The genome is a term that simplifies the entirety of an individual's heritable information DNA is the information for the production of proteins, which can influence and alter the body's appearance in a variety of ways. You can think of DNA a bit like the blueprint of a computer program. The information stored on the DNA is translated into amino acids by special helper molecules during translation, from which the proteins in our bodies are ultimately made. We'll spare you the details; that would be a bit too much biochemistry at once.
Millions of cells divide in our bodies every day, which means that the genetic information also needs to be copied.This means that each cell contains a copy of approximately 3 billion so-called base pairs, ideally in the correct order. It's almost inevitable that something can go wrong. Our body is equipped with a whole range of helpers that can correct errors during the copying process.These helpers are also deployed in cases of damage from "external" sources.
In youth, this highly complex system (mostly) works perfectly, but with age, more and more errors creep in. So-called genomic instability is one of the Hallmarks of AgingThese hallmarks are an attempt to explain the aging process scientifically and at the molecular level. Here we will introduce the first hallmark in more detail and investigating the question of why people age.
If too much DNA damage accumulates (for example, due to genomic instability), the cell dies or becomes degenerate.
Genomic instability – the external threat
Among the threats external origin to count chemical or biological agents, and thus, for example, medicationsIn addition, physics can also explain UV light, in particular. UV-C light, which damages DNA.
If you've ever had a sunburn, then you know what we're talking about. UV light penetrates our skin and, when it hits the DNA, can break off entire pieces.If the UV radiation is low, or if we have applied sunscreen, the damage is minor and our body can repair it.
In the other case, the DNA is damaged so severely that the cell is no longer functional. It dies. If this occurs on a large scale, we see it as skin reddening or, even more dramatically, as blistering. In the long term, this UV damage can severely harm the skin and lead to "skin cancer"..
Fortunately, it doesn't always have to come to the worst, but prolonged high UV exposure without protection also ages the skin. In particular the structural molecule Collagen is gradually destroyed by solar radiation.
Did you know? With approximately 30% Collagen is the most abundant protein in our bodyIt is found in the skin, bones, and tendons. UV radiation can destroy collagen in two ways.On the one hand, the fibroblasts (these cells produce collagen) are inhibited in their activity, and on the other hand, UV radiation activates so-called collagenases, which "eat" functional collagen. The good news is that we can obtain collagen in the form of Collagen peptides They can also be supplied from the outside and thus support our skin.
Collagen peptides (also known as collagen hydrolysate) are a scientifically recognized method for increasing collagen levels in cells.
Genomic instability from within
Let's turn to the threats. of endogenous originDuring cell division, one cell produces two daughter cells. Both daughter cells must naturally receive the same genetic information in order to develop according to their intended purpose. For this to happen, the DNA duplicates itself during cell division (replication) and is then divided equally between the two newly formed cells. This process sometimes results in so-called DNA replication errors, 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 stations are built into this cycle. If an error is detected, cell division stops, and ideally, the error is repaired. If the repair system cannot fix the damage, the cell enters a state of... Senescence displaced.
We'll talk about senescence later, but to give you a better idea: this cell is just put into "zombie mode"She is neither alive nor truly dead.
Quercesome – 20 times higher bioavailability compared to conventional quercetin powder. Thanks to phospholipids from sunflowers and natural vitamin C.
Free radicals and reactive oxygen species – what do these have to do with aging?
Free radicals and reactive oxygen species sound a bit like explosive biochemistry. And they are. Especially during energy-intensive metabolic processes in the body, z.B. in the Mitochondria, free radicals may be producedThese are particularly reactive molecules that can disrupt the reaction equilibrium and thus hinder reactions that are beneficial to the body.
If this involves an oxygen molecule, these molecules are referred to in technical jargon as reactive oxygen species. The body also has a response to this, because Antioxidants These troublemakers can be neutralized to a certain extent. The most important naturally occurring antioxidant in the body is glutathione, which we discussed in our article about GlyNAC have brought closer.
There is even a theory of aging that focuses almost exclusively on free radicals. In short, constant exposure to these reactive molecules is supposed to cause us to age. This theory is now somewhat outdated, as it is now 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 &nuclear envelope defects
The aforementioned damage, regardless of its external or internal origin, constitutes a direct lesion of our blueprint, our DNA. In addition, Defects in the cell nucleus architecture can also cause instability of the genome.This works as follows.
The cell nucleus is a separate space surrounded by a membrane and is the place in the cell where the DNA is located. The cell nucleus's outer layer 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 membrane to function properly.
It It behaves similarly to a house roof.The nuclear envelope must be neither too rigid nor too flexible in order to distribute the loads as effectively as possible. If a problem arises in connection with these "layer proteins" of the nuclear envelope, the genome becomes unstable. This is because the DNA is connected to the nuclear envelope via molecules.
Let's look at a real-world example. There are people who can only produce a shortened form of a specific lamin. This shortened protein is known as... Progerin The disease is therefore referred to as... Progeria (=accelerated aging). In these people, the nuclear envelope is not sufficiently stable. The result is a five- to ten-fold increased rate of aging.Those affected often die in childhood or adolescence.
Did you know? Researchers at the Technical University of Munich have taken a closer look at the clinical picture of progeria and made an exciting discovery. Defective progerin also occurs in normal cells.However, in people with progeria, about 20 times more progerin is produced, causing the cells' waste disposal systems to become clogged. Autophagy, also one of the hallmarks of aging, no longer works for these people either.
The second exciting discovery of the study was that through the gift of Sulforaphan, a secondary plant compound from broccoli, which could increase autophagy and the "cells' garbage cans" (proteasomes) started working 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 progerias are extremely rare diseases, with a frequency of 1 in 1 million, the underlying defect is relevant to each and every one of us. Scientists have demonstrated that progerin, which disrupts the core architecture, also forms in people with a normal aging process..
The genome is therefore constantly unstable due to a variety of influences, both external and internal. No human being 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 are not working.Repairing becomes increasingly suboptimal with age.
The question of why some people age more slowly can probably be answered by the fact that these individuals possess good repair mechanisms to limit genomic instability.. Recent publications on this 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 discuss the second sign of aging: the Telomere abrasion.
