11 replies to this topic

[Tom Andre F. (ex shinobi)]

Hello,

I would like to know what you think about this study:

http://www.ncbi.nlm....pubmed/20663290

I really dont understand what they mean: PQQ decrease GSH and increase ROS ??

[blood]

Is it possible that PQQ produces quite different effects in cancer cells vs healthy cells?

Edited by blood, 18 January 2014 - 11:16 PM.

[Tom Andre F. (ex shinobi)]

Yes and this would not be the first time.. But why a depletion in glutathion ?? why an increase in ROS ? im not so confortable with this study.. Someone can help to understand it better ?

[Turnbuckle]

Active mitochondria is necessary for apoptosis, and PQQ can stimulate mitochondria which will then produce more ROS, using up glutathione. The same appears to be true for C60, which is why I take a gram of reduced glutathione and three grams of Vitamin C every day.

Edited by Turnbuckle, 19 January 2014 - 06:19 PM.

[Tom Andre F. (ex shinobi)]

very interesting turnbuckle !! I didnt know C60 would do that... actually the purpose of C60 is to inhibit every radical species... including ROS.. You really shock me actually

Im not sure about large vit C dose.. But resveratrol and high ORAC value would be great..

Edited by Shinobi, 19 January 2014 - 07:48 PM.

[Kevnzworld]

Active mitochondria is necessary for apoptosis, and PQQ can stimulate mitochondria which will then produce more ROS, using up glutathione. The same appears to be true for C60, which is why I take a gram of reduced glutathione and three grams of Vitamin C every day.

I was unaware that C60 "stimulate " mitochondria, all that I read is that C60 protects mitochondria from ROS. Given that Baati found C60 hepato protective, it doesn't make sense that it would also deplete glutathione, the livers primary antioxidant protection.
PQQ does stimulate mitochondria and contribute to their biogenesis , something that may deplete anti oxidants like glutathione. So if it does, why not take NAC vs reduced GSH or vitamin C ?..bioavailability of GSH is always an issue. What form do you take?
I supplement both PQQ and C60, I find them complimentary not redundant ....

[Turnbuckle]

Active mitochondria is necessary for apoptosis, and PQQ can stimulate mitochondria which will then produce more ROS, using up glutathione. The same appears to be true for C60, which is why I take a gram of reduced glutathione and three grams of Vitamin C every day.

I was unaware that C60 "stimulate " mitochondria, all that I read is that C60 protects mitochondria from ROS. Given that Baati found C60 hepato protective, it doesn't make sense that it would also deplete glutathione, the livers primary antioxidant protection.
PQQ does stimulate mitochondria and contribute to their biogenesis , something that may deplete anti oxidants like glutathione. So if it does, why not take NAC vs reduced GSH or vitamin C ?..bioavailability of GSH is always an issue. What form do you take?
I supplement both PQQ and C60, I find them complimentary not redundant ....

If PQQ, which is said to be an anti-oxidant and to stimulate cellular respiration, depletes glutathione, why would C60 not do the same? I noticed an uptick in aerobic capacity with PQQ, and a much greater uptick with C60. No one has studied it yet, but I don't believe you get that for free. You're unlikely to get more cellular respiration without creating more ROS, and there's no reason to believe C60 will be different in principle from PQQ. Thus more glutathione should be helpful, and I have found this to be the case. As for reduced glutathione v NAC, I have tried both and have found the effects to be similar, but I could not tolerate NAC for long. It is very hard on the digestive system, whereas reduced glutathione seems to have no negative digestive effects.

[hav]

Turnbuckle, what do you think of the Acetyl version of l-glutathione? Seems to be a bit more expensive.

Howard

Edited by hav, 20 January 2014 - 05:39 PM.

[Turnbuckle]

Turnbuckle, what do you think of the Acetyl version of l-glutathione? Seems to be a bit more expensive.

Howard

I haven't tried it.

[OpaqueMind]

If PQQ, which is said to be an anti-oxidant and to stimulate cellular respiration, depletes glutathione, why would C60 not do the same? I noticed an uptick in aerobic capacity with PQQ, and a much greater uptick with C60. No one has studied it yet, but I don't believe you get that for free. You're unlikely to get more cellular respiration without creating more ROS, and there's no reason to believe C60 will be different in principle from PQQ. Thus more glutathione should be helpful, and I have found this to be the case. As for reduced glutathione v NAC, I have tried both and have found the effects to be similar, but I could not tolerate NAC for long. It is very hard on the digestive system, whereas reduced glutathione seems to have no negative digestive effects.

Would your body not theoretically adapt to the increased ROS by boosting its own antioxidant defences, kind of like the adaptation to exercise? Are ROS implicated in exercise? If so, a similar mechanism might occur here. Then again, it might not.

[Turnbuckle]

If PQQ, which is said to be an anti-oxidant and to stimulate cellular respiration, depletes glutathione, why would C60 not do the same? I noticed an uptick in aerobic capacity with PQQ, and a much greater uptick with C60. No one has studied it yet, but I don't believe you get that for free. You're unlikely to get more cellular respiration without creating more ROS, and there's no reason to believe C60 will be different in principle from PQQ. Thus more glutathione should be helpful, and I have found this to be the case. As for reduced glutathione v NAC, I have tried both and have found the effects to be similar, but I could not tolerate NAC for long. It is very hard on the digestive system, whereas reduced glutathione seems to have no negative digestive effects.

Would your body not theoretically adapt to the increased ROS by boosting its own antioxidant defences, kind of like the adaptation to exercise? Are ROS implicated in exercise? If so, a similar mechanism might occur here. Then again, it might not.

There are likely feedback loops that control the level of glutathione. Methionine restriction, for instance, increases blood glutathione and longevity in rats. And this may be how calorie restriction works--by lowering the intake of methionine and thus increasing the level of glutathione. The situation with PQQ with leukemia cells as in the paper cited in the OP is a special case (the Warburg effect, where mitochondria are shut down) and doesn't necessarily apply to normal cells. But it suggests that PQQ (and probably C60) would tend to kill at least some cancer cells.

Cancer cells often show heightened expression of an uncoupling protein (UCP2) that turns off the mitochondria. One hypothesis of how C60 heightens aerobic activity is that it somehow inhibits UCP2. Now it's interesting when you look at that protein, as it has a spherical depression with a hole in the center, while C60 looks like it might serve as an excellent plug.

Uncoupling proteins (UCPs) are mitochondrial transporters present in the inner membrane of mitochondria. They are found in all mammals and in plants. They belong to the family of anion mitochondrial carriers including adenine nucleotide transporters. The term “uncoupling protein” was originally used for UCP1, which is uniquely present in mitochondria of brown adipocytes, the thermogenic cells that maintain body temperature in small rodents. In these cells, UCP1 acts as a proton carrier activated by free fatty acids and creates a shunt between complexes of the respiratory chain and ATP synthase. Activation of UCP1 enhances respiration, and the uncoupling process results in a futile cycle and dissipation of oxidation energy as heat. UCP2 is ubiquitous and highly expressed in the lymphoid system, macrophages, and pancreatic islets. UCP3 is mainly expressed in skeletal muscles. In comparison to the established uncoupling and thermogenic activities of UCP1, UCP2 and UCP3 appear to be involved in the limitation of free radical levels in cells rather than in physiological uncoupling and thermogenesis. Moreover, UCP2 is a regulator of insulin secretion and UCP3 is involved in fatty acid metabolism...

UCP2 expression is increased in most human colon cancers, and the level of expression appears to correlate with the degree of neoplastic changes. These findings may foster the idea that UCP2 is part of a novel adaptive response by which oxidative stress is modulated in colon cancer.

http://diabetes.diab...ppl_1/S130.full

Edited by Turnbuckle, 21 January 2014 - 01:00 AM.

[Tom Andre F. (ex shinobi)]

kind of conflicting story here:

PQQ (mitochondria promoter), diminshes the inflammation response:

Harris CB, Chowanadisai W, Mishchuk DO, Satre MA, Slupsky CM, Rucker RB. Dietary pyrroloquinoline quinine (PQQ) alters indicators of inflammation and mitochondrial-related metabolism in human subjects. J Nutr Biochem. 2013 Dec;24(12):2076-84. doi: 10.1016/j.jnutbio.2013.07.008.

and here: http://www.ncbi.nlm....pubmed/17268846

and here: http://www.ncbi.nlm....pubmed/22843070

Edited by Shinobi, 05 February 2014 - 10:02 AM.