5 replies to this topic

[nickdino]

http://www.ncl.ac.uk...nger-for-longer

https://www.fightagi...nt.php#comments

[hav]

Wow, they tested hydrogen per oxide as a suntan lotion... presumably in vitro:

Comparing the effects of mitochondrial targeted and localized antioxidants with cellular antioxidants in human skin cells exposed to UVA and hydrogen peroxide.

Howard

[PWAIN]

It would be interesting to feed this to mice and see if it has any positive effects.

[niner]

I don't have access to the full text, but looking at the structure of Tiron, the purported mitochondrial antioxidant, I find myself wondering what makes them think it's in fact a mitochondrial antioxidant. It's a benzene ring with two SO3(-) groups and two hydroxyls. That's going to be extremely hydrophilic, and isn't even the right charge to be attracted by the mitochondrial membrane potential. I guess they've come to this conclusion through some means or another, but I don't see it. I've seen Tiron variously called a ROS scavenger or a superoxide scavenger, and those are certainly generated in mitochondria, but that doesn't mean that Tiron specifically localizes there.

[Logic]

I don't have access to the full text, but looking at the structure of Tiron, the purported mitochondrial antioxidant, I find myself wondering what makes them think it's in fact a mitochondrial antioxidant. It's a benzene ring with two SO3(-) groups and two hydroxyls. That's going to be extremely hydrophilic, and isn't even the right charge to be attracted by the mitochondrial membrane potential. I guess they've come to this conclusion through some means or another, but I don't see it. I've seen Tiron variously called a ROS scavenger or a superoxide scavenger, and those are certainly generated in mitochondria, but that doesn't mean that Tiron specifically localizes there.

It seems that iron is freed from iron-sulphur enzymes within the cell by UVA.
The free iron reacts with ROS causing irreversible oxidative damage.
Tiron is able to chelate the iron inside the mitochondria.


"...In terms of mechanism, our study shows that UVA irradiation enhanced the increase in ROS production caused by the presence of the RC inhibitors. In this context, it has been postulated that iron may play a critical role in the modulation of UVA-induced oxidative damage. An increased presence of free iron further exacerbates oxidative damage through interaction with reactive oxygen intermediates via Fenton reactions. Studies have reported an increased level of iron subsequent to UVA irradiation, which has been shown to potentiate irreversible oxidative damage [43], [44] and [45]. Enzymes with iron–
sulphur (Fe–S) centres have been shown to be sensitive to modification by UVA rendering the enzyme inactive [46] and consequently resulting in the release and accumulation of free intracellular iron [47]. Interestingly, Fe–S centres are integral to the RC complexes I, II and III [48] which may make them vulnerable targets for photosensitisation and a potential hotspot for iron-mediated oxidative damage. Indeed our group has recently shown that tiron (4,5-dihydroxy-1,3-benzenedisulfonic) which chelates iron (and other metals), exhibits ROS scavenging properties and enters mitochondria, is able to prevent UVA and hydrogen peroxide induced mitochondrial DNA damage in human skin cells..."
http://www.sciencedi...213231714000950

So is the iron-triton product then able to leave the mitochondria, then the cell and be excreted, or are we just swapping the immediate problem for a buildup of molecules that will cause issues later?

Edited by Logic, 18 September 2014 - 06:35 AM.

[APBT]

FULL TEXT:  Comparing the effects of mitochondrial targeted and localized antioxidants with cellular antioxidants in human skin cells exposed to UVA and hydrogen peroxide