635 replies to this topic

[HighDesertWizard]

Baati, et al, used CCl4 as a toxic substance to determine, among other things, the potential health effects of C60 vis-a-vis Toxins. Are there any other studies in which CCI4 was used in a similar way to test the potency of an anti-oxidant and in which the anti-oxidant treated animals survived? If yes, could someone provide study reference links?

[Turnbuckle]

Baati, et al, used CCl4 as a toxic substance to determine, among other things, the potential health effects of C60 vis-a-vis Toxins. Are there any other studies in which CCI4 was used in a similar way to test the potency of an anti-oxidant and in which the anti-oxidant treated animals survived? If yes, could someone provide study reference links?

 

 

http://www.ncbi.nlm....Cl4 ANTIOXIDANT

[Kalliste]

This is a paywalled article but for those of you who can get it I recommend it. No real news for those of us who spent some time reading about C60 specifically but it is an excellent primer on antioxidants and mitochondria in general. I'll come back with some more quotes later if that is appreciated by someone.

 

 

Biotechnol Adv. 2013 Sep-Oct;31(5):563-92. doi: 10.1016/j.biotechadv.2012.09.005. Epub 2012 Sep 27.

Mitochondria-targeted antioxidants and metabolic modulators as pharmacological interventions to slow ageing.

Gruber J¹, Fong S, Chen CB, Yoong S, Pastorin G, Schaffer S, Cheah I, Halliwell B.

Author information

Abstract

Populations in many nations today are rapidly ageing. This unprecedented demographic change represents one of the main challenges of our time. A defining property of the ageing process is a marked increase in the risk of mortality and morbidity with age. The incidence of cancer, cardiovascular and neurodegenerative diseases increases non-linearly, sometimes exponentially with age. One of the most important tasks in biogerontology is to develop interventions leading to an increase in healthy lifespan (health span), and a better understanding of basic mechanisms underlying the ageing process itself may lead to interventions able to delay or prevent many or even all age-dependent conditions. One of the putative basic mechanisms of ageing is age-dependent mitochondrial deterioration, closely associated with damage mediated by reactive oxygen species (ROS). Given the central role that mitochondria and mitochondrial dysfunction play not only in ageing but also in apoptosis, cancer, neurodegeneration and other age-related diseases there is great interest in approaches to protect mitochondria from ROS-mediated damage. In this review, we explore strategies of targeting mitochondria to reduce mitochondrial oxidative damage with the aim of preventing or delaying age-dependent decline in mitochondrial function and some of the resulting pathologies. We discuss mitochondria-targeted and -localized antioxidants (e.g.: MitoQ, SkQ, ergothioneine), mitochondrial metabolic modulators (e.g. dichloroacetic acid), and uncouplers (e.g.: uncoupling proteins, dinitrophenol) as well as some alternative future approaches for targeting compounds to the mitochondria, including advances from nanotechnology.

Copyright © 2012 Elsevier Inc. All rights reserved.

 

http://www.ncbi.nlm....pubmed/23022622

[Turnbuckle]

Here is a link for a pdf download of the paper "Mitochondria-targeted antioxidants..."--

 

https://www.google.c...od-bBT8jqDAHD9w

Edited by Turnbuckle, 04 April 2015 - 01:00 PM.

[Kalliste]

Here is the mention fullerenes get in this review of many different antioxidants.

 

 

7.4. Carbon based nano-antioxidants
In addition to solid nanoparticles, another allotropic form of carbon
(besides nanotubes) known as fullerene has been shown to be an antioxidant
in vitro (Andrievsky et al., 2009; Cai et al., 2008; Chen et al.,
2004; Elswaifi et al., 2009; Krusic et al., 1991; Sun, 2006) through a
complex mechanism: fullerenes seem to act as 1) protectants against
oxidative damage by crossing the cell membrane and localizing preferentially
in the mitochondria; and 2) efficient radical scavengers,
through a hydrated free radical recombination (self-neutralization) of
hydroxyl radicals (•OH), which is catalyzed by specific water structures
ordered by the fullerene molecules. Therefore, it has been suggested
that efficient uptake and precise subcellular distribution at the mitochondrial
level are key requirements to inhibit ROS formation
(Ali et al., 2004; Foley et al., 2002). However, some contrasting observations
were associated with this material, since fullerenes and their
derivatives have also been reported to increase oxidative stress. Data
by Gharbi et al. indicate that aqueous suspensions of fullerene (C60)
protected against toxicity induced by carbon tetrachloride (CCl4)
(Gharbi et al., 2005). In fact, 24 h after CCl4 injection, most animals
pretreated with C60 at high doses (≥0.5 g/kg), presented livers with
normal morphology (Ali et al., 2004; Foley et al., 2002). CCl4 undergoes
metabolism by cytochrome P450 enzymes and generates a reactive
trichloromethyl radical CCl3• which, in the presence of oxygen, gives
rise to trichloromethylperoxy radical CCl3OO• and lipid peroxidation.
Therefore, the mechanism of protection against CCl4 toxicity in rats
was proposed to be due to the ability of C60 to scavenge these radicals
in vivo.
In addition, in a recent study, oral administration of C60 suspended in
olive oil (0.8 mg/ml) at repeated doses (1.7 mg/kg of body weight)
resulted in almost doubling of lifespan and significant protection in an
experimental model of CCl4 intoxication in rats and erratum (Baati et
al., 2012a,b). These findings are encouraging but should be considered
carefully, especially the animal lifespan results, as olive oil administration
alone already resulted in significant increase in
median lifespan, raising questions regarding the choice of solvent

for C60 administration. Strikingly, median lifespan was extended to
42 months in C60-treated rats, compared to 22 months in water controls
and 26 months in the olive oil group. Themedian lifespan in the
C60 group is surprising and needs to be validated in future in vivo
studies to make sure the results are reproducible.
Another interestingwork has been recently published by Cirillo et al.
inwhich a covalent functionalization based on radical graftingwas used
to incorporate gallic acid on carbon nanotubes without losing any of its
antioxidant properties. This result, although limited to preliminary in
vitro studies and in the absence of any cytotoxicity evaluation (which
is important, because gallic acid can readily oxidize to produce ROS
Wee et al., 2003), may pave the way for the integration of radical scavengers
onto suitable nano-carriers through new methods of covalent
linkage (Cirillo et al., 2011). Despite that, no categorical statement can
be made about the safety of these carbon-based agents; differences in
the purity of the samples, in the incorporation of bioactive molecules
through several chemical procedures and in the doses used during the
experiments do not allowany definite conclusion about the documented
higher efficacy or their toxicological profile.Many questions regarding
the safety of nanoparticles are still unanswered, the main concern
being their ability to trigger intense chemical reactions and anomalies
as nanospecies, while escaping from the normal phagocytic defenses
and depositing into organs and tissues. At the moment, available information
concerning the health risks to the environment and humans is
poor. The encouraging results that have been achieved so far suggest
that they are worth further investigation, although it is imperative to
fully address the biocompatibility of these formulations before concluding
that nano-carriers are safe delivery systems.

 

Here is another part from later on regarding antioxidants and nano-stuff in general which is of some relevance.

 

 

7.9. Perspectives in nano-carrier systems
Why is there such an explosion of work aiming to explore
nano-technology to combat ROS, given the vast array of conventional
antioxidants that is already available? Ironically, the use of antioxidants
in the treatment of diseases associated with ROS has met with
little success thus far. Conventional antioxidants such as vitamins C
and E and N-acetyl cysteine can be metabolized or inactivated even
before reaching their target sites. Additionally, many antioxidants
can only quench a single free radical per molecule. Thus, in order to
elicit detectable changes in ROS levels at the site of damage, continued
and high dosing is necessary in cases where no efficient antioxidant
recycling machinery exists (Elswaifi et al., 2009). With respect to
this, nano-carriers loaded with antioxidants or nanoparticle antioxidants
such as CeONP, which appear to accumulate in the tissue and
cells, seem favorable, especially if their active compartments can be
regenerated in vivo or if they have catalytic ROS-removal properties.
The surface area of nano-structured antioxidants also confers advantages
since the nano-scale imparts a dramatic increase in the exposed
area. The increase in surface area could not only be utilized for improved
ROS scavenging, but also for functionalization on the surface
with other moieties that may provide selective targeting and delivery.
Overall, despite the growing interest in the field of nanotechnology,
great caution needs to be employed when interpreting the effects of
these nano-carriers. That also justifies the current debate between the
enthusiastic application of nano-systems in everyday life and the
distrustful vision towards any nano-application. What is needed is
an in depth investigation that goes beyond a few interesting observations
and provides clear evidence of 1) the long-term biocompatibility
including bio-distribution and metabolism (if any) of these
nano-carriers; 2) fully standardized protocols for the preparation of
the nano-DS, so that the results becomemore reproducible and comparable
among different groups of research; 3) extensive in vitro and
in vivo experiments that show advantages over conventional approaches
and comprehensive understanding of the intracellular trafficking
and mechanisms of actions responsible for their antioxidant
properties.
To reiterate, it is too early to say whether these “nano-structures”
will successfully overcome current limitations of non-specific targeting
or monumentally backfire to be hazardous, but they seemto have a potential
worth exploring in depth.

 

 

Gruber J, et al, Mitochondria-targeted antioxidants and metabolic modulators as pharmacological interventions to
slow ageing, Biotechnol Adv (2012), http://dx.doi.org/10...adv.2012.09.005

[sagafemina]

Ok, so based on a rat study with a sample size of 6 (HELLO!!), some people are drinking the C60 olive oil mixture. I know there is not much evidence of acute toxicity with fullerenes, but it seems kind-of premature to start dosing with this stuff. What do you expect to feel, experience, produce, with this supplement at such an early stage in its investigation? What bio-markers might be tested. How long before you expect to see results? At least with resveratrol there was a bit longer history, more research, etc... before people started taking it en masse. Derived from plant material at least gives resveratrol the aura (if not reality) of being non-toxic. I wouldn't be so comfortable saying the same for fullerenes.

See here to get a good dose of skepticism.

 

This link results in a 404 error.  I would like to see this dose of skepticism.

I would also like to see a link to the Baati article that started the discussion...it's not obvious to me!

Thanks
 

[sagafemina]

Another interesting fullerene study:
http://144.206.159.1...025/1303213.pdf

This study below is even more interesting: note the results on table 1, showing the protective effects of fullerene in a number of in vivo and in vitro experiments.

http://www.thebronxp...elated 2001.pdf

Toxicity appears minimal. I would hazard a guess that those large rats who are experimenting with very low dosages are possibly not being so rash.
It isn't as though the rat study that started this thread is the first fullerene study to show remarkable effects.

Even if it does not affect overall human lifespan, looking at the data, it appears it could possibly affect the quality of that lifespan in a positive manner - at least this is the hypothesis, in the absence of any human or higher primate studies.

 

The first link resulted, for me (twice) in a time-out error.  Can you provide a working link?  Thanks!
 

[Turnbuckle]

 

 

The first link resulted, for me (twice) in a time-out error.  Can you provide a working link?  Thanks!
 

 

 

 

You're pulling up stuff from three years ago. The internet is more fluid than that.

[niner]

I would like to see this dose of skepticism.

The early skepticism was knee-jerk, and some of it was frankly kind of ignorant. I wish that the information wasn't hidden in a bunch of giant threads. Try looking at newer threads in the c60health forum, or starting at the end of big threads and working backwards.  If things are still unclear, just ask.

[sagafemina]

Thanks, 

 

Spent all afternoon reading this thread which I only just discovered.  Eventually ran across both references.  Thanks for your assistance. 

 

Here (I believe) is the skepticism  article (or at least A skepticism article)  

 

And here of course is the Baati article.  For the benefit any other new seekers/finders out there.  Not sure why it wasn't right at the top considering it spawned this entire 600+ message thread!  (But who knew?)

 

My cache is about to explode with downloaded articles, may take me a week to digest them all. 

 

Speaking of digestion, I am amazed that the EVOO article (the one about being toxic to all cancer cell lines) didn't make more headlines.  I never saw it before.   We should all be guzzling the stuff.  Would help pass gallstones too.  OOPS off topic sorry.  Good from now on. 

[niner]

Not sure why it wasn't right at the top considering it spawned this entire 600+ message thread!  (But who knew?)
 
Speaking of digestion, I am amazed that the EVOO article (the one about being toxic to all cancer cell lines) didn't make more headlines.

The full text is linked in the first post in this thread. Also the second post. Which EVOO paper are you referring to? Olive oil has very good epidemiology. A lot of us use it pretty heavily.

 

One thing to keep in mind as you go through references is the difference between aggregated forms of c60, sometimes called nC60 or nano-C60, and molecular forms.  C60oo is molecular.  The aggregated forms can cause various problems that aren't seen in molecular forms. 

[Kalliste]

Saga is refering to the Olive oil kills cancer study I posted a few pages back.

[niner]

Saga is refering to the Olive oil kills cancer study I posted a few pages back.

 

You mean this paper on oleocanthal?  It might be overgenerous to say that olive oil kills cancer, since oleocanthal is a minor component of it.  In the paper, the cells were bathed in a solution of pure oleocanthal.  This is not to say that olive oil isn't good-- it is, but these things always require a threshold dose which may or may not be available from the amount of olive oil we could consume.

[Turnbuckle]

 

Saga is refering to the Olive oil kills cancer study I posted a few pages back.

 

You mean this paper on oleocanthal?  It might be overgenerous to say that olive oil kills cancer, since oleocanthal is a minor component of it.  In the paper, the cells were bathed in a solution of pure oleocanthal.  This is not to say that olive oil isn't good-- it is, but these things always require a threshold dose which may or may not be available from the amount of olive oil we could consume.

 

 

 

Really? Because they talk about 10 micro-molar concentrations.

 

And while EVOO contains low concentrations, olive leaf extracts seem to have much more.

Edited by Turnbuckle, 09 April 2015 - 02:29 PM.

[Kalliste]

Maybe C60 binds to that substance and makes it more bioavailable? C60 is explored for that purpose by many. Or is this wishful thinking? That might make what olive oil brand used more important. It might explain why AgVivos animals died of cancer. He was using inferior oil ☺

Edited by Cosmicalstorm, 09 April 2015 - 03:48 PM.

[Kalliste]

Todays harvest of related C60 stuff. The first one is semi-related. The other two I don't know.

 

 

J Appl Toxicol. 2015 Mar 23. doi: 10.1002/jat.3137. [Epub ahead of print]

Comparative effects of sulfhydryl compounds on target organellae, nuclei and mitochondria, of hydroxylated fullerene-induced cytotoxicity in isolated rat hepatocytes.

Nakagawa Y¹, Inomata A, Ogata A, Nakae D.

Author information

Abstract

DNA damage and cytotoxicity induced by a hydroxylated fullerene [C₆₀ (OH)₂₄ ], which is a spherical nanomaterial and/or a water-soluble fullerene derivative, and their protection by sulfhydryl compounds were studied in freshly isolated rat hepatocytes. The exposure of hepatocytes to C₆₀ (OH)₂₄ at a concentration of 50 μM caused time (0 to 3 h)-dependent cell death accompanied by the formation of cell surface blebs, the loss of cellular levels of ATP and reduced glutathione, accumulation of glutathione disulfide, and induction of DNA fragmentation assayed using alkali single-cell agarose-gel electrophoresis. C₆₀ (OH)₂₄ -induced cytotoxicity was effectively prevented by pretreatment with sulfhydryl compounds. N-acetyl-L-cysteine (NAC), L-cysteine and L-methionine, at a concentration of 2.5 mM, ameliorated cell death, accompanied by a decrease in cellular ATP levels, formation of cell surface blebs, induction of reactive oxygen species (ROS) and loss of mitochondrial membrane potential caused by C₆₀ (OH)₂₄ . In addition, DNA fragmentation caused by C₆₀ (OH)₂₄ was also inhibited by NAC, whereas an antioxidant ascorbic acid did not affect C₆₀ (OH)₂₄ -induced cell death and DNA damage in rat hepatocytes. Taken collectively, these results indicate that incubation of rat hepatocytes with C₆₀ (OH)₂₄ elicits DNA damage, suggesting that nuclei as well as mitochondria are target sites of the hydroxylated fullerene; and induction of DNA damage and oxidative stress is ameliorated by an increase in cellular GSH levels, suggesting that the onset of toxic effects may be partially attributable to a thiol redox-state imbalance caused by C₆₀ (OH)₂₄ . Copyright © 2015 John Wiley & Sons, Ltd.

 

 

Carbon-based nanoparticles such as fullerenes have been widely applied in personal care products, drug delivery systems, and solar cells. The properties of nanoparticles have been increasingly studied because of their applications and their potential risks to the environment and human health. Many studies have focused on the environmental fate and properties of C60. However, there is currently limited information available on the environmental properties of functionalised fullerenes. This study focuses on the colloidal stability of two fullerenes (C60 and [6,6]-diphenyl-C62-bis(butyric acid methyl ester)) in water in the presence of dissolved organic carbon (DOC) and different electrolytes (NaCl and CaCl2). Suspended fullerene concentrations were determined with high resolution Orbitrap mass spectrometry. The size was determined by multi-angle light scattering, dynamic light scattering and for the first time flow cytometry. The suspended concentrations of the fullerenes were stabilised by low concentrations of DOC (2 mg C/L) in the presence of NaCl. However, sedimentation of DOC occurred at low concentrations of CaCl2 (>2 mM) which caused removal of (functionalised) fullerenes. The results show that (functionalised) fullerenes can be rapidly removed in natural aqueous systems in the presence of low concentrations of DOC and multivalent inorganic electrolytes.

 

 

 

Chem Phys Lipids. 2015 Apr 4. pii: S0009-3084(15)00029-8. doi: 10.1016/j.chemphyslip.2015.04.001. [Epub ahead of print]

Fullerene up-take alters bilayer structure and elasticity: A small angle X-ray study.

Drasler B¹, Drobne D², Sadeghpour A³, Rappolt M⁴.

Author information

Abstract

The coupling of fullerene (C₆₀) to the structure and elasticity of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine bilayers has been explored by synchrotron small angle X-ray scattering. Multilamellar vesicles were loaded with 0, 2 and 10mol.% of C₆₀ and studied in a temperature range from 15 to 65°C. The addition of C₆₀ caused an increase in the bilayer undulations (∼20%), in the bilayer separation (∼15%), in the linear expansion coefficient and caused a drop in the bending rigidity of the bilayers (20-40%). Possible damaging effects of fullerene on biomembranes are mainly discussed on the basis of altered bilayer fluidity and elasticity changes.

Copyright © 2015. Published by Elsevier Ireland Ltd.

 

[Kalliste]

Preparation of hydrophilic C₆₀(OH)₁₀/2-hydroxypropyl-β-cyclodextrin nanoparticles for the treatment of a liver injury induced by an overdose of acetaminophen

 

Stable hydrophilic C₆₀(OH)₁₀ nanoparticles were prepared from 2-hydroxypropyl-β-cyclodextrin (HP-β-CD) and applied to the treatment of an acetaminophen overdose induced liver Injury. C₆₀(OH)₁₀ nanoparticles were produced by cogrinding α-CD, β-CD, γ-CD and HP-β-CD and characterized in terms of solubility, mean particle diameter, ζ-potential and long term dispersibility in water. Hydrophilic C₆₀(OH)₁₀ nanoparticles with particle sizes less than 50 nm were effectively produced by cogrinding HP-β-CD with C₆₀(OH)₁₀ at a molar ratio of 1:3 (C₆₀(OH)₁₀:CD). The resulting C₆₀(OH)₁₀/HP-β-CD nanoparticles were stable in water and showed no aggregation over a 1 month period. The C₆₀(OH)₁₀/CDs nanoparticles scavenged not only free radicals (DPPH and ABTS radicals) but also reactive oxygen species (O₂^•− and •OH). When C₆₀(OH)₁₀/HP-β-CD nanoparticles were intraperitoneally administered to mice with a liver injury induced by an overdose of acetaminophen (APAP), the ALT and AST levels were markedly reduced to almost the same level as that for normal mice. Furthermore, the administration of the nanoparticles prolonged the survival rate of liver injured mice, while all of the mice that were treated with APAP died within 40 h. To reveal the mechanism responsible for liver protection by C₆₀(OH)₁₀ nanoparticles, GSH level, CYP2E1 expression and peroxynitrite formation in the liver were assessed. C₆₀(OH)₁₀/HP-β-CD nanoparticles had no effect on CYP2E1 expression and GSH depletion, but suppressed the generation of peroxynitrite in the liver. The findings indicate that the protective effect of C₆₀(OH)₁₀/HP-β-CD nanoparticles was due to the suppression of oxidative stress in mitochondria, as the result of scavenging ROS such as O₂^•−, NO and peroxynitrite, which act as critical mediators in the liver injuries.

http://www.sciencedi...142961214012824

Edited by Cosmicalstorm, 16 April 2015 - 07:32 AM.

[niner]

 

 

Saga is refering to the Olive oil kills cancer study I posted a few pages back.

 

You mean this paper on oleocanthal?  It might be overgenerous to say that olive oil kills cancer, since oleocanthal is a minor component of it.  In the paper, the cells were bathed in a solution of pure oleocanthal.  This is not to say that olive oil isn't good-- it is, but these things always require a threshold dose which may or may not be available from the amount of olive oil we could consume.

 

Really? Because they talk about 10 micro-molar concentrations.

 

And while EVOO contains low concentrations, olive leaf extracts seem to have much more.

 

By "pure" I mean uncontaminated, purified, free from its natural matrix.  This is then put into solution at 10 uM.  If cancer cells need to be in contact with that concentration in order to be killed, then you would need to consume enough to generate such concentrations throughout the body, or at least wherever the cancer cells were.  In the face of a gut lined with various enzymes and efflux pumps working to keep strange molecules out of the system and a xenobiotic metabolism system that is busily oxidizing and conjugating the ones that get in, you would need a lot of oleocanthal to get anywhere close to 10 uM.  Evading these systems is the point of much of pharmaceutical design, and is the most likely reason that candidates showing early promise later fail in development. 

[Turnbuckle]

 

 

 

Saga is refering to the Olive oil kills cancer study I posted a few pages back.

 

You mean this paper on oleocanthal?  It might be overgenerous to say that olive oil kills cancer, since oleocanthal is a minor component of it.  In the paper, the cells were bathed in a solution of pure oleocanthal.  This is not to say that olive oil isn't good-- it is, but these things always require a threshold dose which may or may not be available from the amount of olive oil we could consume.

 

Really? Because they talk about 10 micro-molar concentrations.

 

And while EVOO contains low concentrations, olive leaf extracts seem to have much more.

 

By "pure" I mean uncontaminated, purified, free from its natural matrix.  This is then put into solution at 10 uM.  If cancer cells need to be in contact with that concentration in order to be killed, then you would need to consume enough to generate such concentrations throughout the body, or at least wherever the cancer cells were.  In the face of a gut lined with various enzymes and efflux pumps working to keep strange molecules out of the system and a xenobiotic metabolism system that is busily oxidizing and conjugating the ones that get in, you would need a lot of oleocanthal to get anywhere close to 10 uM.  Evading these systems is the point of much of pharmaceutical design, and is the most likely reason that candidates showing early promise later fail in development. 

 

 

 

The real problem seems not the bioavailability, but the low concentration in EVOO--

 

Bioavailability and antioxidant effects of olive oil phenols in humans: a review.

 

 

CONCLUSION:

Although phenols from olive oil seem to be well absorbed, the content of olive oil phenols with antioxidant potential in the Mediterranean diet is probably too low to produce a measurable effect on LDL oxidisability or other oxidation markers in humans. The available evidence does not suggest that consumption of phenols in the amounts provided by dietary olive oil will protect LDL against oxidative modification to any important extent.

 

 

[niner]

The real problem seems not the bioavailability, but the low concentration in EVOO--

 

Well, it's both.  "Good" olive oil (typical robust oil at Amphora Nueva, for example) has 3-400 ppm of total polyphenols, so you'd find ~250 mg in a 750ml bottle.  Although the absorption of these things is pretty good, the metabolism is pretty brutal, so even if you could get enough (say by taking an extract), you'd still have a problem maintaining adequate concentrations.  Nevertheless, the epidemiology on olive oil consumption is outstanding.  In that large study, they saw an effect on CVD and all-cause mortality, but not on cancer mortality.  That probably blows the "olive oil kills cancer" concept, but it's doing something good.   Maybe it's the polyphenols, maybe it's the lipids, maybe the matrix helps the bioavailability and it's both...   I dunno, but I just bought another six bottles of Nov. 2014 Melgarejo oil while I was poking around at Amphora. 

Edited by niner, 17 April 2015 - 12:42 PM.

[Turnbuckle]

In a list of foods by polyphenol content (mg/100 g), EVOO is not even close to the top--

 

Rank    Food                                              Content

 

1          Cloves                                           15,188

2          Peppermint, dried                         11,960

3          Star anise                                       5460

4          Cocoa powder                               3448

5          Mexican oregano, dried                2319

6          Celery seed                                   2094

7          Black chokeberry                          1756

8          Dark chocolate                              1664

9          Flaxseed meal                               1528c

10        Black elderberry                            1359

11        Chestnut                                        1215

12        Common sage, dried                     1207

13        Rosemary, dried                            1018

14        Spearmint, dried                           956

15        Common thyme, dried                  878

16        Lowbush blueberry                       836

17        Blackcurrant                                  758

18        Capers                                           654

19        Black olive                                    569

20        Highbush blueberry                       560

21        Hazelnut                                        495

22        Pecan nut                                      493

23        Soy flour                                       466

24        Plum                                              377

25        Green olive                                    346

26        Sweet basil, dried                         322

27        Curry, powder                               285

28        Sweet cherry                                 274

29        Globe artichoke heads                  260

30        Blackberry                                     260

31        Roasted soybean                           246

32        Milk chocolate                              236

33        Strawberry                                    235

34        Red chicory                                   235

35        Red raspberry                                215

36        Coffee, filter                                 214

37        Ginger, dried                                 202

38        Whole grain hard wheat flour       201c

39        Prune                                             194

40        Almond                                         187

41        Black grape                                   169

42        Red onion                                     168

43        Green chicory                                166

44        Common thyme, fresh                  163

45        Refined maize flour                      153c

46        Soy, tempeh                                  148

47        Whole grain rye flour                    143c

48        Apple                                            136

49        Spinach                                         119

50        Shallot                                           113

51        Lemon verbena, dried                   106

52        Black tea                                       102

53        Red wine                                       101

54        Green tea                                       89

55        Soy yogurt                                    84

56        Yellow onion                                74

57        Soy meat                                       73

58        Whole grain wheat flour               71c

59        Pure apple juice                             68

60        Pure pomegranate juice                 66

61        Extra-virgin olive oil                     62

62        Black bean                                    59

63        Peach                                             59

64        Pure blood orange juice                56

65        Cumin                                           55

66        Pure grapefruit juice                      53

67        White bean                                    51

68        Chinese cinnamon                         48

69        Pure blond orange juice                46

70        Broccoli                                         45

71        Redcurrant                                    43

72        Soy tofu                                        42

73        Pure lemon juice                            42

74        Whole grain oat flour                    37c

75        Apricot                                          34

76        Caraway                                        33

77        Refined rye flour                          31c

78        Asparagus                                     29

79        Walnut                                          28

80        Potato                                            28

81        Ceylan cinnamon                          27

82        Parsley, dried                                25

83        Nectarine                                       25

84        Curly endive                                 24

85        Marjoram, dried                            23

86        Red lettuce                                    23

87        Chocolate beverage with milk      21

88        Quince                                           19

89        Endive (Escarole)                          18

90        Soy milk                                        18

91        Pure pummelo juice                       18

92        Rapeseed oil                                  17

93        Pear                                               17

94        Soybean sprout                             15

95        Green grape                                   15

96        Carrot                                            14

97        Vinegar                                         13

98        Soy cheese                                    12

99        White wine                                    10

100      Rosé wine                                     10

[geo12the]

In a list of foods by polyphenol content (mg/100 g), EVOO is not even close to the top--

 

 

 

The particular type of polyphenols probably has a big effect on health promoting properties.  The ones in OO have been shown to have positive effects in various studies.

[geo12the]

more recent paper:

 

Biological effects of the olive polyphenol, hydroxytyrosol: An extra view from genome-wide transcriptome analysis.

Nan JN1, Ververis K, Bollu S, Rodd AL, Swarup O, Karagiannis TC.

Author information

 

Abstract

Epidemiological and clinical studies have established the health benefits of the Mediterranean diet, an important component of which are olives andolive oil derived from the olive tree (Olea Europea). It is now well-established that not only the major fatty acid constituents, but also the minor phenolic components, in olives and olive oil have important health benefits. Emerging research over the past decade has highlighted the beneficial effects of a range of phenolic compounds from olives and olive oil, particularly for cardiovascular diseases, metabolic syndrome and inflammatory conditions. Mechanisms of action include potent antioxidant and anti-inflammatory effects. Further, accumulating evidence indicates the potential of the polyphenols and potent antioxidants, hydroxytyrosol and oleuropein in oncology. Numerous studies, both in vitro and in vivo, have demonstrated the anticancer effects of hydroxytyrosol which include chemopreventive and cell-specific cytotoxic and apoptotic effects. Indeed, the precise molecular mechanisms accounting for the antioxidant, anti-inflammatory and anticancer properties are now becoming clear and this is, at least in part, due to high through-put gene transcription profiling. Initially, we constructed phylogenetic trees to visualize the evolutionary relationship of members of the Oleaceae family and secondly, between plants producing hydroxytyrosol to make inferences of potential similarities or differences in their medicinal properties and to identify novel plant candidates for the treatment and prevention of disease. Furthermore, given the recent interest in hydroxytyrosol as a potential anticancer agent and chemopreventative we utilized transcriptome analysis in the erythroleukemic cell line K562, to investigate the effects of hydroxytyrosol on three gene pathways: the complement system, The Warburg effect and chromatin remodeling to ascertain relevant gene candidates in the prevention of cancer.

PMID:   24392471   [PubMed - in process]

 

[Turnbuckle]

 

In a list of foods by polyphenol content (mg/100 g), EVOO is not even close to the top--

 

 

 

The particular type of polyphenols probably has a big effect on health promoting properties.  The ones in OO have been shown to have positive effects in various studies.

 

 

 

Of course the components vary considerably between plant sources, and there are non-food sources that have even more polyphenols than these--such as olive leaf extract.

 

See table 2 in  http://www.ncbi.nlm....es/PMC3779014/ 

[smithx]

This just came out: 

 

Article:

http://www.genengnew...ruses/81251164/

 

Paper:

http://www.sciencema...aa7516.abstract

 

What interested me was this:

 

 

 

Through interaction with CR6 interacting factor (CRIF1), LEM controlled the levels of oxidative phosphorylation (OXPHOS) complexes and respiration resulting in the production of pro-proliferative mitochondrial Reactive Oxygen Species (mROS). LEM provides a link between immune activation and the expansion of protective CD8⁺ T cells driven by OXPHOS and represents a pathway for the restoration of long-term protective immunity based on metabolically modified CTL.

 

If the production of ROS is protective against viruses and cancer, could putting C60 into the mitochondrial membrane and quenching the ROS cause problems? I know that the one rat study seemed to indicate the reverse, but if the ROS is actually protective, how would quenching them be other than non-protective? 

 

 

[niner]

This just came out: 

 

Article:

http://www.genengnew...ruses/81251164/

 

Paper:

http://www.sciencema...aa7516.abstract

 

What interested me was this:

 

Through interaction with CR6 interacting factor (CRIF1), LEM controlled the levels of oxidative phosphorylation (OXPHOS) complexes and respiration resulting in the production of pro-proliferative mitochondrial Reactive Oxygen Species (mROS). LEM provides a link between immune activation and the expansion of protective CD8⁺ T cells driven by OXPHOS and represents a pathway for the restoration of long-term protective immunity based on metabolically modified CTL.

 

If the production of ROS is protective against viruses and cancer, could putting C60 into the mitochondrial membrane and quenching the ROS cause problems? I know that the one rat study seemed to indicate the reverse, but if the ROS is actually protective, how would quenching them be other than non-protective? 

 

ROS mostly drives cancer rather than protecting us against it.  ROS are involved in initiation of cancer, in proliferation, angiogenesis, and metastasis.  If you can reduce mitochondrial ROS with a mitochondrial antioxidant (c60oo, mitoQ, mitoTEMPO, etc), you can suppress cancer.  However, ROS are also involved in signalling that is good for us-- in this case, LEM is up-regulating ROS to cause immune cell proliferation.  This is proliferation we want, unlike the proliferation of cancer cells that we don't want.  Biology being the diabolical thing that it is, ROS also activate several tumor suppressor genes like p53.  However, p53 is not normally located near the mitochondria, so it isn't as susceptible to mitochondrial ROS as are many pro-cancer genes.

 

The balance of all these ROS effects appears to be that c60oo is a net positive with respect to cancer, even if it theoretically subverts the action of LEM.  

[Kalliste]

Nature is promiscuous, everything gets used and reused a dozen times. I have not really seen anything that would indicate that viral infections are becoming worse by mito-stuff. Been wondering about it too of course. The paper on oxidative stress in Annelids did say very large doses of IAC decreased lifespan so if we megadose C60 all the time it might interfer with some vital pathway, there is a lot of crosstalk between ROS and other repair-systems.

 

Re hep C infection

 

CONCLUSIONS:

Administration of the mitochondria-targeted anti-oxidant mitoquinone significantly decreased plasma ALT and aspartate aminotransferase in patients with chronic HCV infection, and this suggests that mitoquinone may decrease necroinflammation in the liver in these patients. As mitochondrial oxidative damage contributes to many other chronic liver diseases, such as steatohepatitis, further studies using mitochondria-targeted anti-oxidants in HCV and other liver diseases are warranted.

http://www.ncbi.nlm....7?dopt=Abstract,

 

Re cancer

 

Abstract

Metastatic dissemination is of poor prognosis for cancer patients. When exploring glucose metabolism in metastatic progenitor cells, we recently found that several different dysfunctions sharing the ability of inducing mitochondrial superoxide production also promote tumor metastasis. Selective targeting of mitochondrial superoxide prevented spontaneous metastasis in mice, opening a new avenue for therapy.

 

Re the immunesystem

 

ABSTRACT

Barrier dysfunction of airway epithelium may increase the risk for acquiring secondary infections or allergen sensitization. Both rhinovirus (RV) and polyinosinic-polycytidilic acid [poly(I·C)], a double-stranded RNA (dsRNA) mimetic, cause airway epithelial barrier dysfunction, which is reactive oxygen species (ROS) dependent, implying that dsRNA generated during RV replication is sufficient for disrupting barrier function. We also demonstrated that RV or poly(I·C)-stimulated NADPH oxidase 1 (NOX-1) partially accounts for RV-induced ROS generation. In this study, we identified a dsRNA receptor(s) contributing to RV-induced maximal ROS generation and thus barrier disruption. We demonstrate that genetic silencing of the newly discovered dsRNA receptor Nod-like receptor X-1 (NLRX-1), but not other previously described dsRNA receptors, abrogated RV-induced ROS generation and reduction of transepithelial resistance (R_T) in polarized airway epithelial cells. In addition, both RV and poly(I·C) stimulated mitochondrial ROS, the generation of which was dependent on NLRX-1. Treatment with Mito-Tempo, an antioxidant targeted to mitochondria, abolished RV-induced mitochondrial ROS generation, reduction in R_T, and bacterial transmigration. Furthermore, RV infection increased NLRX-1 localization to the mitochondria. Additionally, NLRX-1 interacts with RV RNA and poly(I·C) in polarized airway epithelial cells. Finally, we show that NLRX-1 is also required for RV-stimulated NOX-1 expression. These findings suggest a novel mechanism by which RV stimulates generation of ROS, which is required for disruption of airway epithelial barrier function.

 

[tunt01]

 

If the production of ROS is protective against viruses and cancer, could putting C60 into the mitochondrial membrane and quenching the ROS cause problems? I know that the one rat study seemed to indicate the reverse, but if the ROS is actually protective, how would quenching them be other than non-protective? 

 

This is my main concern.  C60 seems a lot like glisodin to me, in that regard.  I'd like to see evidence that C60 doesn't shutdown endogenous antioxidant levels.  I think taking C60 effectively means you are on this product for life, because it becomes your body will become trained to different levels of ROS now that C60 is quenching a lot of this behavior.

 

And without knowing the correct human dosage, it may make it a very calculated risk as to what is the right amount over an extended period of time.

[sagafemina]

 

 

In a list of foods by polyphenol content (mg/100 g), EVOO is not even close to the top--

 

 

 

The particular type of polyphenols probably has a big effect on health promoting properties.  The ones in OO have been shown to have positive effects in various studies.

 

 

 

Of course the components vary considerably between plant sources, and there are non-food sources that have even more polyphenols than these--such as olive leaf extract.

 

See table 2 in  http://www.ncbi.nlm....es/PMC3779014/ 

 

 

This gets me a PNF error...do you have name/author?
 

[Turnbuckle]

Somehow the link is adding an extra backslash. Just delete it and the link will work.

 

Here it is again--

 

http://www.ncbi.nlm....cles/PMC3779014