For some strange reason, cancer has the key to aging. When in 2009 Elizabeth H. Blackburn and her colleagues won the Nobel Prize in Medicine for the discovery of telomerase (an enzyme that extends the life of cells) they realized that cancer cells were the only ones that could use this enzyme. miraculous’ to be immortal.
One of the causes of aging, besides shortening the length of telomeres (ends of chromosomes) is oxidative stress. The accumulation of reactive oxygen species causes damage to the DNA and also changes in the cell’s protein and lipid molecules. The cell finally loses its functionality and dies.
Now, precisely at the German Cancer Research Center in Heidelberg, they have found a key protein in the aging process. It is a protein molecule called TXNIP (an interactive protein with thioredoxin). This molecule is responsible for transforming reactive oxygen molecules from vital to harmful, and thus accelerate or slow down the aging process.
But, a moment, was not oxidative stress a cause of aging? Do reactive oxygen molecules have any benefit in cells? That’s right: Reactive oxygen species do more than harm DNA. For example, they are essential for the T cells of the immune system to be activated.
And how does the body eliminate harmful oxygen species to use those that are ‘beneficial’? One way is its conversion from harmful to vital: thioredoxin-1 enzyme (TRX-1). It has been shown that TRX-1 plays a role in protecting DNA against oxidative stress and slowing aging processes. But the protagnonista molecule of the study, which is its opposite (TXNIP) inhibits thioredoxin-1 and therefore ensures that reactive oxygen molecules are retained, accelerating aging.
Therefore, we might think that aging is precipitated by a set of reactive oxygen molecules, one ‘beneficial’ (TRX-1) and the other, harmful (TXNIP); in which it ends up winning the noxious. The researchers developed the hypothesis that the latter accelerates its production with age, boycotting the work of TRX-1 protection against oxidative stress and causing aging of cells.
TXNIP, the aging molecule
To find out if more TXNIP is formed in the body over the years, they compared T cells from the blood of a group of volunteers older than 55 years with T cells from younger blood donors, who were between 20 and 25 years old. years.
Finally, it turned out that cells from older subjects produce significantly more TXNIP. DKFZ scientists have also observed similar findings in other types of human cells and tissues.
The researchers also found that more TXNIP is produced in the Drosophila fly as age increases. To test whether the TXNIP is really responsible for aging, they raised flies that produce significantly more TXNIP than their relatives, as well as flies in which the synthesis of TXNIP is greatly reduced.
“The flies that produced the most TXNIP lived on average much shorter, while the flies with less TXNIP had a longer average life”, summarizes Tina Oberacker, researcher responsible for the experiments with flies.
In fact, “TRX-1 and its opponent TXNIP are almost intact in the course of evolution, and they hardly differ between flies and humans,” explains Krammer. If more TXNIP occurs with age, this means that TRX gradually disconnects with its protection function.
This leads to increased oxidative stress, which damages cells and tissues and ultimately causes death.