526 replies to this topic

[smccomas01]

Discussing C60 and cancer has anyone read this? 

 

RESULTS:

The C(60)FAS at low single therapeutic dose of 5 mg/kg inhibited the growth of transplanted malignant tumor (antitumor effect) and metastasis (antimetastatic effect): the maximum therapeutic effect was found to be of 76.5% for the tumor growth inhibition; the increase of animal life span by 22% was found; the metastasis inhibition index was estimated as 48%.

CONCLUSION:

It was found that water-soluble pristine С(60) fullerenes efficiently inhibit the transplanted malignant tumor growth and metastasis.

 

 

Source 

http://www.ncbi.nlm....pubmed/21956470

[McK]

Don't forget one of those glowing studies was recently revised down.  I forget the title but it was the one done in France that is always quoted as evidence of longevity. When it was revised down it showed neither longevity or cancer protection.  

 Maybe Turnbuckle remembers the title of the study, but the revision was recent and the journal that published the original was very upset.

[Turnbuckle]

Don't forget one of those glowing studies was recently revised down.  I forget the title but it was the one done in France that is always quoted as evidence of longevity. When it was revised down it showed neither longevity or cancer protection.  

 Maybe Turnbuckle remembers the title of the study, but the revision was recent and the journal that published the original was very upset.

 

 

Must be in the past few days, because I don't see any evidence of it.

[Hebbeh]

 

Good post Pone; yes we must face the possibility that C60 is neither protective and may actually be a factor in cancer development.  In humans I think the numbers are that one in eight will have cancer over their lifetime, all these mice had it.

I was considering trying C60 but I think I will stick to my TA-65 and Stem Cell 100 by Lifecode for now.

 

 

In mice it is one in four. And yes, that the C60/EVOO actually caused the cancer is certainly a possibility. I was never clear on where this C60 came from. Did AgeVivo make it himself, or did he get it from the researchers, and if the latter, was this from their original batch? Because olive oil does go rancid and I doubt even C60 will protect it forever. And as rancid oil is known to cause cancer in mice, it could be the oil and not the C60 that caused the cancer.

 

 

I don't have time to go back and reference it but I'm positive that AgeVivo stated multiple times that he was in contact with the Baati people and they made several donations to him of C60/OO that was left over from their original rat toxicity study....so yes, it was the original and old left over Baati (and very possibly rancid) oil that AgeVivo definitely used for the duration on his mice...and a good point.

[Turnbuckle]

 

 

Good post Pone; yes we must face the possibility that C60 is neither protective and may actually be a factor in cancer development.  In humans I think the numbers are that one in eight will have cancer over their lifetime, all these mice had it.

I was considering trying C60 but I think I will stick to my TA-65 and Stem Cell 100 by Lifecode for now.

 

 

In mice it is one in four. And yes, that the C60/EVOO actually caused the cancer is certainly a possibility. I was never clear on where this C60 came from. Did AgeVivo make it himself, or did he get it from the researchers, and if the latter, was this from their original batch? Because olive oil does go rancid and I doubt even C60 will protect it forever. And as rancid oil is known to cause cancer in mice, it could be the oil and not the C60 that caused the cancer.

 

 

I don't have time to go back and reference it but I'm positive that AgeVivo stated multiple times that he was in contact with the Baati people and they made several donations to him of C60/OO that was left over from their original rat toxicity study....so yes, it was the original and old left over Baati (and very possibly rancid) oil that AgeVivo definitely used for the duration on his mice...and a good point.

 

 

It's what I suspected as he never gave his procedure for making it. I keep mine in the freezer, where it should age about 16 times slower.

[niner]

 

Good post Pone; yes we must face the possibility that C60 is neither protective and may actually be a factor in cancer development.  In humans I think the numbers are that one in eight will have cancer over their lifetime, all these mice had it.

I was considering trying C60 but I think I will stick to my TA-65 and Stem Cell 100 by Lifecode for now.

 

In mice it is one in four. And yes, that the C60/EVOO actually caused the cancer is certainly a possibility. I was never clear on where this C60 came from. Did AgeVivo make it himself, or did he get it from the researchers, and if the latter, was this from their original batch? Because olive oil does go rancid and I doubt even C60 will protect it forever. And as rancid oil is known to cause cancer in mice, it could be the oil and not the C60 that caused the cancer.

 

I think it's even worse than that- Cancer in mice is awfully common.  I'm sure it varies from breed to breed, and these were Pet Shop Mice, so breed is unknown.  We have strong suspicions that c60oo will suppress metastasis (Porporato et al. 2014), and my recollection is that AgeVivo's mice had single tumors, but were not tumor-ridden, as is sometimes seen.  It's even possible that they didn't die of the tumor they had, but of something else.  These results are essentially anecdotal.   Moussa said, in reference to the Wistar rats they used, that they all get cancer, but that none of the treatment group did.  That's a pretty strong signal, but it's only one genotype of one species.  

 

Very good point on the age of the c60oo that AV used.  I think Moussa's lab ran a sample on HPLC, and said it was ok, but I'm not sure that they could tell if the oil was rancid if they were just looking at a c60 signal. 

 

I suspect that there have been more humans using c60oo than either TA-65 or Stem Cell 100. 

[Turnbuckle]

While the following is about nC60/water and not C60/EVOO, it's interesting that the toxicity is attributed to lipid peroxidation, and the solution is very simple--

 

This study examines the biological effects of water-soluble fullerene aggregates in an effort to evaluate the fundamental

mechanisms that contribute to the cytotoxicity of a classic engineered nanomaterial. For this work we used a water-soluble fullerene

species, nano-C60, a fullerene aggregate that readily forms when pristine C60 is added to water. Nano-C60 was cytotoxic to human

dermal fibroblasts, human liver carcinoma cells (HepG2), and neuronal human astrocytes at doses X50 ppb (LC50 ¼ 2–50 ppb,

depending on cell type) after 48 h exposure. This water-soluble nano-C60 colloidal suspension disrupts normal cellular function

through lipid peroxidation; reactive oxygen species are responsible for the membrane damage. Cellular viability was determined

through live/dead staining and LDH release. DNA concentration and mitochondrial activity were not affected by the nano-C60

inoculations to cells in culture. The integrity of cellular membrane was examined by monitoring the peroxy-radicals on the lipid

bilayer. Subsequently, glutathione production was measured to assess the cell’s reaction to membrane oxidation. The damage to cell

membranes was observed both with chemical assays, and confirmed physically by visualizing membrane permeability with high

molecular weight dyes. With the addition of an antioxidant, L-ascorbic acid, the oxidative damage and resultant toxicity of nano-C60

was completely prevented.

 

http://nanonet.rice....ytotoxicity.pdf

 

 

 

I use C and reduced glutathione, which is the endogenous antioxidant in the mitochondria.

[pone11]

 

While the following is about nC60/water and not C60/EVOO, it's interesting that the toxicity is attributed to lipid peroxidation, and the solution is very simple--

 

This study examines the biological effects of water-soluble fullerene aggregates in an effort to evaluate the fundamental

mechanisms that contribute to the cytotoxicity of a classic engineered nanomaterial. For this work we used a water-soluble fullerene

species, nano-C60, a fullerene aggregate that readily forms when pristine C60 is added to water. Nano-C60 was cytotoxic to human

dermal fibroblasts, human liver carcinoma cells (HepG2), and neuronal human astrocytes at doses X50 ppb (LC50 ¼ 2–50 ppb,

depending on cell type) after 48 h exposure. This water-soluble nano-C60 colloidal suspension disrupts normal cellular function

through lipid peroxidation; reactive oxygen species are responsible for the membrane damage. Cellular viability was determined

through live/dead staining and LDH release. DNA concentration and mitochondrial activity were not affected by the nano-C60

inoculations to cells in culture. The integrity of cellular membrane was examined by monitoring the peroxy-radicals on the lipid

bilayer. Subsequently, glutathione production was measured to assess the cell’s reaction to membrane oxidation. The damage to cell

membranes was observed both with chemical assays, and confirmed physically by visualizing membrane permeability with high

molecular weight dyes. With the addition of an antioxidant, L-ascorbic acid, the oxidative damage and resultant toxicity of nano-C60

was completely prevented.

 

http://nanonet.rice....ytotoxicity.pdf

 

 

 

I use C and reduced glutathione, which is the endogenous antioxidant in the mitochondria.

 

 

What is really surprising about this result is that:

 

1) They added the Vitamin C 40 hours into a 48 hour test, yet still avoided the peroxidation.  How did that work?

 

2) Vitamin C has a half life of something like 30 minutes?   So interesting that they were able to dose it a single time and it still worked.

[Turnbuckle]

 

 

While the following is about nC60/water and not C60/EVOO, it's interesting that the toxicity is attributed to lipid peroxidation, and the solution is very simple--

 

This study examines the biological effects of water-soluble fullerene aggregates in an effort to evaluate the fundamental

mechanisms that contribute to the cytotoxicity of a classic engineered nanomaterial. For this work we used a water-soluble fullerene

species, nano-C60, a fullerene aggregate that readily forms when pristine C60 is added to water. Nano-C60 was cytotoxic to human

dermal fibroblasts, human liver carcinoma cells (HepG2), and neuronal human astrocytes at doses X50 ppb (LC50 ¼ 2–50 ppb,

depending on cell type) after 48 h exposure. This water-soluble nano-C60 colloidal suspension disrupts normal cellular function

through lipid peroxidation; reactive oxygen species are responsible for the membrane damage. Cellular viability was determined

through live/dead staining and LDH release. DNA concentration and mitochondrial activity were not affected by the nano-C60

inoculations to cells in culture. The integrity of cellular membrane was examined by monitoring the peroxy-radicals on the lipid

bilayer. Subsequently, glutathione production was measured to assess the cell’s reaction to membrane oxidation. The damage to cell

membranes was observed both with chemical assays, and confirmed physically by visualizing membrane permeability with high

molecular weight dyes. With the addition of an antioxidant, L-ascorbic acid, the oxidative damage and resultant toxicity of nano-C60

was completely prevented.

 

http://nanonet.rice....ytotoxicity.pdf

 

 

 

I use C and reduced glutathione, which is the endogenous antioxidant in the mitochondria.

 

 

What is really surprising about this result is that:

 

1) They added the Vitamin C 40 hours into a 48 hour test, yet still avoided the peroxidation.  How did that work?

 

2) Vitamin C has a half life of something like 30 minutes?   So interesting that they were able to dose it a single time and it still worked.

 

 

They say there is likely an induction period due to the initial presence of antioxidants.

In most of our experiments, the cell

culture media itself contains antioxidants at relatively

low concentrations. It may be that peroxidative

processes begin at time zero, and that it takes more

than 30 h to deplete the antioxidants in the cell culture

media. In this interpretation, protection is extended

beyond 48 h when L-ascorbic acid is added. Additional

ascorbic acid is needed to protect the astrocytes, which

are lipid rich cells. NHA were grown in media containing

1% ascorbic acid which protects these cells from

oxidative stress generated during normal incubation.

This initial concentration of L-ascorbic acid is substantially

lower than the L-ascorbic acid added during the

48 h of nano-C60 exposure.

 

 

 

[sensei]

The clearance half life of ascorbic acid is 2 +/- .5 hours (not 30 minutes)

 

http://link.springer...0280-013-2179-9

[pone11]

The clearance half life of ascorbic acid is 2 +/- .5 hours (not 30 minutes)

 

http://link.springer...0280-013-2179-9

 

And this study says that it is 30 minutes:

 

http://www.ncbi.nlm....pubmed/18450228

 

But in fairness to your point in the abstract they say that is controversial.

 

If you end up trying to reconcile the difference please summarize why for us.   Amazing that such a basic and easily measured fact of science cannot be agreed on by qualified scientists....

[Raphy]

Don't forget one of those glowing studies was recently revised down.  I forget the title but it was the one done in France that is always quoted as evidence of longevity. When it was revised down it showed neither longevity or cancer protection.  

 Maybe Turnbuckle remembers the title of the study, but the revision was recent and the journal that published the original was very upset.

 

Any source to backup this?

[hav]

 

The clearance half life of ascorbic acid is 2 +/- .5 hours (not 30 minutes)

 

http://link.springer...0280-013-2179-9

 

And this study says that it is 30 minutes:

 

http://www.ncbi.nlm....pubmed/18450228

 

But in fairness to your point in the abstract they say that is controversial.

 

If you end up trying to reconcile the difference please summarize why for us.   Amazing that such a basic and easily measured fact of science cannot be agreed on by qualified scientists....

 

 

 

That abstract doesn't sound like authority for the proposition, it just mentioned it in passing without a cite in a manner that sounds kind of dismissive to me:

 

There is a strong advocacy movement for large doses of vitamin C. Some authors argue that the biological half-life for vitamin C at high plasma levels is about 30 minutes, but these reports are the subject of some controversy. NIH researchers established the current RDA based upon tests conducted 12 hours (24 half lives) after consumption.

 

Keep in mind that the 30-minute advocates are arguing over the value of taking massive amounts of Vitamin C and are probably measuring peak levels after those high doses and citing a number for a 50% drop in those peaks.  Whereas the 2-1/2 hour number is from this study (actually, 2.0 h ± 0.6 h) trying to maintain stead-state levels in the bloodstream to evaluate its value for treating advanced cancer.  So the cancer study 50% drop starts at a more reasonable level where the kidneys wouldn't be working overtime to remove.

 

Howard

[pone11]

 

 

The clearance half life of ascorbic acid is 2 +/- .5 hours (not 30 minutes)

 

http://link.springer...0280-013-2179-9

 

And this study says that it is 30 minutes:

 

http://www.ncbi.nlm....pubmed/18450228

 

But in fairness to your point in the abstract they say that is controversial.

 

If you end up trying to reconcile the difference please summarize why for us.   Amazing that such a basic and easily measured fact of science cannot be agreed on by qualified scientists....

 

 

 

That abstract doesn't sound like authority for the proposition, it just mentioned it in passing without a cite in a manner that sounds kind of dismissive to me:

 

There is a strong advocacy movement for large doses of vitamin C. Some authors argue that the biological half-life for vitamin C at high plasma levels is about 30 minutes, but these reports are the subject of some controversy. NIH researchers established the current RDA based upon tests conducted 12 hours (24 half lives) after consumption.

 

Keep in mind that the 30-minute advocates are arguing over the value of taking massive amounts of Vitamin C and are probably measuring peak levels after those high doses and citing a number for a 50% drop in those peaks.  Whereas the 2-1/2 hour number is from this study (actually, 2.0 h ± 0.6 h) trying to maintain stead-state levels in the bloodstream to evaluate its value for treating advanced cancer.  So the cancer study 50% drop starts at a more reasonable level where the kidneys wouldn't be working overtime to remove.

 

 

Maybe half life of a massive dose is different than half life of a small dose.   I guess there are many variables.      My only point is that if you look in the literature you will find the 30 minute figure, and I leave it to others to figure out why different studies report different half lives.

 

If it is the case that a massive dose has a half life of two hours, and a small dose has a half life of 30 minutes, then let's use the 30 minute figure, because that will reflect the kind of doses that we are taking orally.

[niner]

 

 

While the following is about nC60/water and not C60/EVOO, it's interesting that the toxicity is attributed to lipid peroxidation, and the solution is very simple--

 

This study examines the biological effects of water-soluble fullerene aggregates in an effort to evaluate the fundamental

mechanisms that contribute to the cytotoxicity of a classic engineered nanomaterial. For this work we used a water-soluble fullerene

species, nano-C60, a fullerene aggregate that readily forms when pristine C60 is added to water. Nano-C60 was cytotoxic to human

dermal fibroblasts, human liver carcinoma cells (HepG2), and neuronal human astrocytes at doses X50 ppb (LC50 ¼ 2–50 ppb,

depending on cell type) after 48 h exposure. This water-soluble nano-C60 colloidal suspension disrupts normal cellular function

through lipid peroxidation; reactive oxygen species are responsible for the membrane damage. Cellular viability was determined

through live/dead staining and LDH release. DNA concentration and mitochondrial activity were not affected by the nano-C60

inoculations to cells in culture. The integrity of cellular membrane was examined by monitoring the peroxy-radicals on the lipid

bilayer. Subsequently, glutathione production was measured to assess the cell’s reaction to membrane oxidation. The damage to cell

membranes was observed both with chemical assays, and confirmed physically by visualizing membrane permeability with high

molecular weight dyes. With the addition of an antioxidant, L-ascorbic acid, the oxidative damage and resultant toxicity of nano-C60

was completely prevented.

 

http://nanonet.rice....ytotoxicity.pdf

 

I use C and reduced glutathione, which is the endogenous antioxidant in the mitochondria.

 

What is really surprising about this result is that:

 

1) They added the Vitamin C 40 hours into a 48 hour test, yet still avoided the peroxidation.  How did that work?

 

2) Vitamin C has a half life of something like 30 minutes?   So interesting that they were able to dose it a single time and it still worked.

 

Since it's an in vitro experiment, the in vivo half life doesn't matter.  There are a number of processes that remove xenobiotics from the body, but almost none of them are present in a Petri dish.

[hotbit]

I have spent the whole evening reading this thread on interesting home-experiment. Sad thing they always end with death

Great job and thank you, AgeVivo.

[AnahimSkywalker]

Those lazy bed-rats!