31 replies to this topic

[cbohrson]

From
Bio-Applications of Nanoparticles

Chapter 13:
Toxicity Studies of Fullerenes and Derivatives

See the later part of:

Abstract
Due to their unique properties, fullerenes, a model of carbon-based nanoparticles, have
attracted considerable interest in many fields of research including material science
and biomedical applications. The potential and the growing use of fullerenes and
their mass production have raised several questions about their safety and environmental impact.
Available data clearly shows that pristine C60 has no acute or sub-acute toxicity in a large
variety of living organisms, from bacteria and fungal to human leukocytes, and also in drosophila,
mice, rats and guinea pigs. In contrast to chemically—either covalently or noncovalently—
modified fullerenes, some C60 derivatives can be highly toxic. Furthermore, under light exposure,
C60 is an efficient singlet oxygen sensitizer. Therefore, if pristine C60 is absolutely nontoxic
under dark conditions, this is not the case under UV-Visible irradiation and in the presence of
O2 where fullerene solutions can be highly toxic through 1O2 formation.

Papers that were referenced in support of this later in the chapter (I haven't had time to look at them):

Sera N, Tokiwa H, Miyata N. Mutagenicity of the fullerene C60-generated singlet oxygen dependent
formation of lipid peroxides. Carcinogenosis 1996; 17(10):2163-9.

Yamago S, Tokuyama H, Nakamura E et al. In vivo biological behavior of a water-miscible fullerene:
14C labeling, absorption, distribution, excretion and acute toxicity. Chem Biol 1995; 2:385-9.

Boutorine AS, Tokuyama H, Takasugi M et al. Fullerene-oligonucleotide conjugates: Photoinduced
sequence-specific DNA cleavage. Angew Chem Int ed Engl 1994; 33(23-24):2462-5.

Thoughts?

[niner]

This sounds like it's based on in vitro experiments, where the light intensity, UV content, and concentration of free oxygen can be vastly higher than inside the human body, particularly inside the membranes where C60-oo localizes. If the light-induced singlet oxygen production they're considering were a problem in vivo, then you'd expect to see photo-sensitization, and people would be getting sunburned from small amounts of sun exposure. Instead, we're seeing just the opposite, where it's taking more sun exposure than prior to C60-oo use to induce a burn.

[cbohrson]

That makes sense. However, is it true that the damage to biomolecules or DNA caused by singlet oxygen would manifest itself as a sunburn, or even cause pain or discomfort?

My understanding is that sunburn is caused by "direct DNA damage", or the dimerization of thymine base pairs on exposure to UV-B radiation. Singlet oxygen wouldn't necessarily work this way. The studies seem to document just a general increase in ROS.

[niner]

That makes sense. However, is it true that the damage to biomolecules or DNA caused by singlet oxygen would manifest itself as a sunburn, or even cause pain or discomfort?

My understanding is that sunburn is caused by "direct DNA damage", or the dimerization of thymine base pairs on exposure to UV-B radiation. Singlet oxygen wouldn't necessarily work this way. The studies seem to document just a general increase in ROS.

ROS and singlet oxygen are generally inflammatory and can oxidatively damage DNA, so if they were being generated in the upper layers of skin in sufficient numbers, I'd expect a sunburn-like response. UVB does cause thymine dimers, but there is also other free radical damage. It looks like TT dimerization is the biggest factor, but I suspect that free radical damage is responsible for at least some of the inflammation. If T-T creation exceeds the capacity of DNA repair systems, that's probably what triggers the apoptotic response seen in a bad sunburn, which shows up as peeling. I would imagine that other forms of radical-induced damage could also trigger apoptosis.

You're probably right that a small amount of singlet oxygen could cause damage that we wouldn't feel. If sunburn is mostly due to direct photo-induced TT dimerization, and C60 reduces sunburn response, one has to wonder how that's occurring. Is the C60 acting as a chromophore, absorbing UV before it hits the DNA, but creating species that are ultimately more harmful than a TT dimer? Or, in the environment of the cell, does something more benign happen? C60 seems to be extremely good at disarming ROS, so maybe if one molecule creates a radical, another will catch it? Somewhere along the line, there has to be an ultimate reducing agent that is the sink for these electrons, but I'm not sure what that is going to be.

Someone should do an in vivo experiment where an animal is dosed with C60-oo, exposed to UV, and effect on ROS levels in skin are compared to un-dosed animals.

[Lister]

I’ve spent more time in the sun this summer than I did last summer. Last summer I burnt and peeled regularly. While I’ve burnt a few times this summer there’s never been any peeling and it fades extremely quickly (within 12 hours). I didn't use sunscreen at all this summer.

It seems as though we can credit the OO alone for some of the skin regeneration. I get the impression though the extended periods of sun exposure I can endure without burning is down to the C60. If I had to put a figure on it I would add an extra 60 minutes of sun exposure while dosing C60 over not.

This result seems to be similar to others regardless of dose size/frequency. (I’m at 2mg/day)

Beyond this though if there is deeper harm being caused I can't tell.

Edited by Lister, 31 August 2012 - 07:14 PM.

[cbohrson]

Also found this, which documents increased ROS production after intragastric administration of C60 suspended in corn oil.

http://ehp03.niehs.n....1289/ehp.11922

[Turnbuckle]

Also found this, which documents increased ROS production after intragastric administration of C60 suspended in corn oil.

http://ehp03.niehs.n....1289/ehp.11922

And they found corn oil was even worse--

Suspension of particles in saline solution or corn oil yielded a similar extent of genotoxicity, whereas corn oil per se generated more genotoxicity than the particles.

[platypus]

I’ve spent more time in the sun this summer than I did last summer. Last summer I burnt and peeled regularly. While I’ve burnt a few times this summer there’s never been any peeling and it fades extremely quickly (within 12 hours). I didn't use sunscreen at all this summer.

Excuse me but why do you choose to burn several times per summer, i.e. what are the benefits? My motto has always been "only idiots burn", which sometimes hits some if I've forgotten to reapply sunscreen often enough.

[cbohrson]

Also found this, which documents increased ROS production after intragastric administration of C60 suspended in corn oil.

http://ehp03.niehs.n....1289/ehp.11922

And they found corn oil was even worse--

Suspension of particles in saline solution or corn oil yielded a similar extent of genotoxicity, whereas corn oil per se generated more genotoxicity than the particles.

Wow, that's a huge caveat. Sorry for not reading more carefully.

Still note, however:

ROS-generating ability

Figure 1 shows ROS generation of particles in aqueous solution. The ROS generation was 3.3-fold (95% CI, 2.1–4.5) and 5.5-fold (95% CI, 4.2–6.6) in incubations containing SWCNT at 1 and 10 μg/mL, respectively. The C₆₀ fullerenes increased ROS production at the highest dose by 1.6-fold (95% CI, 1.5–1.9). SRM2975 and carbon black increased the level of ROS production by 4.4-fold (95% CI, 4.3–4.5) and 7.6-fold (95% CI, 7.4–7.9), respectively, at 10 μg/mL (Figure 1).

Ans also:

Oxidatively damaged DNA

Figure 2 shows the level of 8-oxodG in colon, liver, and lung tissue of rats administered C₆₀ fullerenes and SWCNT dispersed in either saline or corn oil. We observed significant single-factor effects of corn oil, which was associated with 25% (95% CI, 12–40), 30% (95% CI, 20–40), and 38% (95% CI, 29–47) higher level of 8-oxodG in the colon, liver, and lung, respectively.
We found no interactions between type of vehicle and particle exposure, indicating that particles in corn oil generated the same level of DNA damage as particles in saline. The generation of 8-oxodG is based on data from both types of vehicles (corresponding to estimates of single-factor effects). In the liver, the exposure to C₆₀ fullerenes was associated with 17% (95% CI, 4–34) and 25% (95% CI, 11–41) increases of 8-oxodG in groups treated with the low dose and high dose of particles, respectively. Exposure to SWCNT increased the level of 8-oxodG in the liver by 22% (95% CI, 8–38) and 20% (95% CI, 7–36) in the rats given the low dose and high dose, respectively. There were increased levels of 8-oxodG in the lung after exposure to SWCNT at both the low [21% (95% CI, 9–33)] and high doses [23% (95% CI, 11–35)], whereas only the high dose of C₆₀ fullerenes was associated with significantly elevated levels of 8-oxodG in the lung [18% (95% CI, 4–31)]. Oral exposure to particles was not associated with increased levels of 8-oxodG in colon mucosa tissue.

This still seems odd, especially given how significant C60 fullerene's effects are supposed to be.

Edited by cbohrson, 01 September 2012 - 05:37 PM.

[Turnbuckle]

This still seems odd, especially given how significant C60 fullerene's effects are supposed to be.

Perhaps not since these particles were not dissolved and previous poor results for C60 have been blamed (correctly or incorrectly) on the presence of incompletely dissolved particles.

[zorba990]

Also found this, which documents increased ROS production after intragastric administration of C60 suspended in corn oil.

http://ehp03.niehs.n....1289/ehp.11922

And they found corn oil was even worse--

Suspension of particles in saline solution or corn oil yielded a similar extent of genotoxicity, whereas corn oil per se generated more genotoxicity than the particles.

Wow, that's a huge caveat. Sorry for not reading more carefully.

Still note, however:

ROS-generating ability

Figure 1 shows ROS generation of particles in aqueous solution. The ROS generation was 3.3-fold (95% CI, 2.1–4.5) and 5.5-fold (95% CI, 4.2–6.6) in incubations containing SWCNT at 1 and 10 μg/mL, respectively. The C₆₀ fullerenes increased ROS production at the highest dose by 1.6-fold (95% CI, 1.5–1.9). SRM2975 and carbon black increased the level of ROS production by 4.4-fold (95% CI, 4.3–4.5) and 7.6-fold (95% CI, 7.4–7.9), respectively, at 10 μg/mL (Figure 1).

Ans also:

Oxidatively damaged DNA

Figure 2 shows the level of 8-oxodG in colon, liver, and lung tissue of rats administered C₆₀ fullerenes and SWCNT dispersed in either saline or corn oil. We observed significant single-factor effects of corn oil, which was associated with 25% (95% CI, 12–40), 30% (95% CI, 20–40), and 38% (95% CI, 29–47) higher level of 8-oxodG in the colon, liver, and lung, respectively.
We found no interactions between type of vehicle and particle exposure, indicating that particles in corn oil generated the same level of DNA damage as particles in saline. The generation of 8-oxodG is based on data from both types of vehicles (corresponding to estimates of single-factor effects). In the liver, the exposure to C₆₀ fullerenes was associated with 17% (95% CI, 4–34) and 25% (95% CI, 11–41) increases of 8-oxodG in groups treated with the low dose and high dose of particles, respectively. Exposure to SWCNT increased the level of 8-oxodG in the liver by 22% (95% CI, 8–38) and 20% (95% CI, 7–36) in the rats given the low dose and high dose, respectively. There were increased levels of 8-oxodG in the lung after exposure to SWCNT at both the low [21% (95% CI, 9–33)] and high doses [23% (95% CI, 11–35)], whereas only the high dose of C₆₀ fullerenes was associated with significantly elevated levels of 8-oxodG in the lung [18% (95% CI, 4–31)]. Oral exposure to particles was not associated with increased levels of 8-oxodG in colon mucosa tissue.

This still seems odd, especially given how significant C60 fullerene's effects are supposed to be.

Study says :
Oral exposure to low doses of C₆₀ fullerenes and SWCNT.

So they would need to remove the SWCNT, single waled carbon nanotubes from the equation for this to be an issue with C60. UNless they kept things really pristine (no cross contaminations).

Edited by zorba990, 01 September 2012 - 09:31 PM.

[Hebbeh]

So they would need to remove the SWCNT, single waled carbon nanotubes from the equation for this to be an issue with C60. UNless they kept things really pristine (no cross contaminations).

My understanding is they didn't dose C60 and SWCNT concurrently but seperately and the results were measured and reported seperately.

[Turnbuckle]

Study says :
Oral exposure to low doses of C₆₀ fullerenes and SWCNT.

So they would need to remove the SWCNT, single waled carbon nanotubes from the equation for this to be an issue with C60. UNless they kept things really pristine (no cross contaminations).

No, you really need to go to the study. They looked at several things, C60, carbon tubes, printer's black, and they were all suspended in corn oil or water, not dissolved. In Figure 1 you see a significant bump over the controls when you get to the highest dose, but not for C60, which was almost flat for all doses.

Attached Files

•  C60 in corn oil.png   71.74KB   24 downloads

Edited by Turnbuckle, 01 September 2012 - 10:00 PM.

[niner]

This is a really screwy study. They say:

We observed an effect of corn oil in all three organs. This was not part of our a priori hypothesis. We chose the volume of corn oil to be identical to that of the saline solution (200 μL), which would allow a reasonable volume for the suspension in the aqueous solution. It should be emphasized that corn oil is rich in polyunsaturated fatty acids and was sonicated, which might produce genotoxic compounds. In addition, rat studies indicated that a diet rich in corn oil increased 8-oxodG excretion in urine (Loft et al. 1998) as well as the levels of 5-hydroxymethyl-2′-deoxyuridine, another marker of oxidatively damaged DNA in blood and mammary gland tissue (Djuric et al. 2001).

They mention this rather briefly, but doesn't it kind of blow their hypothesis? They really had some large vehicle effects in vivo, although they claim statistical significance for effects in some tissues, though they aren't much larger than controls, if you look at fig 2, for example. I don't know what to make of their light scattering results. They sonicated these mixtures, 10 hours a day for five days! How the hell do they even know what they have at that point, if they don't do any chemical analysis on it? They wonder how the particulates could have had a systemic effect, but maybe there were various and sundry dissolved compounds, with god only knows what properties, as a result of all that sonication. Shouldn't they have ended up with polyhydroxy C60 agglomerates in the aqueous medium? And corn oil being a triglyceride, they should have gotten some adducts there, I'd think. I didn't see any mention of color change in the corn oil, but I might have missed it.

Technical note: The word "sonication" was not in FireFox's spell checker, though it helpfully suggested that I meant "fornication". Maybe it has a point...

[sanjosegeek]

Funny, I just put some c60 in corn oil tonight, this is what it looks like after 2 hours:  c6cornOil1.jpg   64.8KB   8 downloads

It has a deep red color already.

I plan to start a canola oil solution tomorrow.

And in answer to the unanswered question, I really, seriously dislike the taste of olive oil.

Edited by Some_Asshole, 02 September 2012 - 07:41 AM.

[Turnbuckle]

They sonicated these mixtures, 10 hours a day for five days! How the hell do they even know what they have at that point, if they don't do any chemical analysis on it?

Spot on.

But I take back what I said about these things not being dissolved. The there must have been a supersaturated solution with all this sonication. So when Fig. 1 shows an almost flat curve for a C60 concentration over four orders of magnitude, we can reasonably conclude it has almost no impact on the level of ROS.

Edited by Turnbuckle, 02 September 2012 - 12:19 PM.

[niner]

Funny, I just put some c60 in corn oil tonight, this is what it looks like after 2 hours: [pic]
It has a deep red color already.

I plan to start a canola oil solution tomorrow.

And in answer to the unanswered question, I really, seriously dislike the taste of olive oil.

First of all, Best Name Ever! Thanks for the lulz. Corn oil reacted really quickly; that's a lot faster than olive oil, isn't it? Maybe higher concentrations of PUFA react faster? Some olive oil tastes horrible, others not- It's really variable. If you got a "light" olive oil, it would probably taste like the other vegetable oils, though you'd be giving up the beneficial polyphenols.

[mikey]

I've heard sonication used in reference to making liposomal nutrients. For instance, vitamin C, water and lecithin, which yields phosphatidylcholine are sonicated in an ultrasonic device to create liposomal vitamin C. That's vitamin C encapsulated in a lipid bilayer that matches the lipid bilayer on cell walls. Since the liposomal bilayer docks up to the cell wall, vitamin C is delivered into the cell at a tremendously higher rate than if it was just vitamin C, which is water soluble. Liposomal vitamin C is said to be absorbed into cells at about 90%, where IV vitamin C is about 20%. See lots of data on one of the best vendors of liposomal nutrients at: http://www.livonlabs.com/

This is a really screwy study. They say:

We observed an effect of corn oil in all three organs. This was not part of our a priori hypothesis. We chose the volume of corn oil to be identical to that of the saline solution (200 μL), which would allow a reasonable volume for the suspension in the aqueous solution. It should be emphasized that corn oil is rich in polyunsaturated fatty acids and was sonicated, which might produce genotoxic compounds. In addition, rat studies indicated that a diet rich in corn oil increased 8-oxodG excretion in urine (Loft et al. 1998) as well as the levels of 5-hydroxymethyl-2′-deoxyuridine, another marker of oxidatively damaged DNA in blood and mammary gland tissue (Djuric et al. 2001).

They mention this rather briefly, but doesn't it kind of blow their hypothesis? They really had some large vehicle effects in vivo, although they claim statistical significance for effects in some tissues, though they aren't much larger than controls, if you look at fig 2, for example. I don't know what to make of their light scattering results. They sonicated these mixtures, 10 hours a day for five days! How the hell do they even know what they have at that point, if they don't do any chemical analysis on it? They wonder how the particulates could have had a systemic effect, but maybe there were various and sundry dissolved compounds, with god only knows what properties, as a result of all that sonication. Shouldn't they have ended up with polyhydroxy C60 agglomerates in the aqueous medium? And corn oil being a triglyceride, they should have gotten some adducts there, I'd think. I didn't see any mention of color change in the corn oil, but I might have missed it.

Technical note: The word "sonication" was not in FireFox's spell checker, though it helpfully suggested that I meant "fornication". Maybe it has a point...

[cbohrson]

Ok -- I referred to this other study because I thought perhaps there might be a connection to light exposure here. But it seems like we can account for the ROS produced in this experiment by other means.

Does anyone have any further insights on this light issue? Could fur, or the fact that the rats were likley kept indoors, have confounded results in the Baati stud? Note that in the studies I referred to in the first post both visible and UV light caused C60 to induce increased oxidative stress.

[jakeb]

Anyone have any other thoughts on what to make of this? I'm trialling topical c60 for hairloss and I'm concerned about the UV issue. I'm applying at night and attempt to avoid excessive UV exposure, but I certainly don't want to make things worse.

[Kevnzworld]

Anyone have any other thoughts on what to make of this? I'm trialling topical c60 for hairloss and I'm concerned about the UV issue. I'm applying at night and attempt to avoid excessive UV exposure, but I certainly don't want to make things worse.

From this
http://www.anti-agin...012/11/12/1424/

These factors have led many scientists to caution about possible biological impacts of C60.  One known negative impact is that C60 cannot be used as a basis of a skin cream because when it is photo-excited it produces destructive singlet oxygen radicals. In general, there seems to be
mixed evidence and little agreement about overall negative effects of C60. 

http://ijt.sagepub.c.../3/197.abstract
Is the study VG may have relied on.

Edited by Kevnzworld, 22 November 2012 - 03:11 AM.

[Anthony_Loera]

I guess he saw the interview with Professor Fathi Moussa.

Great!

A

[niner]

Anyone have any other thoughts on what to make of this? I'm trialling topical c60 for hairloss and I'm concerned about the UV issue. I'm applying at night and attempt to avoid excessive UV exposure, but I certainly don't want to make things worse.

From this
http://www.anti-agin...012/11/12/1424/

These factors have led many scientists to caution about possible biological impacts of C60. One known negative impact is that C60 cannot be used as a basis of a skin cream because when it is photo-excited it produces destructive singlet oxygen radicals. In general, there seems to be
mixed evidence and little agreement about overall negative effects of C60.

http://ijt.sagepub.c.../3/197.abstract
Is the study VG may have relied on.

Has anyone ever seen any evidence that c60 could be a problem with both realistic concentrations of c60 and realistic light intensity? I don't recall any. When cells are soaked for hours in high concentrations of c60 compounds, then illuminated with lasers or high intensity lamps, stuff happens. The relevance of this to humans is questionable, to say the least.

[cbohrson]

Hello again,

I did find this, which I believe is the primary source for the authors of the reference I posted originally for saying that C60 can produce singlet oxygen when irradiated.

Mutagenicity of the fullerene C60-generated singlet oxygen
dependent formation of lipid peroxides

The methods section of this paper is pushing the limits of my understanding. Its clear they discuss the light intensity here:

Mutagenicity test
The mutagenicity test was performed according to the procedure reported
previously (15). All of the procedures of the plate incorporation assay with
or without S9 in the absence of cofactors were performed under irradiation
by visible light (100 W fluorescent light with 400-600 nm at a distance of
25 cm) for 20 nun or without irradiation in the dark room, and the plates
were then incubated aerobically for 48 h or in anaerobic Gas Pak jars (BBL
Microbiology Systems, Cockeysville, MD) for 16 h and incubated aerobically
for an additional 32 h.

I'm having more difficulty, however, deciphering how exactly they exposed cells to C60. I'd appreciate a second set of eyes here. I'm pretty sure this part is important:

Mutagenicity of C6o after irradiation by visible light
C60 is a non-polar compound, insoluble in distilled water and
dimethylsulfoxide, but was soluble at a concentration of 300
microgram/ml in PVP as a cofacter of solubility. To determine the
mutagenicity of Qo in Salmonella strains TA102, TA104 and
YG3OO3, C60 dissolved in PVP was bioassayed in the presence
or absence of S9 fraction without cofactor.

Edited by cbohrson, 16 January 2013 - 05:49 PM.

[Chupo]

Is irradiation by light different from irradiation by x-ray? Is there any need to worry if our C60oo gets x-rayed during transport? I would think it only matters in vivo and that the C60 would be protective, no?

[niner]

Is irradiation by light different from irradiation by x-ray? Is there any need to worry if our C60oo gets x-rayed during transport? I would think it only matters in vivo and that the C60 would be protective, no?

Visible light and x-rays are both photons, but they are wildly different in energy and interact with matter in very different ways. If c60 is x-rayed in transport, I think that it would be very difficult to tell a difference, mostly because the x-ray flux is so low. I don't think there's anything to worry about there.

[Chupo]

Is irradiation by light different from irradiation by x-ray? Is there any need to worry if our C60oo gets x-rayed during transport? I would think it only matters in vivo and that the C60 would be protective, no?

Visible light and x-rays are both photons, but they are wildly different in energy and interact with matter in very different ways. If c60 is x-rayed in transport, I think that it would be very difficult to tell a difference, mostly because the x-ray flux is so low. I don't think there's anything to worry about there.

Ahh. Thank you, Niner.

[cbohrson]

Okay, some quick analysis:

100W light bulb, distance of 25 cm = .25 m

Power per unit meter = (4*pi*r^2)/(bulb power) = (4*pi*.25^2)/100 = 127 Wm^-2
All of this is visible light in the 400-600 nm range.

According to wikipedia, the intensity of sunlight at the Earth's surface in the visible range is 445Wm^-2.
In the study above cells were exposed to this light for only 20 minutes.

I'm not trying to be alarmist, but people get at least comparable visible light exposure on a daily basis from the sun, and in actuality probably well more than what was used in the study. It seems plausible to me that UV/visible light could penetrate the top layers of the skin and produce significant amounts of singlet oxygen through interaction with C60. Consequences due to this type of interaction may not have been noticed in the rat life extension study because of the fact that the rats were kept in a laboratory environment and rarely (if ever) exposed to light intensity comparable to that used in the study or sunlight.

That said, I will admit I'm not in a good position to evaluate whether the concentration used in the study is comparable to what might be found in human skin after supplementation with C60 in OO. For anyone who wants to venture an answer in this study the authors used 300 micrograms of C60 dissolved in polyvinylpyrrolidone (PVP). Don't raise your eyebrows over the PVP part -- I think its unlikely that it has any role in the singlet oxygen production http://en.wikipedia....inylpyrrolidone.

[niner]

That said, I will admit I'm not in a good position to evaluate whether the concentration used in the study is comparable to what might be found in human skin after supplementation with C60 in OO. For anyone who wants to venture an answer in this study the authors used 300 micrograms of C60 dissolved in polyvinylpyrrolidone (PVP). Don't raise your eyebrows over the PVP part -- I think its unlikely that it has any role in the singlet oxygen production http://en.wikipedia....inylpyrrolidone.

Concentration is really where this paper falls apart. 300 ug/ml is 0.3mg/ml, which is more than one third the concentration of the c60-oo products on the market (which are 800ug/ml = 0.8mg/ml). We are consuming a relatively small number of ml of the c60-oo solution orally, which means that is it diluted wildly, having an entire human to disperse into, not to mention whatever amount is eliminated, which may be non-trivial. In the paper, the cells that they are looking at are literally soaked in this high concentration, and all of the mechanisms that would normally prevent the c60 from reaching the cell have been circumvented. I would guesstimate that the concentration of c60-oo in our cells might be 1/10,000 the level in this experimental system. After being drenched with c60, these naked cells that were never expected to see the light of day are exposed to a moderately intense photon flux. In humans, on the other hand, our skin is covered with an outer layer that absorbs and diffuses light. The rest of our cells are buried, so photo-produced radicals aren't going to be an issue. The salmonella strain that they're using as their experimental system is rather mutation-prone, probably a lot more so than human cells. I don't know if PVP entered into these results or not, but it has a fair amount of biological activity, as Miyata's group has noted in some of their other papers. It's also worth considering the difference between pristine c60 in PVP versus c60-oo. Because of its amphipathic nature, c60-oo will preferentially localize in membranes, while the c60 PVP concoction is more strange. The c60 will be enclosed in the PVP, maybe a little bit like a micelle, which might keep it in the aqueous phase, where the nucleic acids would be found. It's just a very different situation.

So far, the observation of a number of people using c60-oo and exposing themselves to a lot of sunlight is usually a suppression of sunburn. I don't think there have been any reports of a higher level of sunburn for a given exposure, so that would seem to be evidence against there being a dangerous photo effect with c60-oo.

[cbohrson]

I agree with most of your points about the flawed direct applicability of the study. However, what it still does tell us is that in some concentration, and under some intensity of UV/visible light, C60 is capable of producing singlet oxygen.

This is the point I have trouble with, per arguments discussed earlier in the thread about the mechanism behind sunburn:

So far, the observation of a number of people using c60-oo and exposing themselves to a lot of sunlight is usually a suppression of sunburn. I don't think there have been any reports of a higher level of sunburn for a given exposure, so that would seem to be evidence against there being a dangerous photo effect with c60-oo.

The mechanism behind sunburn does not have to do with singlet oxygen or even increased ROS exposure. Apparently the latest research shows it has to do with direct damage to RNA (edit: better link here) which sets off a cascade of inflammatory responses. Less incidence of sunburn among C60 users could indicate that this damaged RNA is somehow being repaired with increased frequency, but I see this as unlikely. The more likely scenario I think is that the C60 is directly capturing some of the incident radiation and preventing RNA damage in that way. Singlet oxygen production could be increasing and the skin would remain unburned.

Note that it has been shown before that certain sunscreens increase ROS exposure in the skin. Insofar as it could be a cellular sunscreen, C60 could be doing something similar. I don't agree with the logical step that less sunburn implies no dangerous photo effect with c60-oo. In fact I almost see it as more likely, because we need to account for where the energy in the UV light is going and the only published results on the interaction between light and C60 indicate increased singlet oxygen production.

Edited by cbohrson, 18 January 2013 - 06:25 AM.