Chris Driver wrote:
>The free radical theory has been around for nearly five decades now. Time
>enough for workers to tie it down and develop commercial anti-oxidants
>which will substantially extend human lifespan. This has not happened.
I think you made a very good point here. It seems clear to me that the most
popular version of the free radical theory of aging, as presented by the
media and vitamin industry, and promoting antioxidants as the fountain of
youth, is false.
In response to Chris Driver, Peter Proctor wrote:
>See my review in CRC Handbook of Free Radicals
>and Antioxidants, vol 1, 1989. Hundreds of diseases. IMHO, the
>expression " Free Radical Pahology " is redundant.
>>As for atherosclerosis, cancer, etc. The vast majority of the people
>reading this post will die of a free radical-related disease.
It is very easy to suggest, e.g. in the discussion of a scientific paper,
that a certain disease may be caused by free radicals. Because of the
elusive and ubiquitous nature of free radicals, it would be very difficult
for anyone to prove the author wrong.
If you want to be absolutely sure that your hypothesis can never be
proven wrong, you can always say that free radicals "may be involved"
in the pathogenesis of the disease. It is a lot easier to say that than to
say: "In conclusion, we really don't have a clue what causes this
>Don't confuse the experimental difficulties and the limitations
>of ( e.g., ) antioxidant supplimentation with evidence against
>a role for free radiacals in aging. We may be looking at the wrong
>thing. E.g., antioxidants may not work in mitochondrial radical-induced
Mitochondria would certainly be the first place look for free radical
induced damage. But the evidence for such damage occurring at a
significant level in aging is still missing.
It was recently shown by Hayashi et al. (J Biol Chem, 269(9):6878-
6883, 1994) with a very neat experiment that the age-related
mitochondrial hypofunction found in human skin fibroblasts is not
caused by defects in the mitochondrial DNA (mtDNA). Intercellular
transfer of HeLa nuclear genome to fibroblasts from an aged donor
restored the activity of the mitochondrial enzyme cytochrome oxidase
(COX), a marker of mitochondrial function.
Also, transfers of mtDNA from old and young subjects to HeLa cells
that don't have mtDNA showed that mtDNA from old subject was
functionally intact. The levels of COX activity and synthesis of
mitochondrial proteins was the same, irrespective of whether the
mtDNA was from aged or fetal donors.
Kimmo Hatanpaa, M.D.