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C60 and ROS as a "good signaling" blocker

ros c60 mitohormesis mitophagy fasting nrf2 ros c60 fasting mitohormesis

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#1 BieraK

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Posted 13 December 2015 - 05:53 AM


Hello, apparently this question has already been discussed, however It has been hard for me to reach a conclusion

Some people says thay c60 produces ROS and block ROS at the same time. Other people says that c60 just only block ROS.

The problem with ROS blockade is the hormetic response of ROS as signaling for the upregulation of some genes like endogenous antioxidant defenses, as it indicated in the blog of Vince Giuliano ROS could work as signaling that promotes health and longevity: http://www.anti-agin...5/mitohormesis/

The same can goes for fasting, wich produces mitophagy, as I understand mitophagy is crucial for get rid of mutated mitochondria. And as I understand fasting can clean "bad" mitochondria and produce more healthy and efficient mitochondria.

What is the case of c60? With the new studies and experiences with c60, could it produce both a blockade and a generation of ROS? or on the contrary could it prevent adaptation to stress through ROS?... Could c60 decrease the effects of fasting, and by that block mitophagy and mitohormesis?

 


Edited by BieraK, 13 December 2015 - 05:55 AM.


#2 AdamI

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Posted 13 December 2015 - 11:09 AM

Fasting leeds to upregulated DNA repair of cells instead of  creating new cells. Don't think the repair is specified to only Mitochondria.



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#3 ambivalent

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Posted 13 December 2015 - 02:51 PM

Hi,

 

Fasting triggers stem cell regeneration.

 

also

 

This paper gives evidence of NAC blocking some autophagy except fasting induced autophagy. 

 

 

 

 

 



#4 niner

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Posted 15 December 2015 - 01:10 AM

This paper gives evidence of NAC blocking some autophagy except fasting induced autophagy. 

 

I wonder if NAC is blocking autophagy that was necessary, or if it reduced the level of oxidative damage, resulting in less autophagy being needed?


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#5 BieraK

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Posted 15 December 2015 - 02:28 AM

from anti-aging firewalls blog:

 

Consistently, abrogation of this mitochondrial ROS signal by antioxidants impairs the lifespan-extending and health-promoting capabilities of glucose restriction and physical exercise, respectively. In summary, the findings discussed in this review indicate that ROS are essential signaling molecules which are required to promote health and longevity

 

 

Reactive Oxygen Species (ROS) are important signaling molecules(ref),  increased ROS expression up to a certain point may be good instead of bad for you(ref)(ref), the stress induced by ROS leads (via the Nrf2 pathway) to activation of multiple endogenous antioxidant and other protective genes(ref)(ref).  And, in fact, suppression of ROS by taking antioxidants can be health-damaging and life-shortening(ref). 


"Antioxidants" is an ambigous concepts because can be applied to a several of substances with different mechanism, Vitamin C is so different compared to Resveratrol, however both are called antioxidants. The same for Beta-Carotene and Curcumin or the Nrf2 enhancer Milk Thistle or Andrographis Paniculata (Apparently the best Nrf2 enhancer, and by that is best compared with Milk Thistle for liver protection, and of course for alcohol intake when social interaction demands the sacrifice).
 

 

I don't think that c60 could be "life shortening", but the ROS blockade could be interfering with interventions like fasting, fasting is one of the best tools that we have for health and longevity, stem cell proliferation, hormonal balance and autophagy. In my judgement autophagy is one of the best effects of fasting, specially mitophagy, with fasting bad or mtDNA damaged mitochondria can be cleaned, and on the otherhand mitophagy could produce more efficient mitochondrian.

MitoQ, a "mitochondrial targeted antioxidant" similar to c60, mitochondrial antioxidants are different compared with other antioxidants like NAC, it is possible that these antioxidants do not produce the same effects as NAC in relation to the ROS blockade (ROS as a signal for hormetic response). So I've found this reseach that talks about MitoQ:
http://www.ncbi.nlm....pubmed/20805228

 

The antioxidant transcription factor Nrf2 negatively regulates autophagy and growth arrest induced by the anticancer redox agent mitoquinone.

Abstract

Mitoquinone (MitoQ) is a synthetically modified, redox-active ubiquinone compound that accumulates predominantly in mitochondria. We found thatMitoQ is 30-fold more cytotoxic to breast cancer cells than to healthy mammary cells. MitoQ treatment led to irreversible inhibition of clonogenic growth of breast cancer cells through a combination of autophagy and apoptotic cell death mechanisms. Relatively limited cytotoxicity was seen with the parent ubiquinone coenzyme Q(10.) Inhibition of cancer cell growth by MitoQ was associated with G(1)/S cell cycle arrest and phosphorylation of the checkpoint kinases Chk1 and Chk2. The possible role of oxidative stress in MitoQ activity was investigated by measuring the products of hydroethidine oxidation. Increases in ethidium and dihydroethidium levels, markers of one-electron oxidation of hydroethidine, were observed at cytotoxic concentrations of MitoQ. Keap1, an oxidative stress sensor protein that regulates the antioxidant transcription factor Nrf2, underwent oxidation, degradation, and dissociation from Nrf2 in MitoQ-treated cells. Nrf2 protein levels, nuclear localization, and transcriptional activity also increased following MitoQ treatment. Knockdown of Nrf2 caused a 2-fold increase in autophagy and an increase in G(1) cell cycle arrest in response to MitoQ but had no apparent effect on apoptosis. The Nrf2-regulated enzyme NQO1 is partly responsible for controlling the level of autophagy. Keap1 and Nrf2 act as redox sensors for oxidative perturbations that lead to autophagy. MitoQ and similar compounds should be further evaluated for novel anticancer activity.

 
 

However this is on cancer cells.

From the study cited above
 


Induction of Autophagy by MitoQ

Our findings indicate that apoptosis may not be the major mechanism responsible for the antiproliferative activity of MitoQ. We therefore hypothesized that MitoQ may induce autophagy that leads to inhibition of proliferation. Autophagy is one of the consequences of stressing cells, and it is emerging as an important mechanism to explain drug responses in cancer cells (27,29). Autophagy is characterized by formation of autophagic vacuoles (autophagosomes) (3031), which can be seen by transmission electron microscopy (31). Autophagosomes were observed after 24 h of incubation with 1 μm MitoQ (Fig. 3A). The presence of mitochondria within the autophagic vacuole (“mitophagy”) was also noted (labeled by arrowheads) (32). Mitophagy is a potential mechanism for turnover of dysfunctional mitochondria, in agreement with the rapid membrane depolarization and cytochrome c release

 

I will read the study with more details, time and patience.


Edited by BieraK, 15 December 2015 - 02:57 AM.


#6 ambivalent

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Posted 15 December 2015 - 03:41 PM

 

This paper gives evidence of NAC blocking some autophagy except fasting induced autophagy. 

 

I wonder if NAC is blocking autophagy that was necessary, or if it reduced the level of oxidative damage, resulting in less autophagy being needed?

 

 

Hi niner,

 

I suppose it raises the question of what is going on in fasting induced autophagy. In layman's terms do the two types of autophagy perform separate processes or the same processes but different threshold levels?

 

I'd made the rather the basic assumption that c60oo would improve the efficacy of fasting because it seems likely it would improve lysosome function:

 

http://www.ncbi.nlm....pubmed/24089192

 

 

 



#7 Kalliste

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Posted 16 December 2015 - 05:55 AM

I've fasted with C60 in my system (stopped taking 1.5mg/day the day before the fast started) and I've fasted with weeks free of C60 before the fast started. Can't say the fasting felt differently, the various processes that happen to the body were mostly the same so I very much doubt C60 would be able to cancel the fasting benefits.

 

Fasting probably affects far too many pathways.

 

If you wanna be on the safe side stop C60 for several weeks, then do a long fast and some HIT to cycle out any faulty mitos before restarting the C60 :)

 

The last time I fasted I stopped C60 three days in advance, the most distinguishable effects was that without C60 my weekly bike riding gave me a lot more muscle soreness in the legs.



#8 ambivalent

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Posted 16 December 2015 - 10:35 PM

I've fasted with C60 in my system (stopped taking 1.5mg/day the day before the fast started) and I've fasted with weeks free of C60 before the fast started. Can't say the fasting felt differently, the various processes that happen to the body were mostly the same so I very much doubt C60 would be able to cancel the fasting benefits.

 

Fasting probably affects far too many pathways.

 

If you wanna be on the safe side stop C60 for several weeks, then do a long fast and some HIT to cycle out any faulty mitos before restarting the C60 :)

 

The last time I fasted I stopped C60 three days in advance, the most distinguishable effects was that without C60 my weekly bike riding gave me a lot more muscle soreness in the legs.

 

 

I've not fasted enough with c60 to make an concrete observations. I suppose the distinction between the non-fasting and fasting induced autophagy 

is the recycling criteria; I seem to recall Longo describing the fasting effect being comparable to trying to lighten the load in a hot-air-balloon. 







Also tagged with one or more of these keywords: ros c60 mitohormesis mitophagy fasting nrf2, ros, c60, fasting, mitohormesis

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