I want to say a bit on the phenomenology of antioxidants. Phenomenology here means "what we think we know", a phenomenological theory is usually the first thing scientists construct before they get a really good grip on things, and that's sort of where we're at.
Anti-oxidant means it's stopping an oxidant, which should be a clue here that the focus is on the oxidant, not the antioxidants, those just block it.
The oxidant, the enemy, is this guy:
http://en.wikipedia.org/wiki/Hydroxyl_radical#Biological_significance
Unlike superoxide, which can be detoxified by superoxide dismutase, the hydroxyl radical cannot be eliminated by an enzymatic reaction. Mechanisms for scavenging peroxyl radicals for the protection of cellular structures includes endogenous antioxidants such as melatonin and glutathione, and dietary antioxidants such as mannitol and vitamin E
Hydroxyl reacts with anything, so pretty much any one antioxidant is as good as another -- except thiols a la NAC, which serve a totally different purpose. This means that there is no one "super" antioxidant that will save you.
Antioxidant activity is measured by exposing a substance
or a group of substances to an oxidizer, and seeing how well they neutralize it.
The thing is, any compound, literally any compound, is toxic at some point, so you can't just pick one antioxidant, be it resveratrol, vitamin E, quercetin or whatever, and take lots of it. You'll hit the toxic level long before you reach enough antioxidant activity to do yourself any good.
It is better to have a lot of different antioxidants than any one compound. This way, the antioxidant activity is increased without bringing on the potentially toxic effects caused by overdoing it with this, that, or the other. This is why you will never hear a nutritionist who is not trying to sell you something say you need a particular antioxidant, they always say antioxidants in the plural. You get plural antioxidants by eating a varied diet with lots of vegetables, consuming varied and different things, tea, coffee, honey, rooibos, wine, beer, cannabis*, et cetera.
Studies that try to measure the effects of this-or-that antioxidant are, in my totally unqualified opinion, playing whack-a-mole when the right option is simply to hit all the holes at once, see if it gets away from us then.
Of course, this leaves one gaping hole that is oh-so-relevant:
mitochondrial hormesis, the theory that oxidative stress induces the body's natural healing mechanism:
http://www.cell.com/cell-metabolism/retrieve/pii/S1550413107002562
There is also a proposed role of reactive oxygen species in regulation of normal bodily functions:
http://jcb.rupress.org/content/194/1/7.short
I am afraid these theories do not quite satisfy me because they fail to explain why we do indeed see increased lifespan in people who consume antioxidant-rich diets, tea etc, generally referred to as "plant-based diet" because animal tissues are poor sources of antioxidants (except GSH):
http://en.wikipedia.org/wiki/Longevity#Longevity_and_lifestyle
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A bit on the history of pyrroloquinoline quinone, aka PQQ, aka the novel putative vitamin. Historically, many, many compounds have been proposed as vitamins and then withdrawn. This is why the sequence of B vitamins includes B1 thiamin, B2 riboflavin, B3 niacin, B5 pantothenate, B6 pyridoxal, B7 biotin, B9 folate, B12 cobalamin -- B4, B8, B10, and B11 were later withdrawn as were B13, B14, B15, B16 and B17. The jury remains out on PQQ (jury also still out on choline), but let's go to the record.
In 2003, the famous Kasahara and Kato publish a report in
Nature detailing the role of PQQ in lysine metabolism, suggesting it may be a novel vitamin in mammals.
http://www.shanghaimed.cn/bookpic/upFileDown/201051818383010617.pdf (Kasahara and Kato, 2003)
Two years later, two papers in
Nature, one by Rucker et al, one by Felton and Anthony, attack this hypothesis. Rucker states that PQQ status does not affect the presence or absence of lysine-metabolizing enzymes, a biomarker for lysine metabolism. Fenton and Anthony state that the proposed PQQ-dependent enzyme was misidentified, and has a novel structure but does not use PQQ.
Nature was furious, and published both.
http://www.nature.com/nature/journal/v433/n7025/abs/nature03323.html (Rucker et al 2005)
http://www.nature.com/nature/journal/v433/n7025/abs/nature03322.html (Fenton and Anthony 2005)
The next year, Bauerly et al publish a report in
Biophysica Acta confirming K&K and stating that PQQ status does indeed affect lysine metabolism, regardless of alpha-aminoadipate semialdehyde dehydrogenase! The authors go on to state that PQQ's known, novel and poorly understood role in mitochondriogenesis -- the generation of new mitochondria -- may explain its role in lysine metabolism.
Nature has had more than enough of this bullshit.
http://cat.inist.fr/?aModele=afficheN&cpsidt=18265312 (Bauerly et al 2006)
In 2009, Rucker, Chowanadisai and Nakano -- the same Rucker as before -- publish an article in
Alternative Medicine stating "PQQ is a novel biofactor for which a proposition can be made for physiological importance." Again he cites the role of PQQ in mitochondriogenesis. This represents a partial -- mind you I said
partial -- reversal of Rucker's initial position, but
not a suggestion that PQQ is a mammalian enzyme cofactor:
http://www.researchgate.net/publica...quinoline_quinone/file/d912f50609e366fa89.pdf (Rucker et al 2009)
Anthony, by contrast, remains firmly in the "not a cofactor, not a vitamin" camp, with a well-cited presentation on his website of why he thinks so.
http://www.chris-anthony.co.uk/myresearch.html#pqqvit
So, is PQQ vital to life?
http://www.youtube.com/watch?v=fpaQpyU_QiM
*smoking is bad
