20 April 2009

Don't get old, don't get sick, don't breathe...

A single cellular mechanism helps to age and tolerate a lack of oxygenThe ability to tolerate oxygen starvation, delayed aging and reduced formation of toxic proteins responsible for Alzheimer's and Huntington's diseases may be caused by a violation of the signaling cascade "tied" to the VHL-1 molecule.

Matt Kaberlein from the University of Washington and his colleagues began their work on nematodes Caenorhabditis elegans, which have long become model animals for both geneticists and gerontologists. Scientists significantly reduced the level of the VHL-1 signaling protein and found that this not only increased the resistance of worms to hypoxia (which they tried to achieve), but also significantly slowed the aging of nematodes, which usually live no more than two weeks.

Although the details of the molecular mechanism have yet to be established, the authors of the publication in Science believe that the reason is a change in the function of proteosomes. These intracellular organelles are usually engaged in destroying "aged" proteins, and are present in all animals. Moreover, the newly discovered mechanism does not depend on hydrogen sulfide, insulin-like factor, diet and sirtuins, with the help of which the lifespan of yeast was increased by 10 times.

It is unlikely that Kaberlein is familiar with the technique of Buteyko, who trained his followers to be resistant to hypoxia, nevertheless, his work adds a reasonable link to this set of exercises. However, do not forget that Kaberlein and colleagues, firstly, worked on worms, and so living in less pleasant conditions, and secondly - they trained their wards to hypoxia resistance at the genetic level, which does not mean that it is possible to do it with breathing exercises.

An alternative find is the second publication in the journal Science, in which Jean–Claude Martinou from the University of Geneva managed to grow worms that tolerate a complete lack of oxygen for 48 hours. To do this, scientists caused a defect in the hyl-2 gene, also independent of all the aforementioned signaling pathways. However, this did not affect life expectancy in any way, so if there is an application, it is more likely among divers, pilots and cosmonauts than among the rapidly aging population of developed countries. 

"Newspaper.Ru»Portal "Eternal youth" www.vechnayamolodost.ru

20.04.2009

Found a typo? Select it and press ctrl + enter Print version