The genome is a term that simplifies the totality of the heritable information of an individual This is information for the production of proteins, which can determine and change the appearance of the body in many different ways. You can imagine DNA a bit like the code plan of a computer program. The information stored on the DNA is translated by special helpers into amino acids, which ultimately become the proteins in our body. We'll spare you the details, that would be a bit too much biochemistry at once.
Every day, millions of cells divide in our body, which means that genetic information must also be copiedThis means that each cell has a copy of around 3 billion so-called base pairs, ideally in the right order. It is almost obvious that something can go wrong. Our body is equipped with a whole range of helpers that can correct errors during the copying processThese helpers are also used in the event of damage from “outside”.
When we are young, this highly complex system (mostly) functions perfectly, but as we get older, more and more errors creep in. The so-called genomic instability is one of the Hallmarks of Aging. These Hallmarks are an attempt to explain the aging process scientifically and on a molecular level. Here we will introduce you to the first Hallmark in more detail and investigate the question of why people age.
If too much DNA damage accumulates (for example due to genomic instability), the cell dies or degenerates.
Genomic instability – the threat from outside
Among the threats external origin to count chemical or biological active substances and thus, for example, medicinesIn addition, physics can also be used to study UV light, in particular UV-C lightthat damage DNA.
If you've ever been sunburned, you know what we're talking about. UV light penetrates our skin and, when it hits the DNA, can break off entire piecesIf the UV radiation is low or we have applied sunscreen, the damage is small and our body can repair it.
In the other case, the DNA is damaged so severely that the cell can no longer function. It dies. If this happens on a large scale, we see it as reddening of the skin or, even more impressively, in the form of blistering. In the long term, this UV damage can be very damaging to the skin and lead to “skin cancer”.
Fortunately, things don't always have to go to the worst, but constant high UV exposure without protection also causes the skin to age. In particular, the structural molecule collagen is gradually destroyed by solar radiation.
Did you know? At about 30%, Collagen is the most common protein in our body. It is found in the skin, bones and tendons. UV radiation can destroy collagen in two ways.On the one hand, the fibroblasts (these cells form collagen) are inhibited in their work and secondly, UV radiation activates so-called collagenases, which "eat up" functional collagen. The good news is that we can get collagen in the form of collagen peptides also from the outside and thus support our skin.
Collagen peptides (also called collagen hydrolysate) are a scientifically recognized method for increasing collagen levels in cells.
Genomic Instability from Within
Let's get to the threats endogenous originDuring cell division, two daughter cells are created from one cell. Both daughter cells naturally need to receive the same genetic information so that they can develop according to their purpose. To do this, the DNA duplicates itself during cell division (replication) and is then divided equally between the two new cells that are created. This sometimes results in so-called DNA replication errors, for example incorrect pairings between the two strandsThis is suboptimal, but the body is prepared for it.
Cell division is organized as a cycle and control stations are built into this cycle. If an error is detected, cell division stops and the error is repaired in the best case. In the event that the repair system cannot repair the damage, the cell is returned to the state of senescence offset.
We will talk about senescence later, but to give you a better picture: this cell is just been put into "zombie mode". She is neither alive nor really dead.
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Free radicals and reactive oxygen species – what do they have to do with aging?
Free radicals and reactive oxygen species sound a bit like explosive biochemistry. And that's exactly what it is. Especially in energy-intensive metabolic processes in the body, e.g. in the mitochondria, free radicals may be formedThese are particularly reactive molecules that can disrupt the reaction equilibrium and thus hinder reactions that are beneficial to the body.
If it is an oxygen molecule, these molecules are referred to in technical jargon as reactive oxygen species. The body has an answer to this too, because antioxidants can neutralize these troublemakers to a certain extent. The most important antioxidant in the body is glutathione, which we will explain in our article about GlyNAC brought closer.
There is even a theory of aging that is based almost exclusively on free radicals. In short, constant exposure to these reactive molecules is said to cause us to age. This theory is now somewhat outdated, as we now know that a certain amount of free radicals can be beneficial for the body.Only when the balance tips do free radicals pose a threat to our genomic stability.
Genomic Instability & Nuclear Envelope Defects
The damage mentioned, whether of external or internal origin, is one of the direct lesions of our blueprint, the DNA. In addition, Defects in nuclear architecture can also cause genome instability. It works like this.
The cell nucleus is a separate space surrounded by a membrane and is the place in the cell where DNA is located. The shell of the cell nucleus is made up of many different proteins, including proteins from the lamin family. "Lamina" is Latin and means plate, disc or layer. These "layer proteins" must be formed correctly for the shell to function properly.
It behaves similarly to a house roof, which must be neither too rigid nor too soft in order to distribute the loads as best as possible. If a problem occurs in connection with these "layer proteins" of the nuclear envelope, the genome becomes unstable. The reason for this is the fact that the DNA is connected to the nuclear envelope via molecules.
Let's look at a real example. There are people who can only produce a shortened form of a specific lamin. The shortened protein is called progerin Accordingly, the disease is referred to as Progeria (=accelerated aging). In these people, the nuclear envelope is not sufficiently stable. The result is a five to tenfold increase in aging rateThose affected often die in childhood or adolescence.
Did you know? Researchers at the Technical University of Munich have taken a closer look at the disease progeria and made an exciting discovery. Faulty progerin also occurs in normal cellsHowever, in people with progeria, about 20 times more progerin is produced, which clogs the cells’ garbage cans. autophagy, also one of the Hallmarks of Aging, no longer works for these people.
The second exciting discovery of the study was that by giving sulforaphane, a secondary plant substance from broccoli, which increased autophagy and the “garbage cans of the cells” (proteasomes) worked better again.
If the nuclear envelope is damaged or unstable, cell health is significantly impaired. Genomic instability is one cause of this.
Genomic Instability in the Future
Even though progeria is an extremely rare disease, with a frequency of 1:1 million, the underlying defect is also relevant to each and every one of us. Scientists have shown that even in people with normal aging processes, progerin is formed, which disrupts the nuclear architecture.
The genome is therefore constantly unstable due to the various influences, whether from outside or from inside. No human is exempt from this. The good news is that our bodies are prepared for many of these challenges. However, efforts to keep the instability in check or to repair it become less effective as we age.
The question of why some people age more slowly can probably be answered by the fact that these individuals have good repair mechanisms to limit genomic instabilityThe recent publications on the topic not only deepen our knowledge but also show possible ways in which we can keep genomic instability in check.
The next article in this series will focus on the second hallmark of aging: telomere attrition.
