When the body fights oxidative damage, it calls up a reservist enzyme that protects cells – but only if those cells are relatively young, a study has found.
Biologists at USC discovered major declines in the availability of an enzyme, known as the Lon protease, as human cells grow older.
A protease is an enzyme that breaks down peptides (pieces of protein). So this enzyme does not neutralize free radicals. It breaks down proteins damaged by chemicals that rampage thru the cell doing damage. Without enough Lon (and other proteases as well) damaged pieces will accumulate in a cell. This has a number of undesirable consequences such as taking up space that would get used by functional proteins. Also, the damaged proteins will in some cases do wrong things such as generate reactive species that do even more damage. Aging is a vicious cycle where damage causes even more damage.
Would a drug be capable of boosting Lon activity? Is that even the right response to the problem found by these researchers?
The finding may help explain why humans lose energy with age and could point medicine toward new diets or pharmaceuticals to slow the aging process.
The researchers showed that when oxidative agents attack the power centers of young cells, the cells respond by calling up reinforcements of the enzyme, which breaks up and removes damaged proteins.
As the cells age, they lose the ability to mobilize large numbers of Lon, the researchers reported in The Journals of Gerontology.
A cell that does not have enough Lon protease has likely accumulated a lot of damage. The low Lon protease might even be the result of damage to mitochondria where the cell loses the ability to generate enough energy. It would not surprise me if the cell basically turns off optional systems like Lon when energy levels drop too lo. So just trying to boost Lon might not work.
If boosting Lon is either not practical or useful then what? I see two options: Fix the root cause of low Lon. If the root cause is damaged mitochondrial DNA then send in gene therapy to fix the mitochondria. Another option: Try to kill cells that do not make enough Lon. Then neighboring cells or stem cells could divide to replace them. That's an approach that would need selective control so that you don't die due to an organ suddenly failing due to excessive cell loss. Also, cell therapies would be needed to replace cells in organs that have limited repair capability (e.g. the heart).
|Share |||Randall Parker, 2011 September 10 08:59 AM Aging Mechanisms|