potential, which can attract more C60. In addition, they supposedly have less peroxidated lipids, less aldehydes and less cross-linked proteins than older, less fit and heavy alcohol consumers do. C60 is lipid soluble so, it may stay in fat tissue reserves as depot very long. Therefore, I can speculate that, in the best case, if one is physically unfit, fat, old drunk and all these things put together then he will be less susceptible to C60. Because C60 will be chemically bonded and can not reach the mitochondrion to produce ATF.
This does not mean that older will benefit less; just it will be difficult to overdose.

1. Mitochondrial membrane potential has little to do with its attractiveness to C60oo.
2. Your speculation that a "physically unfit, fat, old drunk" should be "less susceptible to [the benefits of] C60" is not supported by the observation that old dogs had the most dramatic response to C60oo (minus them being old drunks of course lol).
3. C60 has demonstrated its affinity to mitochondrial membranes, but this does not mean that it is directly involved in ATP production (I know your ATF means ATP, but in English phosphate starts with P and not F like fosfat in Bulgarian or Russian).
4.Not sure what the last sentence means other than it contradicts what you said above about old drunks being "less susceptible to C60." Re overdose, those who took a lot of C60oo are conspicuously silent about the results.



In any rate, thank you for taking time to put your thoughts on C60oo mode of action. It's good to consider strengths and weaknesses of other people's hypotheses, 'cause it helps honing our own knowledge and understanding.

Yeah, I too have a hypothesis but I am reluctant to share it, because it requires certain familiarity with qi of qigong and the meridian system of TCM. The connection to the modern western medicine/physiology is the primo-vascular system that is believed to serve as physical channel for the "flow of qi". For the vast majority of people here the light is brighter under the street poles other than this, and that's where they are looking for answers.

Edited by xEva, 25 February 2014 - 10:35 AM.

[somecallmetim]

Yeah, I too have a hypothesis but I am reluctant to share it, because it requires certain familiarity with qi of qigong and the meridian system of TCM. The connection to the modern western medicine/physiology is the primo-vascular system that is believed to serve as physical channel for the "flow of qi". For the vast majority of people here the light is brighter under the street poles other than this, and that's where they are looking for answers.

Please reconsider sharing your hypothesis with us. I am familiar with subtle energies such as qi, and would be interested in reading your thoughts on what effects C60 has on the meridians etc. Besides, at this point, your view on what C60 & C60oo does in the body is just as valid as anyone else's here.

[smithx]

The ryanodine receptor would not be expected to be oxidized in younger individuals, and would therefore not be causing problems.

In older individuals with a higher ROS load, it would get oxidized and less efficient. This would definitely affect stamina as well as strength, in that opposing muscle pairs would be pulling on each other.

So you would only expect to see a C60 effect on that receptor in older individuals.

My hypothesis is that C60 reduces the ROS load in older individuals and therefore reduces the oxidation of enzymes such as the ryanodine receptor. When these enzymes are replaced through natural turnover, the animal experiences the benefits we see in terms of increased activity levels because the replacements are able to stay functional for longer without getting oxidized.

Here's full text of the article "Ryanodine Receptor Oxidation Causes Intracellular Calcium Leak and Muscle Weakness in Aging"
http://www.ncbi.nlm....les/PMC3690519/

C60 might either get into the cell membrane and deoxidize the ryanodine receptors to some extent, repairing the calcium leakage, and/or they could get into the mitochondrial membrane and reduce superoxide, which would also decrease the oxidation of those receptors (and many other things).

Since the ryanodine receptors along with other proteins are likely to be recycled and replaced at some point, reduced superoxide would allow new receptors to keep working better for longer before they become oxidized.

Yes, in fact, in the paper you linked, it says:

Jang et al showed that ablation of the antioxidant enzyme superoxide dismutase 1 (SOD1) increased superoxide levels in murine skeletal muscle resulting in reduced specific force and accelerated age-dependent muscle pathology.

This shows that increased superoxide causes muscle dysfunction; it stands to reason that decreased superoxide would help. I don't know of anyone old enough to suffer from noticeable sarcopenia who has taken c60-oo. I'd love to run the experiment of trying 60-oo in the extreme elderly or someone with heart failure, but I don't want to recommend it to anyone like that because I wouldn't want to be responsible if something bad happened. It might be interesting to give it to a very old rat.

If there's an interaction between the ryanodine receptor and c60-oo, I suspect it's mediated through ROS. I think there are some other candidate enzymes, like aconitase, that may have more explanatory power. With c60 use, we're seeing increased endurance, but not particularly increased force generation. That suggests, at least in the young-ish clientele that are using c60 at the moment, that the RyR isn't a big factor. In the elderly, OTOH, it might come into play.

[Geoffrey1]

interesting re c-60 from Vince:

http://www.anti-agin...s-in-olive-oil/

begin quote: >>As I understand it, the process goes like this:

1.  The outer mitochondrial membrane is charged positively and the inner membrane is charged negatively.   This is because free electrons are spun off in the complexes in the electron transfer chain.  As the chain becomes less efficient and there is decline in expression of mitochondrial antioxidants, the more there is a charge differential. “Accumulation of Skulachev ions in the mitochondria is based on the transmembrane potential difference generated as a result of electron transport chain activity. The outer side of inner membrane of mitochondria has positive charge and the inner side has negative charge.”  The actions of the electron transport chain involve four complexes, and you can get a fair idea how they work by viewing one of these animations.

2.  Superoxide is created as a result of the cross-membrane charge differential, the amount being a nonlinear function of the differential. “The specific feature attributable to the generation of ROS by mitochondria is related to the fact that the higher is the membrane potential (the larger is the difference in the concentration of protons inside and outside the mitochondria), the higher is the level of the superoxide anion production. As it was shown [29], there is steep dependence of mitochondrial superoxide-anion-radical generation on transmembrane potential (Δ). Even a small (10–15%) decline of Δ resulted in tenfold lowering of ROS production rate.”

3.  In the case of C60, the modeling studies suggest that the fullerenes are initially electrically neutral and penetrate easily to the center of the mitochondrial membranes. “Wong-Ekkabut et al. showed using molecular dynamics simulations [20] that C60fullerene is capable of penetrating into membrane and accumulates in the middle of lipid bilayer.”

4.  There, a fullerene may pick up as many as six protons, according to the quantum wave-function model.

5.  The electrical gradient then sucks the positively charged fullerene across the inner mitochondrial membrane into the interior of the mitochondria.  “DFT simulations allowed us to propose the following mechanism. C60 fullerene molecules enter the space between inner and outer membranes of mitochondria, where the excess of protons has been formed by diffusion. In this compartment fullerenes are loaded with protons and acquire positive charge distributed over their surface. Such “charge-loaded’’ particles can be transferred through the inner membrane of the mitochondria due to the potential difference generated by the inner membrane, using electrochemical mechanism described in detail by Skulachev et al. [18,24]. In this case the transmembrane potential is reduced, which in turn significantly reduces the intensity of superoxide anion-radical production.”

6.  Once a positively charged fullerene is inside the mitochondria, the charge differential between the inner and the outer membrane is automatically reduced.

7.  A net result is that a relatively small reduction in the charge differential can essentially turn down or turn off the production of superoxide.

8.  This mechanism is completely independent of any antioxidant properties of the fullerene itself.  Basically, the superoxide production is reduced through the C60 being in the role of a charge transporter.

9.  If the fullerene has an antioxidant property once inside the mitochondria, that is an additional mechanism for reduction of ROS.

We note that a similar mechanism of action may explain the effectiveness of MitoQwhich is commonly called a “mitochondrial antioxidant.”  MitoQ is designed to be a molecule having a powerful positive charge, consisting of the cation triphenylphosphonium (TPP) covalently bonded to coenzyme Q-10.    The result is a positively charged molecule.  It is thought that the charge is sufficient to propel the molecule through the mitochondrial membrane into the interior of the mitochondria.   Once inside a mitochondrion, as in the case of a C-60 fullerene, a MitoQ molecule reduces the charge differential across the mitochondrial membrane.  This again should result in reduction of superoxide production.  If the Q-10 moiety has an antioxidant function on Complex 2, that too enhances the antioxidant impact.<< end quote

[Kalliste]

Has somebody done some kind of followup on this? Googling leads me to a bunch of people who want to sell me this and that. What is a good news resource on this subject?

[niner]

Has somebody done some kind of followup on this? Googling leads me to a bunch of people who want to sell me this and that. What is a good news resource on this subject?

 

This thread, and other threads in this forum.  There is nowhere else on the net that you will find much on c60 other than uninformed speculation or hype.