The free radical debate continues
Many believe that free radicals – potentially toxic by–products of the body's vital activity - are one of the main components of the aging process. However, a number of studies conducted in recent years indicate the validity of the opposite hypothesis.
Canadian researchers from McGill University, working under the leadership of Professor Siegfried Hekimi, confirmed previously obtained data that free radicals increase the lifespan of experimental model organisms – roundworms Caenorhabditis elegans. They found that free radicals act on a molecular mechanism that, under other conditions, triggers the process of programmed cell death – apoptosis.
Apoptosis is the self–destruction of a damaged cell that occurs in various situations: to prevent cell malignancy or the development of an autoimmune disease, or to destroy cells infected with viruses. The key molecular mechanism of apoptosis has remained virtually unchanged in all animals, but it was first discovered in experiments on C.elegans and brought researchers the Nobel Prize.
The authors found that when adequately stimulated by free radicals, this molecular cascade strengthens the cell's defense mechanisms and increases the lifespan of the organism.
According to Professor Hekimi, the mechanisms of apoptosis of human cells have been very actively studied due to their exceptional importance in the functioning of immune mechanisms and the development of malignant tumors. To date, there are already quite a large number of pharmacological drugs that affect the signaling cascade that triggers apoptosis. However, finding ways to increase life expectancy by influencing this mechanism is not an easy task.
Hekimi also believes that targeting the mechanism of apoptosis may be particularly useful in the treatment of neurodegenerative diseases. Due to the complexity of replacing dying neurons with new cells, apoptotic signals in the central nervous system can be partially redirected to increase the viability of damaged cells, rather than their self-destruction.
Article by Callista Yee et al. The Intrinsic Apoptosis Pathway Mediates the Pro-Longevity Response to Mitochondrial ROS in C. elegans published in the journal Cell.
Evgeniya Ryabtseva
Portal "Eternal youth" http://vechnayamolodost.ru based on the materials of McGill University:
What doesn’t kill you may make you live longer.
12.005.2014