In article <drierac.47.00127105 at deakin.edu.au>, drierac at deakin.edu.au (Chris Driver) writes:
> Since posting my comments on free radical damage and ageing I have seen a
> number of comments posted on the bulletin board and some directed to me
> personally, some of them quite insulting. Nevertheless I want to thank all
> people who responded. I still think you have no case.
>> Some clear thinking is needed here. Proteins, and lipids can be damaged by
> many processes including free radicals. For some cells which no longer have
> the ability to renew these components, this matters. Thus there is convincing
> evidence that the deterioration of sperm cells and erythrocytes involves free
> radical damage.
>> In addition hypoxia/ischemia may impair cells ability to respond to stress and
> replace damaged proteins, etc. I will concede that it is likely that free
> radical damage contributes to the damage associated with
> ischemeia/reperfusion.
>> Therefore it seems likely that free radical blockers may contribute to the
> extension of good health, at least in some cases. So does safe driving!
>> However the best efforts of cell biologists have failed to find any consistent
> effect of radicals in cell culture. There is consistently a big zero on this
> one.
>> Furthermore in old age there are many cells which are still functionally
> intact. This most marked in the brain where some cells appear to deteriorate
> rapidly and neighbouring cells are uneffected. I read this in the mammalian
> literature and am finding it in Drosophila.
>> Furthermore it is possible to take cells from a very old human, transform them
> and produce immortal cell lines. There is not sufficient mutational damage to
> kill them.
Could you suggest any literature source? I don't really know a lot about
cell cultures, but as far as I know cells behave differently in the culture
than in the organism, and the mutational load might have nothing to do
with the immortality of a cell culture.
> Finally there is not one case in the literature that I can find where free
> radical blockers, retard a number of normal physiological declines. Without
> this data you have no case.
With respect to this notion, I was surprised to read a couple days ago that
overexpression of SOD leads to overexposure(!) to oxidative damage (the
examples given were the Down's syndrom and trangenic mice). Not that I
doubt the free radical theory in any way, it was just something unexpected.
>> Yours in hope, Chris Driver
Sincerely,
Alex Nikitin
