Scientists have found 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.
“Variations in the way just a few genes work 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 factors that directly affect the rate of aging of the body,”said Jose Enriquez from the National Center for Cardiovascular Research in Madrid (Spain).
Enriquez and his colleagues observed how the “cell powerhouses” - mitochondria - worked in several generations of mice and found the key to healthy aging. They also found that modern technologies for conceiving a child from three people can have extremely negative consequences for their health.
As scientists explain, the human genome and DNA of all animals can be divided into two unequal parts. Most of it is located inside the nucleus, and a relatively small fraction of DNA, which includes only 37 genes, is located in mitochondria. This small handful of genes is directly responsible for converting the energy contained in glucose molecules and other nutrients into "formats" that the cell can understand and destroying cellular "debris".
The authors of the article were interested in how small variations in the structure of these genes, which do not cause serious metabolic problems, affect how the body ages in humans and animals with the onset of old age. To do this, scientists took two breeds of mice, swapped their mitochondria in places, and tracked what changed in the work of their bodies and the nature of their aging.
Much to the surprise of scientists, the replacement of mitochondria in the cells of mice from the most popular laboratory breed for similar bodies from cells of another popular breed led to the fact that their average life expectancy increased by almost 20%, and the mice themselves are much less frequent than rodents with "normal" genome, suffered from obesity, cancer, diabetes and other consequences 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 less oxidants during the oxidation of sugars and the production of cellular "energy currency", and also influenced in a special way the work of nuclear DNA, forcing the cells of their owners to more actively oxidize fats and resist inflammation. How this all happens is still a mystery.
“The interaction of the nuclear and mitochondrial genome is reflected in 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 emergence of old age diseases, then we will be able to maintain health during old age for a very long time,”concludes Ana Latorre-Pellicer. a colleague of Henriquez.
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