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) (30, 31), 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.