Mitochondrial genes and aging
Biologists have found the key to healthy aging and a long life
Scientists have found out that the rate of aging of our body depends on small mutations in the DNA of mitochondria, anomalies in the work of which lead to accelerated decrepitude of the body and the development of senile diseases, according to an article published in the journal Nature (Mitochondrial and nuclear DNA matching shapes metabolism and healthy aging).
"Variations in the work of just a few genes determine how well we age. It turned out that there are differences in the work of mitochondria caused not by diseases and pathologies, but by other causes that directly affect the rate of aging of the body," said Jose Enriquez from the National Center for Cardiovascular Research in Madrid (in a press release The interaction between our 2 genomes, nuclear and mitochondrial, is the key to healthy aging – VM).
Henriques and his colleagues observed how the "energy stations of cells" – mitochondria – worked in the body of several generations of mice, and found the key to healthy aging. They also found out that modern technologies of conceiving a child from three people can have extremely negative consequences for their health.
As scientists explain, the human genome and the DNA of all animals can be divided into two unequal parts. Most of it is located inside the nucleus, and a relatively small proportion of DNA, which includes only 37 genes, is located in the mitochondria. This small handful of genes is directly responsible for converting the energy contained in glucose molecules and other nutrients into "formats" understandable to the cell and destroying cellular "garbage".
The authors of the article were interested in how small variations in the structure of these genes, which do not cause serious problems with metabolism, affect how the human and animal bodies age with the onset of old age. To do this, scientists took two breeds of mice, swapped their mitochondria in places, and traced what changed in the work of their body and the nature of their aging.
To the great surprise of scientists, the replacement of mitochondria in the cells of mice from the most popular laboratory breed with similar corpuscles from cells of another popular breed led to the fact that their average life expectancy increased by almost 20%, and the mice themselves (in the picture on the right – VM) suffered much less than rodents with a "normal" genome from obesity, cancer, diabetes and other effects of aging. Interestingly, all these differences appeared only in old age, and young mice looked and lived the same.
The reason for this, as shown by cell analysis, was that the mitochondria of mice from the NZB breed produced fewer oxidants during the oxidation of sugars and the production of cellular "energy currency", and also had a special effect on the work of nuclear DNA, forcing the cells of their owners to actively oxidize fats and resist inflammation. How it all happens is still a mystery.
"The interaction of the nuclear and mitochondrial genome affects the entire course of human or animal life. If we can uncover the biological processes that are the basis of healthy aging and prevent the appearance of senile diseases, then we will have the opportunity to maintain health during old age for a very long time," concludes Ana Latorre–Pellicer, a colleague of Henriques.
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07.07.2016