331 replies to this topic

[anagram]

what I meant by xenobiotic was specifically substances which the body does not use directly in metabolism. Astaxanthin may be broken down by enzymes in the liver, but for the rest of the body which does not contain those enzymes, Astaxanthin accumulates in cell membranes. that is what xenobiotics are, things which cannot be directly broken down by mitochondria, like sugars, amino acids, vitamins.

My point was sort of that If you look at riboflavin's chemical structure(a key vitamin), it looks like it could be a fairly good antioxidant, and for that matter, a lot of things including amino acids look like they could be antioxidants, however the metabolism and usage of compounds by mitochondria determines they're in vivo antioxidant behaviors. this is why 100 g of l-lysine supplementation will not protect people against Parkinson's but 10mg of selegiline will.

c60 looks very strange to our cells, and I doubt that mitochondria can even degrade c60. so because of this, I assume that mitochondria try to stop antioxidants from exerting effects inside cells, leaving only the weird looking compounds(xenobiotics) that our cells don't properly know how to degrade/modify, to stay in our cells, and act as antioxidants.

Edited by anagram, 23 January 2013 - 09:06 PM.

[niner]

what I meant by xenobiotic was substances which the body does not use directly in metabolism. theoretically, all mitochondria need are the constitutes of the krebs cycle, vitamines, and amino acids to sustain themselves, though we add a variety of other nutrients to our diet because just giving what mitochondria what they need is not enough.
things like asprin, a xenobiotic, however don't serve any direct purpose to our body, and are treated differently than metabolically "useful" compounds like sugar. If you look at riboflavin's chemical structure,a required nutrient, it looks like it could be a fairly good antioxidant, and for that matter, a lot of things like amino acids look like they could be antioxidants, however the metabolism and usage of compounds by mitochondria determines they're in vivo behaviors, whether they act like antioxidants or not.
c60 looks very strange to our cells which are accustomed to glucose and amino acids, I doubt that mitochondria can even degrade c60, so based on this I assume that mitochondria try to stop antioxidants from entering cells, only the weird looking compounds(xenobiotics) that our cells don't properly know how to degrade can get through un noticed, and act as antioxidants.

Mitochondria don't degrade anything. That's not their job. They can't "stop" anything from entering cells; they are inside the cell. They don't act like little traffic cops. Metabolism doesn't have anything to do with whether or not something is an antioxidant. Metabolism is the main determinant of how long a compound will stay in the body. If a compound is rapidly metabolized and excreted, then it isn't going to be a very good drug, antioxidant or otherwise, but while it's in the body it will act in the way its chemistry dictates.

[anagram]

what I meant by xenobiotic was substances which the body does not use directly in metabolism. theoretically, all mitochondria need are the constitutes of the krebs cycle, vitamines, and amino acids to sustain themselves, though we add a variety of other nutrients to our diet because just giving what mitochondria what they need is not enough.
things like asprin, a xenobiotic, however don't serve any direct purpose to our body, and are treated differently than metabolically "useful" compounds like sugar. If you look at riboflavin's chemical structure,a required nutrient, it looks like it could be a fairly good antioxidant, and for that matter, a lot of things like amino acids look like they could be antioxidants, however the metabolism and usage of compounds by mitochondria determines they're in vivo behaviors, whether they act like antioxidants or not.
c60 looks very strange to our cells which are accustomed to glucose and amino acids, I doubt that mitochondria can even degrade c60, so based on this I assume that mitochondria try to stop antioxidants from entering cells, only the weird looking compounds(xenobiotics) that our cells don't properly know how to degrade can get through un noticed, and act as antioxidants.

Mitochondria don't degrade anything. That's not their job. They can't "stop" anything from entering cells; they are inside the cell. They don't act like little traffic cops. Metabolism doesn't have anything to do with whether or not something is an antioxidant. Metabolism is the main determinant of how long a compound will stay in the body. If a compound is rapidly metabolized and excreted, then it isn't going to be a very good drug, antioxidant or otherwise, but while it's in the body it will act in the way its chemistry dictates.

sorry, I put it in a bad/confusing way.
what I was trying to say was that I think that a lot of common nutrients like carbohydrates are not "antioxidant" in nature, simply because they don't stay in mitochondria for long enough to do anything very positive.
I think that the long lasting effect of c60 on health is partially because if its unmetabolizable nature.
I must disagree with you niner because the addition of hyroxyl groups to certain compounds does influence the behavior of a lot of compounds. An example of something that is formed by mitochondrial metabolism is the asprin metabolite 2,3-Dihydroxybenzoic acid, which has iron chelating and antioxidant effects in vivo.

Edited by anagram, 23 January 2013 - 09:03 PM.

[niner]

what I meant by xenobiotic was substances which the body does not use directly in metabolism. theoretically, all mitochondria need are the constitutes of the krebs cycle, vitamines, and amino acids to sustain themselves, though we add a variety of other nutrients to our diet because just giving what mitochondria what they need is not enough.
things like asprin, a xenobiotic, however don't serve any direct purpose to our body, and are treated differently than metabolically "useful" compounds like sugar. If you look at riboflavin's chemical structure,a required nutrient, it looks like it could be a fairly good antioxidant, and for that matter, a lot of things like amino acids look like they could be antioxidants, however the metabolism and usage of compounds by mitochondria determines they're in vivo behaviors, whether they act like antioxidants or not.
c60 looks very strange to our cells which are accustomed to glucose and amino acids, I doubt that mitochondria can even degrade c60, so based on this I assume that mitochondria try to stop antioxidants from entering cells, only the weird looking compounds(xenobiotics) that our cells don't properly know how to degrade can get through un noticed, and act as antioxidants.

Mitochondria don't degrade anything. That's not their job. They can't "stop" anything from entering cells; they are inside the cell. They don't act like little traffic cops. Metabolism doesn't have anything to do with whether or not something is an antioxidant. Metabolism is the main determinant of how long a compound will stay in the body. If a compound is rapidly metabolized and excreted, then it isn't going to be a very good drug, antioxidant or otherwise, but while it's in the body it will act in the way its chemistry dictates.

sorry, I put it in a bad/confusing way.
what I was trying to say was that I think that a lot of common nutrients like carbohydrates are not "antioxidant" in nature, simply because they don't stay in mitochondria for long enough to do anything very positive.
I think that the long lasting effect of c60 on health is partially because if its unmetabolizable nature.
I must disagree with you niner because the addition of hyroxyl groups to certain compounds does influence the behavior of a lot of compounds. An example of something that is formed by mitochondrial metabolism is the asprin metabolite 2,3-Dihydroxybenzoic acid, which has iron chelating and antioxidant effects in vivo.

Once a compound is metabolized, its chemistry is different. Its ability to act as an antioxidant may change then, but not before then. Compounds don't need to be in mitochondria to be antioxidants. Most antioxidants, in fact, aren't found there. The very few compounds that preferentially localize to mitochondria, like c60 or SkQ1 are far more effective for that reason.

[Fred_CALICO]

Thank you for your answers.
I return to the notion of xenobiotic.
While astaxanthin is not a nutrient common to all peoples, in usual doses, it does not appear toxic.
Consumption of shrimp has exploded 20 years (Production multiplied by 9). Worldwide, there are approximately 4 million tons of shrimp are consumed either 300% per year.
http://www.planetosc...s-le-monde.html
If the definition is: A xenobiotic is a substance that is foreign to a living organism, so it must be admitted that much of our food is xenobiotic. Thus the term provides no information ... is noise!
Some notes:
1/Des lab experiments show that bacteria and mushrooms are able to rewrite their DNA to adapt to a substrate previously unknown to them.
2/Chez man state Americans rotting cheese with maggots is toxic during the early weeks of ingestion. French for Corsica is a good source of protein and vitamins from his childhood.
3/Chardon is a generic term for several species of thorny plants mainly belonging to the family Asteraceae (Compositae), especially the genera Carduus (thistle proper). A priori only consumes goats, not humans.
I made an anecdotal experience: Place a sheet with thorn thistle on the tongue. Let saliva for a few minutes (2 or 3). The spines are soft. Repeat the experiment several days now. The time of action of saliva for spines degradation becomes short.

What I'm trying to illustrate is that the notion of xenobiotic is poor.
The concept of toxicity must be relativized.
Some nutrients are toxic, others simply unknown by the body at time t.
And body (DNA) does not govern the same way according to their needs and environment.

The memory included in the DNA is a resource plastic.

[Turnbuckle]

But at any rate, it looks to me that C60 is a mimic for catalase, superoxide dismutase and glutathione.

That is an interesting suggestion, but after reading a paper on the toxic effects of C60 on embryonic zebrafish, it might be just the opposite. The researchers used various levels of C60 in the presence of chemicals that suppress glutathione, and found that C60 became much more toxic to zebrafish embryos.

Fullerene C60 exposure elicits an oxidative stress response in embryonic zebrafish

Chemical depletion of GSH [glutathione]

BSO and DEM, known inhibitors of glutathione synthesis, were used to determine if C60 exerts a toxic response through depletion of glutathione. DEM was found to have a maximum tolerable concentration (MTC) of 50 nM and BSO had a MTC of 5 μM. These concentrations of DEM and BSO were used for each co-incubation with graded concentrations of C60 (50–300 ppb) and 1% DMSO controls. Both DEM and BSO increased the embryo’s sensitivity to C60, with increased mortality within the first 24 hours of exposure (figure 4). Embryos were more sensitive to DEM than BSO. There was not a significant increase in mortality between controls for either DEM or BSO and control embryos.

http://www.ncbi.nlm....les/PMC2421009/

See the figure below.

They suggested that C60 is a pro-oxidant (and that whatever it is doing also occurs in the absence of light). Thus it occurred to me that a supplement to stimulate glutathione would be useful. I gave that a quick try this morning, and found that 2 mg of C60-EVOO + 1800 mg NAC worked very well together in the gym. I was easily lifting much more weight--one third more.

I will try this over the next few days. If it continues to work, glutathione depletion may be an alternative explanation of the fading effects that many see with C60.

Attached Files

•  C60.jpg   40.39KB   18 downloads

[ClarkSims]

But at any rate, it looks to me that C60 is a mimic for catalase, superoxide dismutase and glutathione.

That is an interesting suggestion, but after reading a paper on the toxic effects of C60 on embryonic zebrafish, it might be just the opposite. The researchers used various levels of C60 in the presence of chemicals that suppress glutathione, and found that C60 became much more toxic to zebrafish embryos.

The zebra fish study was done with pristine c60, that was sonicated and suspended in dmso. This is a totally different chemical than C60 which is adducted to a fatty acid, and incorporated into a mitocondria. IIRC, every study with pristine c60 and suspended c60, has showed that it is an irritant and an oxidizer. I think it is acting as an asbestos mimic, and rupturing cell membranes.

C60 was obtained from Sigma Aldrich, WI (99+%) and dissolved in 100% dimethyl sulfoxide (DMSO). The stock solution of 50 ppm C60 was sonicated for 1.5 hours to ensure a uniform dispersion and size distribution. C60(OH)24 (MER Corp, Arizona) was dissolved in DMSO and sonicated for 5 minutes to ensure uniform distribution. The size range of C60 and C60(OH)24 agglomerates following sonication were measured using photon correlation

Note that C60 does not dissolve in dmso. It was all solid nano particles. The author chose his words poorly.

[ClarkSims]

They suggested that C60 is a pro-oxidant (and that whatever it is doing also occurs in the absence of light). Thus it occurred to me that a supplement to stimulate glutathione would be useful. I gave that a quick try this morning, and found that 2 mg of C60-EVOO + 1800 mg NAC worked very well together in the gym. I was easily lifting much more weight--one third more.

I will try this over the next few days. If it continues to work, glutathione depletion may be an alternative explanation of the fading effects that many see with C60.

I have a hard time believing that 2 mg of C60 OO, could increase performance that much.
That is a small fraction of the doses feed to the mice int the Biati study. You can choose pretty much any allometric scaling factor, and 2 mg will look small. I am taking about 50 mg / day, and I feel pretty normal. I am pretty healthy, but by no means a superman.

Your comment about NAC got me curious though.
I found this:

http://mangans.blogs...erformance.html

Here is another study on a different cystiene donor.

http://jap.physiolog.../87/4/1381.full

I need to read both studies in detail, before I can form an opinion.

[Krell]

They suggested that C60 is a pro-oxidant (and that whatever it is doing also occurs in the absence of light). Thus it occurred to me that a supplement to stimulate glutathione would be useful. I gave that a quick try this morning, and found that 2 mg of C60-EVOO + 1800 mg NAC worked very well together in the gym. I was easily lifting much more weight--one third more.

I will try this over the next few days. If it continues to work, glutathione depletion may be an alternative explanation of the fading effects that many see with C60.

This study suggests that NAC alone can produce a 25% increase in endurance?

http://ajrccm.atsjou...169/9/1022.full

[Turnbuckle]

I have a hard time believing that 2 mg of C60 OO, could increase performance that much.

This was a step change similar to the first time I took it a year ago. I started with 2 mg and bam.

Your comment about NAC got me curious though.
I found this:

http://mangans.blogs...erformance.html

Good find. The comments to it seem to indicate NAC works. The last one says--

NAC works. Been using it for 10 years with great success as a competitive cyclist.

Edited by Turnbuckle, 15 March 2013 - 12:29 AM.

[Turnbuckle]

They suggested that C60 is a pro-oxidant (and that whatever it is doing also occurs in the absence of light). Thus it occurred to me that a supplement to stimulate glutathione would be useful. I gave that a quick try this morning, and found that 2 mg of C60-EVOO + 1800 mg NAC worked very well together in the gym. I was easily lifting much more weight--one third more.

I will try this over the next few days. If it continues to work, glutathione depletion may be an alternative explanation of the fading effects that many see with C60.

This study suggests that NAC alone can produce a 25% increase in endurance?

http://ajrccm.atsjou...169/9/1022.full

Looks like I picked the right dose!

The supplementation consisted of 1,800 mg per day of NAC...

[Turnbuckle]

Note that C60 does not dissolve in dmso. It was all solid nano particles. The author chose his words poorly.

This came up before in the scientific discussion thread--

This says that c60 and dmso have a strong reaction and form c60-DMSO adduct.http://www.publish.c...d=SA0402264.pdf

[mikey]

Well, that third leg does make dosing a difficult balancing act. The rats didn't have to worry so much but it seems like it might be possible to even shorten a human lifespan with overdosed regimen. Or make things worse toward the end. Maybe the C60 studies currently under way will consider taking some measurements. Or the next round of experiments if they need a before and after. Would be good information.

Hmm, cell differentiation kind of seems like the first prospect with real negative connotations for C60oo.

I'm still taking 7 mg every day and the wrinkles on my face are still about 1/4 as deep as before I started C60 in early August, so I doubt that continuous dosing is pushing me towards a shorter lifespan.

No doubt my skin and hair look considerably younger.

As above, so below.

They suggested that C60 is a pro-oxidant (and that whatever it is doing also occurs in the absence of light). Thus it occurred to me that a supplement to stimulate glutathione would be useful. I gave that a quick try this morning, and found that 2 mg of C60-EVOO + 1800 mg NAC worked very well together in the gym. I was easily lifting much more weight--one third more.

I will try this over the next few days. If it continues to work, glutathione depletion may be an alternative explanation of the fading effects that many see with C60.

This study suggests that NAC alone can produce a 25% increase in endurance?

http://ajrccm.atsjou...169/9/1022.full

Looks like I picked the right dose!

The supplementation consisted of 1,800 mg per day of NAC...

I prefer 1,800 mg two or three times a day.

[Turnbuckle]

I prefer 1,800 mg two or three times a day.

So you've been taking this level of NAC concurrently with C60?

[Krell]

I prefer 1,800 mg two or three times a day.

Anyone have any data on the half life of NAC in the body? How soon should I take it before exercise?

I am getting ready for my annual 5k road race, and I am considering adding NAC to my arsenal
along with beetroot juice and C60.

[platypus]

They suggested that C60 is a pro-oxidant (and that whatever it is doing also occurs in the absence of light). Thus it occurred to me that a supplement to stimulate glutathione would be useful. I gave that a quick try this morning, and found that 2 mg of C60-EVOO + 1800 mg NAC worked very well together in the gym. I was easily lifting much more weight--one third more.

Are you an experienced weightlifter? A _third_ more would be off-the-scale exceptional! Lifts going from 60kg -> 80kg for example?

[Turnbuckle]

Anyone have any data on the half life of NAC in the body? How soon should I take it before exercise?

About 6 hours--

Oral supplementation with N-AcetylCysteine (NAC) provides an alternate means of boosting intracellular glutathione via elevated intracellular cysteine. NAC is rapidly absorbed after oral administration and reaches a maximum plasma level in 2-3 hours, with a half-life of about 6 hours.

http://www.benbest.c...trceut/NAC.html

Edited by Turnbuckle, 15 March 2013 - 11:12 AM.

[platypus]

I'm still taking 7 mg every day and the wrinkles on my face are still about 1/4 as deep as before I started C60 in early August, so I doubt that continuous dosing is pushing me towards a shorter lifespan.

Wait, are you saying that C60 took 3/4 of your wrinkle-depth away?

[Turnbuckle]

They suggested that C60 is a pro-oxidant (and that whatever it is doing also occurs in the absence of light). Thus it occurred to me that a supplement to stimulate glutathione would be useful. I gave that a quick try this morning, and found that 2 mg of C60-EVOO + 1800 mg NAC worked very well together in the gym. I was easily lifting much more weight--one third more.

Are you an experienced weightlifter? A _third_ more would be off-the-scale exceptional! Lifts going from 60kg -> 80kg for example?

I'm not a serious weightlifter, however I'd become a fanatic for a while some ten years ago and maxed out the weights on half the Nautilus machines (no free weights). After that I was knocked flat, first by a case of shingles, then by statins. The increase yesterday was dramatic on most of the machines--a one third gain on average--after taking NAC + C60 2 hours before. I was taking NAC all along, but only 600 mg three times a week, and not coordinating it with the gym.

[niner]

I am getting ready for my annual 5k road race, and I am considering adding NAC to my arsenal
along with beetroot juice and C60.

Be sure to post your results, positive or negative. If NAC+c60 turns out to be the new secret weapon, well, that will be something. I would expect to see a lengthening of time-to-fatigue, although I can't see any reason for a dramatic strength increase. If in your 5K, you are near the fatigue limit at the end, then anything that pushes that out should increase your total work output and therefore improve your time. If that's not the failure mode you're experiencing, then maybe not so much help. It might be interesting for c60 non-responders to try combining it with NAC.

[Turnbuckle]

Normally I work out every other day, but I found the C60/NAC combination so intriguing I couldn't wait. This morning I took it again (2 mg C60 & 1800 mg NAC, waiting only an hour this time), and again I could lift more weight. The weight I was lifting several days ago now felt like nothing, and I could lift even more than yesterday during my first trial. And while yesterday I felt nothing out of the ordinary, today I felt a bit too much energy. A bit speedy, snapping the weights up and down. So I will back off a bit and only use this regimen every other day.

[GVA]

But at any rate, it looks to me that C60 is a mimic for catalase, superoxide dismutase and glutathione.

That is an interesting suggestion, but after reading a paper on the toxic effects of C60 on embryonic zebrafish, it might be just the opposite. The researchers used various levels of C60 in the presence of chemicals that suppress glutathione, and found that C60 became much more toxic to zebrafish embryos.

The zebra fish study was done with pristine c60, that was sonicated and suspended in dmso. This is a totally different chemical than C60 which is adducted to a fatty acid, and incorporated into a mitocondria. IIRC, every study with pristine c60 and suspended c60, has showed that it is an irritant and an oxidizer. I think it is acting as an asbestos mimic, and rupturing cell membranes.

C60 was obtained from Sigma Aldrich, WI (99+%) and dissolved in 100% dimethyl sulfoxide (DMSO). The stock solution of 50 ppm C60 was sonicated for 1.5 hours to ensure a uniform dispersion and size distribution. C60(OH)24 (MER Corp, Arizona) was dissolved in DMSO and sonicated for 5 minutes to ensure uniform distribution. The size range of C60 and C60(OH)24 agglomerates following sonication were measured using photon correlation

Note that C60 does not dissolve in dmso. It was all solid nano particles. The author chose his words poorly.

These scientific 'clever mens' have not taken into consideration and have not tried to check up that at ultrasonic treatment of a "C60-DMSO-H2O" mix the products of DMSO oxidation can be formed, for example, DMS-dioxide, methanesulphonic acid and others compounds that can be more or less toxic for Zebra fish. Oh yes, such are realities of 'a modern' science!

[Turnbuckle]

With regard to C60 in DMSO, it's not at all obvious that it can't be dissolved (or reacted) by the use of sonic treatment. After all, C60 can be "dissolved" in water with sonic treatment, and that seems even more unlikely. Furthermore, even though the effects of C60 in EVOO and DMSO may not be the same, it's easy to imagine that, if you were to boost mitochondrial energy production, that would also boost ROS production and pressure would be put on the glutathione system.

[GVA]

With regard to C60 in DMSO, it's not at all obvious that it can't be dissolved (or reacted) by the use of sonic treatment. After all, C60 can be "dissolved" in water with sonic treatment, and that seems even more unlikely. Furthermore, even though the effects of C60 in EVOO and DMSO may not be the same, it's easy to imagine that, if you were to boost mitochondrial energy production, that would also boost ROS production and pressure would be put on the glutathione system.

Ok! Despite your questions, allow to switch you to the modern approach to antioxidants but which, for the clear reasons, does not consider properties C60HyFn. For this PL see Watson J. 2013 Oxidants, antioxidants and the current incurability of metastatic cancers. Open Biol 3: 120144. (http://dx.doi.org/10.1098/rsob.120144)
~

[anagram]

It is more reasonable C60hyn simply extracts H from glutathione, the C60 then has a H at its disposal to preform a "antioxidant" effect. There are documents regarding "permanent oxidants" which are compounds that will continuously drain the reduced NADPH or Glutathione systems of reducing electrons. C60 has a long lasting, DNA scissoring, and pronounced effects on Mouse biology, If C60 lodges itself within the body it could be possible that C60 exerts a oxidizing effect on the surrounding environment. It might seem counter intelligent to say that increased free radicals are a bad thing, however intuitive and well based studies show that ROS's are important to cellular morphology and growth, without intermittent ROS's in a cellular environment cells would be unable to thrive. C60 does not cause ROS damage, but C60 exerts a rather complex pro oxidant effect which simply means it extracts reducing Hydrogen s while simultaneously reducing OO- radical. This is relevant to the concept of Cellular membrane integrity which is a cells membrane's physical strength.

http://www.ncbi.nlm....57/figure/fig4/
http://www.ncbi.nlm....57/figure/fig1/

Visibly on cell culture ©, the cells have a more defined shape and are less strung out than the Cell which have been treated with other C60 derivatives. A specific example of this phenomenon in the real world is as you try and tear a sheet of plastic in half, it is difficult when it is not under stress lateral to the sheet itself. If you can imagine the membrane of a cell as a plastic sheet, the less it is being pulled then the better it will preform under difficult strain. The compound© has the longest amine hydrocarbon tail of any of the other compounds which is of seemingly significant to the absorption of the C60 into the cells. Cells are unlikely to metabolize C60 if it has such long groups attached to it which is lent evidence by the fact that certain short chain C60 derivatives induce senescence perhaps paradoxically, only . This is a incomplete theory however the evidence is that polycarboxylic derivative of fullerene C60 is cytotoxic while the amino adduct derivatives of C60 are "safer", If there is any person whom can give proper evidence for a theory as to why this exists please elaborate on my crude attempt at a pseudo analysis.

Edited by anagram, 15 March 2013 - 09:16 PM.

[mikey]

I'm still taking 7 mg every day and the wrinkles on my face are still about 1/4 as deep as before I started C60 in early August, so I doubt that continuous dosing is pushing me towards a shorter lifespan.

Wait, are you saying that C60 took 3/4 of your wrinkle-depth away?

No question about it. I hadn't seen my body worker, who did Michael Jackson and his entire dance team for the making of Thriller, since before I started C60.

When you first enter his studio, you strip down to your shorts and he looks you over for posture, etc...
The first thing out of his mouth was, "You look younger. What are you doing?"

I said, "Younger, how?"

He said, "Less wrinkles."

Others have made similar remarks about how I am "glowing" or guessing me at 42 years old, where I'm 59.

As well, after Turnbuckle noted that two deep scars had faded I saw that the two deep scars I had on my face are almost invisible.

C60 appears to help collagen health tremendously. Probably because of its antioxidant effect. If skin is protected from free radical damage then perhaps its growth factors can reverse some damage to it.

I will have photos taken shortly to compare to the photos I had taken in 2011.

Then we will see.

[Turnbuckle]

Third try with C60 + NAC and the results in the gym were much the same, except no over-energized feeling this time. If this continues for a week or two without fading, I will be pleased.

Edited by Turnbuckle, 17 March 2013 - 11:28 PM.

[ClarkSims]

Well I just ran about 50 flights of stairs, crawled in bed and went to sleep. By far, not my hardest run, but my hardest run in about 2 years. I am glad everyone else is getting such good results. I don't have anything dramatic to say, but I feel good.

[ClarkSims]

With regard to C60 in DMSO, it's not at all obvious that it can't be dissolved (or reacted) by the use of sonic treatment. After all, C60 can be "dissolved" in water with sonic treatment, and that seems even more unlikely. Furthermore, even though the effects of C60 in EVOO and DMSO may not be the same, it's easy to imagine that, if you were to boost mitochondrial energy production, that would also boost ROS production and pressure would be put on the glutathione system.

In the zebra fish study, they were dealing with a suspension. Quoting from the article, "The stock solution of 50 ppm C60 was sonicated for 1.5 hours to ensure a uniform dispersion and size distribution. C60(OH)24 (MER Corp, Arizona) was dissolved in DMSO and sonicated for 5 minutes to ensure uniform distribution. The size range of C60 and C60(OH)24 agglomerates following sonication were measured using photon correlation "

I they are talking about size distributions, and sizes of agglomerates, that has to be a suspension, not a solution. right? Am I missing something?

[Turnbuckle]

With regard to C60 in DMSO, it's not at all obvious that it can't be dissolved (or reacted) by the use of sonic treatment. After all, C60 can be "dissolved" in water with sonic treatment, and that seems even more unlikely. Furthermore, even though the effects of C60 in EVOO and DMSO may not be the same, it's easy to imagine that, if you were to boost mitochondrial energy production, that would also boost ROS production and pressure would be put on the glutathione system.

In the zebra fish study, they were dealing with a suspension. Quoting from the article, "The stock solution of 50 ppm C60 was sonicated for 1.5 hours to ensure a uniform dispersion and size distribution. C60(OH)24 (MER Corp, Arizona) was dissolved in DMSO and sonicated for 5 minutes to ensure uniform distribution. The size range of C60 and C60(OH)24 agglomerates following sonication were measured using photon correlation "

I they are talking about size distributions, and sizes of agglomerates, that has to be a suspension, not a solution. right? Am I missing something?

C60(OH)24 is soluble in water and other polar solvents like DMSO. In this experiment, the researchers found that C60 (probably a suspension of nC60) and C60(OH)24 had no apparent antioxidant effect. Also, in the previous paper (PMC2186061), nC60 was found to be significantly more toxic than C60(OH)24, which is one reason people here were initially worried about it and took precautions such as filtering the EVOO solution. (I still do.)

Edited by Turnbuckle, 18 March 2013 - 11:14 AM.