Fullerene C60

mmats

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C60

The prolongation of the lifespan of rats by repeated oral administration of [60]
fullerene



a b s t r a c t
Countless studies showed that [60]fullerene (C60) and derivatives could have many potential biomedical
applications. However, while several independent research groups showed that C60 has no acute or subacute
toxicity in various experimental models, more than 25 years after its discovery the in vivo fate and
the chronic effects of this fullerene remain unknown. If the potential of C60 and derivatives in the
biomedical field have to be fulfilled these issues must be addressed. Here we show that oral administration
of C60 dissolved in olive oil (0.8 mg/ml) at reiterated doses (1.7 mg/kg of body weight) to rats not
only does not entail chronic toxicity but it almost doubles their lifespan. The effects of C60-olive oil
solutions in an experimental model of CCl4 intoxication in rat strongly suggest that the effect on lifespan
is mainly due to the attenuation of age-associated increases in oxidative stress. Pharmacokinetic studies
show that dissolved C60 is absorbed by the gastro-intestinal tract and eliminated in a few tens of hours.
These results of importance in the fields of medicine and toxicology should open the way for the many
possible -and waited for- biomedical applications of C60 including cancer therapy, neurodegenerative
disorders, and ageing.
Full text here - http://extremelongevity.net/wp-content/uploads/C60-Fullerene.pdf
 

mmats

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These rats lifespans increased almost 2 fold after only 24 doses. The study states c60 was absorbed and then "eliminated in a few tens of hours", but how would that explain such long term effects? Maybe c60 accumulates in the lipid bilayer of the mitochondrial membrane?

Nevertheless, people are experiencing positive results over the last year - http://www.longecity.org/forum/topic/58783-poll-quantifying-c60oo-data/
 

mmats

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Reasoning for suspending the c60 in EVOO - "The olive oil lipid chains bind to the C60. The resulting lipofullerene can reside in the lipid bilayer of the cell and mitochondial membrane for a long time and act as an infinitely-recyclable antioxidant right where antioxidant action matters most."

Further evidence against combining c60 with water - "Initially, the hydrophobicity of C60 (water solubility <10-9mg/L) was thought to limit its interactions with biological systems and oral administration, skin application, or injection of C60 in rats and other cellsystems revealed no acute toxicity. However, once C60 is introduced into water (either via solvents or by extensive stirring) it forms stable nanoscale suspended aggregates known as fullerene water suspensions (FWS) or nC60 and becomes biologically active. nC60 is highly toxic to eukaryotic cell lines, Daphnia magna and fish."
 

mmats

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Possible explanation for the long term effects of C60 (and importance of a weekly/monthly dosing protocol) -

While C60/EVOO is certainly an anti-oxidant, there is also a spectrum of effects that appear to be persistent if not permanent. One possible explanation is that C60 is modifying the epigenetics of the mitochondrial DNA (mtDNA), as epigenetic changes produce very long lasting effects.

Some background:

The epigenetic content of mtDNA is due to methyl groups that attach to DNA and act as off switches. These are copied after DNA replication to the daughter strand by an enzyme known as methyltransferase, which must contact both strands to copy the switch positions. It is believed from a theoretical study that C60 is attracted to the DNA groove between strands. There it may act as a physical barrier--a methyltransferase inhibitor like procaine*, which is also attracted to the DNA groove and has been shown to extend the lifespan of rats.

The theory:

If the methylation of mtDNA is randomly reduced (and thus has fewer genes turned off) in some fraction of mitochondria this will prove to be advantageous and the population of a cell’s mitochondria (of which there are typically hundreds or thousands) will in time become dominated by the better functioning mitochondria as they are constantly dividing and the defective ones removed by mitophagy. Thus it would be important to take regular breaks from C60 treatment to allow the population of better functioning mitochondria** to increase without further modification--a dosing schedule the Baati rat study may have stumbled upon by accident.

The bottom line:

This process of replication and mitophagy is selection of the fittest at the intracellular level. Taking C60 continuously may result in degrading the better functioning mitochondria as it doesn't allow time for the replication and selection process to work.
 
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