The genome is a term that simply refers to the totality of the inheritable information of an individual . It consists of information for the production of proteins, which can determine and change the appearance of the body in various ways. You can think of DNA a bit like the code plan of a computer program. The information stored in DNA is translated into amino acids by special helpers during translation, from which the proteins in our body are ultimately formed. We will spare you the details; that would be a bit too much biochemistry at once.
Day by day, millions of cells in our body divide, which means that the genetic information also needs to be copied.This means that for each cell there is a copy of about 3 billion so-called base pairs, ideally also in the correct order. That something can go wrong is almost a given. Our body is equipped with a whole range of helpers that can correct errors during the copying process. These helpers also come into play in the case of damage from the "outside." In young years, this highly complex system (usually) works flawlessly, but with age, 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 at the molecular level. Here we will introduce you to the first Hallmark in more detail and explore the question of why people age.
If too many DNA damages accumulate (for example, due to genomic instability), the cell dies or becomes malignant.
Genomic instability – the danger from outside
Among the threats of external origin are chemical or biological agents, including medications. In addition, physics can also damage DNA through UV light, specifically UV-C light.
If you have ever gotten a sunburn, then you know what we are talking about. UV light penetrates our skin and can, when it hits the DNA, break out whole pieces. If the UV radiation is low, or if we have applied sunscreen, the damages are small and our body can repair them.
In the other case, the DNA is damaged so severely that the cell is no longer functional. It dies. If this happens on a large scale, we see it as skin redness or even more impressively in the form of blistering. In the long term, these UV damages can harm the skin significantly and lead to "skin cancer".
Fortunately, it doesn't always have to come to the worst, but prolonged high UV exposure without protection also causes the skin to age. In particular, the structural molecule collagen is gradually destroyed by sunlight.
Did you know? With 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 one hand, fibroblasts (these cells produce collagen) are inhibited in their work, and on the other hand, UV radiation activates so-called collagenases that "eat up" functional collagen. The good news is that we can also supply collagen in the form of collagen peptides from the outside and thus support our skin.
Collagen peptides (also referred to as collagen hydrolysate) are a scientifically recognized method to increase collagen levels in cells. Collagen powder is therefore one of the most popular dietary supplements. Those who prefer a plant-based alternative often opt for vegan collagen boosters, which are based on collagen precursors.
Genomic Instability from Within
Let’s move on to the threats of endogenous origin. During cell division, one cell divides into two daughter cells. Both daughter cells must naturally receive the same genetic information so that they can develop according to their purpose. For this, the DNA doubles during cell division (replication) and then divides evenly between the two new cells that are formed. In this process, so-called DNA replication errors can occur, such as incorrect pairings between the two strands. This is suboptimal, but the body is prepared for it.
Cell division is organized as a cycle, and control checkpoints 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 fix the damage, the cell is put into a state of senescence .
We will talk about senescence later, but to give you a better picture: this cell has just been put into "zombie mode". It is neither alive nor truly 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 they are. Especially in energy-intensive metabolic processes in the body, z.B.In the mitochondria, free radicals can form under certain circumstances. These are particularly reactive molecules that can disturb the reaction equilibrium and thus hinder beneficial reactions in the body.
If it is an oxygen molecule, these molecules are referred to in technical jargon as reactive oxygen species. The body also has a response to this, as antioxidants can neutralize these troublemakers to a certain extent. The most important endogenous antioxidant is glutathione, which we have introduced to you in our article about GlyNAC ..
There is even a theory of aging that almost exclusively refers to free radicals. In short, prolonged exposure to these reactive molecules is said to make us age. This theory is now somewhat outdated, as it is known that a certain level 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 &and defects of the nuclear envelope
The mentioned damages, whether of external or internal origin, are among the direct lesions of our blueprint, the DNA. In addition, defects in the nuclear architecture can also cause instability of the genome. This works as follows.
The nucleus is a distinct space surrounded by a membrane and the location in the cell where the DNA is housed. The envelope of the cell nucleus is made up of many different proteins, including proteins from the lamin family. "Lamina" is Latin and means plate, disk, or layer. These "layer proteins" must be formed correctly for the envelope to function properly.
It behaves similarly to a house roof, which must not be too rigid or too soft in order to distribute the loads as effectively as possible. If a problem occurs with the nuclear envelope in connection with these "layer proteins," 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 form a shortened version of a specific lamin. The shortened protein is referred to as progerin .Accordingly, the disease is referred to as progeria (=accelerated aging). In these individuals, the nuclear envelope is not sufficiently stable. The result is a five- to tenfold increase in aging speed. Affected individuals often die in childhood or adolescence.
Did you know? Researchers at the Technical University of Munich have studied the clinical picture of progeria more closely and made an exciting discovery. Faulty progerin also occurs in normal cells. However, in individuals with progeria, about 20 times more progerin is produced, causing the cells' waste disposal systems to become clogged. The autophagy, also one of the hallmarks of aging, therefore does not function in these individuals either.
The second exciting discovery of the study was that by administering Sulforaphane, a secondary plant compound from broccoli, autophagy could be increased and the "garbage cans of the cells" (proteasomes) worked better again.
If the nuclear envelope is damaged or unstable, then cell health is significantly impaired. Genomic instability is one cause of this.
Genomic instability in the future
Even though progerias are extraordinarily rare diseases, with a frequency of 1 in 1 million, the underlying defect is also relevant for each and every one of us. Researchers have shown that even in people with a normal aging process, Progerin is formed, which disrupts the nuclear architecture.
The genome is therefore constantly unstable due to various influences, whether from outside or inside. No one is exempt from this. The good news is that our body is prepared for many of these challenges. However, the efforts to keep the instability in check or to repair it become increasingly suboptimal with 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 instability.The newer publications on the topic not only deepen our knowledge but also show possible ways to keep genomic instability in check.
In the next article in this series, we will discuss the second hallmark of aging: telomere attrition.
