One day a frail old man with a cane came to see me. He complained of poor vision in both eyes. He was very thin.
Upon examination, initial cataracts and a pronounced “parquet” type of retina were revealed. This indicates that he has discirculatory encephalopathy.
I warned him that he was at risk of having a stroke. To which he replied that he had already had a stroke and myocardial infarction. Moreover, it turned out that he was suffering diabetes mellitus 2 types. But imagine my surprise when I saw his age on the outpatient card. He was only 46 years old.
Why do some people look old at 46 years old, while others look fit and slender at 70? After all, Trump is 71 years old, and Melania is 48 years old, but she looks like a girl.
Why does it happen that some people die old at 46 years old, while others are vigorous and active at 90 years old? A lot has been written about this, and I also wrote about it. To stay healthy for many years, you need the following:
For 30 years I have been talking to my patients about how to eat properly in my understanding. We are not talking about “healthy” food, which is found everywhere on the pages of LJ, the Internet, and on TV.
But yesterday I had a problem new idea, which can also confirm my assumptions. So…
The Hayflick limit or immortality is impossible.
There are two types of cells in the body: germ cells and somatic cells. Reproductive cells are the female egg and male sperm.
Somatic cells are the trillions of all the remaining cells that make up the body of an organism. Somatic cells constantly die and new ones are formed in their place.
So Leonard Hayflick discovered that the number of divisions of somatic cells is approximately 50-52 divisions. This was called the Hayflick limit. It's like in games like Mario. When a character has a certain number of lives. When they run out, he dies.
The human body is completely renewed every seven years.
Swedish neurologist Jonas Friesen found that every adult is on average fifteen and a half years old. That is, almost all cells (with the exception of neurons) are completely renewed. Some cells many times, some several times.
But each time the supply of subsequent possible divisions decreases.
Thus, when the supply comes to an end, life inevitably approaches death.
So the conclusion is that if we want to live longer, then we need to make sure that the cells divide as little as possible.
When cell division increases.
The disease increases cell division
Naturally, if there is some kind of disease, then the cells of this organ begin to divide more often. Inflammation destroys the somatic cells of the organ. To restore them, division is intensified.
If the disease continues, the cells constantly divide and the division reserve comes to an end (the Hayflick limit) and the cells of the organ are replaced by connective tissue, and possibly a tumor.
Conclusion, you need to get sick less.
Gastrointestinal tract (microbial population).
IN gastrointestinal tract contains a huge number of microbes. This number exceeds the number of all human somatic cells. Each microbe is surrounded by antibodies and inhibits their harmful effects. It is the balance between microbes and antibodies that is a component of our health. But this balance can constantly be disrupted.
But for microbes the Hayflick Limit is not written. Why? Yes, because for a moment, freed from microbes, they enter into sexual intercourse with each other and divide both due to somatic division and due to sexual intercourse. So, the microbial population in the stomach and intestines (unlike humans, is eternal), but is also subject to change.
Epithelium of the stomach and intestines
It is interesting that all the “battles” between the microbial population and between our antibodies occur on epithelial cells mucous membranes of the stomach and intestines. These cells divide especially frequently. This division is especially intensified after eating. After all, food is needed not only by our cells, but also by the microbial population located on these intestinal epithelial cells.
Therefore, it is logical to assume that the more often a person eats food (and this could be a small piece of candy or one nut between meals), the more often division occurs and thereby the Hayflick limit decreases.
Naturally, the Hayflick limit for human life huge and we are unlikely to be able to completely exhaust it even in 200 years. Great value Other factors also play a role, which I will write about in future articles. But still, there is no need to shorten it.
You can eat everything, a lot, with pleasure. This is a very pleasant part of life and after eating we feel wonderful relaxation. This also prolongs life.
Epilogue.
Returning to the 46-year-old patient who was at my appointment, I asked him. How does he eat? He replied that 4 - 5 times a day. He also showed his pockets, which contained walnuts. He said that for the past 20 years he has been carrying them in his pockets all the time and eating them periodically. That is, he ate almost continuously. Since the Nobel Prize was awarded in 2009 for the discovery of how telomeres protect chromosomes, laboratories around the world have begun offering telomere length testing to determine “biological age.” For example, in one of the Moscow institutions, this analysis will cost the client 18,000 rubles. What is the essence of this discovery, does telomere length affect a person’s life expectancy and is it worth spending money on this examination - this is what my article is about today.
Hayflick limit
In 1961, Leonard Hayflick, observing the cultivation of human fibroblasts, discovered the death of the culture after 50 divisions. Cells could be transferred from medium to medium, frozen for any period of time, but even after thawing, they somehow “remembered” how many divisions had already occurred and divided as many times as 50 remained. The phenomenon named after the scientist - the Hayflick limit - remained for years inexplicable, but even then they started talking about the human life expectancy programmed in genes.
Only in 1971, Alexey Olovnikov noticed that the Hayflick limit is characteristic of cells with DNA that is not closed in a circle, while bacteria with circular DNA reproduce without restrictions. The scientist put forward a hypothesis marginotomy, which assumed that the limit of division of cells with linear DNA is due to incomplete copying of the terminal sections of the chromosome at the time of cell division. Olovnikov’s idea is ingenious and at the same time simple, it is easy to explain even to a schoolchild. I will try to talk about this in the context of evolutionary theory.
When a cell prepares to divide, the enzyme DNA polymerase travels along the chromosome to make a copy of it. If the chromosome has a circular structure, the enzyme safely completes a full circle, and the ends of the copy stick together to form a chromosome for a new cell. 
In the era of single-celled organisms, chromosomes had a ring structure. But sometimes, as a result of mutations, it happened that the ends of the new chromosome did not stick together to form a ring, and the DNA strand remained open. This is roughly how bacteria with linear chromosomes appeared. The bacterium that received such a chromosome was faced with the problem of copying when it was time for its own division. The polymerase, having reached the end of the linear chromosome, stops and cannot copy the terminal region, which is approximately equal to the enzyme’s own length. 
This idea dawned on Olovnikov when he got on the subway after a lecture on Hayflick’s experiments at Moscow State University. He reasoned: “what happens to polymerase on linear chromosomes is similar to how the second carriage of a train never reaches a dead end and stops at a distance equal to the length of the locomotive.” But let's return to evolutionary theory to understand how nature solved the problem of bacteria with linear chromosomes.
The tendency to form linear chromosomes could be inherited by daughter cells, and with each generation the genome of daughter bacteria was shortened. As soon as a vital gene for the bacterium was not copied, the colony stopped growing and died. Therefore, at first, bacteria with linear chromosomes were quickly eliminated as a result of natural selection. 
However, some of these bacteria, as a result of random viral insertions, received additional ends on their chromosomes, which served as a kind of reserve - these end sections of the chromosome could be shortened with each division without threatening important genes. Olovnikov, assuming the presence of these regions at the ends of linear human chromosomes, called them telogens(modern name - telomeres).
Ok, but sooner or later telomeres will be used up after 50-100-200 divisions, and the death of a colony of bacteria with linear chromosomes seems inevitable. Moreover, linear chromosomes are the only variant of DNA organization for all existing multicellular organisms, including humans. Why did seemingly defective linear chromosomes end up in highly developed organisms? Presumably, for the first multicellular organisms, the ability for unlimited division turned out to be harmful. Just imagine your cells doubling unhindered, turning your beautiful body into embryonic biomass. But the first multicellular organisms did not have immune and hormonal systems and other mechanisms regulating cell division. Perhaps this is why natural selection favored multicellular organisms, which arose from unicellular organisms with linear chromosomes.
So, telomeres are finite, and nature requires procreation. How to explain the formation of the human body into trillions of cells from one zygote without shortening of telomeres? To resolve this contradiction, the brilliant Olovnikov predicted that telomeres are capable of growing with a special enzyme, which he gave the name tandem polymerase(modern name - telomerase). Many years later, American scientists experimentally confirmed Olovnikov’s guesses and proved that telomerase is capable of attaching to the end of a chromosome and, acting as a matrix, growing telomeres, for which they received the Nobel Prize in 2009. 
Hayflick limit in humans
In modern animal and human organisms, the problem of the Hayflick limit is not so relevant - it has not yet been possible to establish a connection between telomere length and life expectancy. Therefore, you should not rush to pay money for research on telomere length. In addition, this mechanism of limiting cell division is unlikely to stop cancer. Both stem and cancer cells easily extend the telomeres of their chromosomes by increasing telomerase activity. A good example is a cell culture obtained 60 years ago from a cervical tumor of the American Henrietta Lacks. Its cells are still used in laboratories around the world, they flew into space and were blown up by an atomic bomb, with their help vaccines and cures for cancer were developed, and this year they even made a feature film about them. The famous HeLa cells (from He nrietta La cks) outlived the woman herself and her children, and in terms of their biomass many times outgrew the mass of all of them combined. Thus, telomerase easily solves the Hayflick limit problem. 
In addition, the ability of stem cells to divide asymmetrically not only solves the problem of the Hayflick limit without the participation of telomerase, but also the problem of the accumulation of mutations, the frequency of which increases with each cell division. New data on stem cell division create the preconditions for the potential immortality of not only individual cells, but also the entire organism.
Asymmetric division - potential for immortality
It is logical that the division of one cell ends with the formation of two daughter cells, one of which contains the original chromosome, and the second gets its copy. Even if we're talking about about the division of a cell with a ring chromosome, then the daughter cells are not equivalent to each other, since during the process of DNA copying errors inevitably occur, which go to the daughter cell that received a copy of the chromosome. If we talk about the division of cells with a linear chromosome, then the daughter cell that receives a copy not only contains more mutations, but will also receive shortened telomeres. Thus, it can be assumed that after many cycles of stem cell divisions in the body there will be one cell with the original chromosome, and all the others will contain shortened copies with mutations. 
Considering that after several cycles of divisions gradual maturation (differentiation) of cells occurs, sooner or later the cell with the original chromosome, like all the cells of its generation, having fulfilled its function, will die, just as billions of blood, skin or intestinal epithelium cells die every day. In this situation, we are forced to admit that all the original stem cells stored in our body in the womb are consumed and mutations inevitably accumulate with age, and telomeres inevitably shorten. This is how the inevitable decrepitude and mortality of our body has long been explained.
However, in 1975, the asymmetric division hypothesis was put forward, suggesting that the division of a stem cell ends with the formation of not two daughter cells, but one, while the second cell remains a stem cell. In 2010, it was experimentally confirmed that the process of distribution of the original chromosome and its copy is asymmetric. It turned out that the original chromosomes remain in the stem cell, which retains its stemness, and the copies end up in the daughter cell, which forms a colony of gradually differentiating cells with a limited lifespan. 
In this situation, stem cells have literally inexhaustible potential for self-sustainment:
1. They preserve the original DNA without accumulating mutations and without the risk of being left without telomeres;
2. Rarely divide, synthesize little proteins and are metabolically weakly active, which means they survive the lack of oxygen and nutrition, intoxication and radiation more easily than other cells;
3. They do not differentiate into mature cells and are not consumed during life.
Conclusion
In my laboratory, I grow these giant colonies of blood cells in just 10 days. Each red spot is thousands of young red blood cells formed from a single stem cell. It is possible that the founder of the colony is somewhere among them and is ready to form more than one such colony - it is enough to change the concentration of hormone-like division stimulants. 
This is roughly what happens in bone marrow each of us throughout our lives. Most mature blood cells live from a few minutes to several months, requiring billions of blood cells to be renewed every day.
But why do the processes of renewal of blood and other body tissues slow down with age? I adhere to the theory that stem cells remain viable throughout our lives. And the slowdown in regeneration processes is due to the “walling up” of stem cells with connective tissues, as a result of which they cease to receive signals from the macroorganism about the need for renewal.
I’ll tell you why this happens next time. So as not to miss updates -! And if you don’t have a LiveJournal account, subscribe to updates on
How to go beyond the Hayflick limit, or all the ways to prolong life
Text: Nadezhda Markina
SO FAR, ROUND PEOPLE DO IT BEST NEMATODE WORMS. SCIENTISTS HAVE INCREASED THEIR LIFESPAN TEN TIMES.
Demographic studies convincingly show: human life expectancy depends mainly on social factors– the standard of living and the state of medicine in the country where he lives. In Japan, for example, average duration life over the past 20 years has increased to 82.15 years, and in the Kingdom of Swaziland has also increased - to 32.3. Therefore, it is difficult to calculate the biological “lifespan” of a person, especially since
Most older people die from disease, not old age. Most, but not all. In the 19th century, scientists discovered a law that bears the names of Gompertz and Makeham and describes the dependence of mortality on age. Initially, as age increases, mortality increases exponentially. It seems clear that more 70-year-olds die than 60-year-olds, and more 80-year-olds die than 70-year-olds. But there is one mystery in the curve that describes the law: after the age of 90, it reaches a plateau. This means that if a person has crossed
(A girl born today can live on average 71 years. At the beginning of the 21st century, this figure was 68 years. Men still live less than women - on average by 5 years. Highest Duration Rates life in Japan: 86 years for women and 79 years for men.)
This age, then the probability of death - at 90, at 100 or more years for him is approximately the same. Scientists cannot explain this phenomenon of centenarians. Most likely, the lucky ones who managed to avoid old age diseases reach the plateau. It can also be assumed that the aging process seems to stop at this advanced age. However, aging poses even more challenges for researchers. mysteries than longevity. This is evidenced primarily by the sheer number of theories of aging.
Aging is... ...a program
This postulate underlies the theory one of the main experts on aging in Russia, Vladimir Skulachev. He introduced the concept of “phenoptosis” - the programmed death of an organism, by analogy with apoptosis, the programmed death of a cell. It would seem, why do we need a program for death? Because it is beneficial to the population and species. According to Skulachev, in nature there is a “samurai law of biology”, which says: “It is better to die than to make a mistake.” This means that an organism that is no longer needed. But since aging is a program, Vladimir Skulachev believes, it means “it can be canceled.” To support his theory, he gives examples of non-aging organisms in nature, in which death occurs without aging.
Other scientists are supporters of evolu tional theories of aging emphasize that the body makes a choice between repair and reproduction. Repairing cells and tissues requires a lot of energy - it’s cheaper to multiply faster.
...accumulation of damage
Since with age the body begins to it works worse, which means something is spoiling in it. The question is what exactly. Some experts believe that the most important thing is that proteins spoil. For example, in collagen molecules, which is about a third of all structural proteins in the body, transverse “bridges” are formed between the long spiral threads, which sew the threads together, as a result of which the tissue loses its elasticity. At the cellular level, mitochondria deteriorate
– cellular energy substations. This can lead to the cell taking the path of programmed death. Telomeres are DNA sections at the ends of chromosomes. They consist of a series of repeating nucleotide sequences, and in all vertebrates these repeats have the same structure (TTA YGG). Telomeres shorten with each cell division and thus serve as a counter for the number of cell divisions. The counter works because the enzyme DNA polymerase, which doubles DNA when a cell divides, cannot read information from its end, so each
the next copy of DNA becomes shorter than the previous one. According to David Sinclair from Harvard, sirtuin proteins play a key role in the mechanisms of gene regulation. These are enzymes involved in the process of packaging the DNA molecule into a protein shell in the cell nucleus in the form of chromatin. In this form, the genes are inactive. In order for genetic information to be counted from them, they must be unpacked. Sirtuins prevent the unpacking of genes that should not work in a given place and at a given moment. Sirtuins play the role of guards: they make sure that silent genes remain silent and do not try to appear where they are not needed. But in addition to regulation, they are also involved in the repair of damaged DNA. Combining two positions - a traffic controller and a repairman - is not for the benefit of the cage. With age, DNA damage accumulates, sirtuins become overloaded with repairs and can no longer cope with gene regulation. As the body ages, more DNA damage occurs, and sirtuins have to increasingly rush to repair. If a traffic controller is constantly leaving his post to fix cars instead of regulating traffic, this will not end well. Gene regulation is disrupted. Genes that are unpacked without supervision can no longer pack up and become silent.
Giant turtles (Megalochelys gigantea).
They live up to 150 years, retain the ability
to reproduction. They die because they
the shell becomes too heavy.
Atlantic salmon (Salmo salar).
Usually aging accelerated “according to the program”
me" - immediately after spawning, and its decomposition
the remaining remains attract crustaceans, which
These serve as food for salmon fry.
He "sacrifices himself."
Wandering Albatrosses (Diomedea
exulans). They live on average 50 years, not
As they age, they lay eggs. And then
die, suddenly, for some unknown reason
reason.
During the work of mitochondria, deadly compounds are formed in them - reactive forms of nitrogen and oxygen. These are free radicals with an unpaired electron. They are very reactive and attack the first molecule they come across indiscriminately, be it DNA or non-DNA. loc. Of course, after such violence, the molecules become inadequate and do not work correctly.
...damage to genes
Finally, genetic damage appears in old age. After an organism stops reproducing, it accumulates harmful mutations. There is no longer a risk of passing them on to offspring, which means you can “spoil” as much as you like. Harmful mutations can lead to disruption of protein synthesis and to cancer, for example. Many people also consider the still mysterious mos to be genetic factors of aging. Bionic elements are short sequences that move along the DNA molecule and affect the functioning of genes. There are more of them with age. And there are mutations that directly cause premature aging - progeria or, conversely, “eternal youth” .... regulation
About ten years ago, American scientists found out why yeast ages - their gene regulation mechanism breaks down. A new study has shown that in mammals everything is exactly the same. This reason is universal, scientists say. This means that the causes of aging may not be genetic, but epigenetic, that is, lying next to genes.
...damage to DNA “packaging”
In the cell nucleus, the DNA molecule is wound around histone proteins. These proteins can be modified, which determines the packing density. With age, the chromatin in the nucleus becomes looser, and this leads to the fact that unnecessary and harmful genes begin to work. Packaging is tight - genes don’t work, packaging
loose - genes work.
...oxidation by free radicals
One of the most popular theories of aging is free radical theory. Its author, Danchen Harman, suggested in 1956: we age because our molecules are exposed to the action of a powerful antioxidant defense system emitted from mitochondria. But it weakens with age, causing free radical damage to increase.
The roots of the evolutionary approach to aging lie in the work of a German biologist
August Weissmann.
He was the first to suggest that aging occurs according to evolutionary
a program that removes old and unnecessary individuals from the population.
Weissmann believed that the key to this was the limited ability of cells
to division.
Hayflick's limit or limit is a theory that explains the nature of the mechanism behind cell aging. According to this theory, a normal human cell is capable of reproducing itself and dividing between forty and sixty times before it loses this ability and collapses through programmed death or apoptosis.
The theory, called the Hayflick limit, prompted scientists to reconsider Alexis Carrel's previous theory, according to which cells can endlessly reproduce themselves.
The history of the creation of Hayflick's theory
Leonard Hayflick (born May 20, 1928 in Philadelphia), a professor of anatomy at the University of California, San Francisco, developed his theory while working at the Wistar Institute in Philadelphia, Pennsylvania, in 1965. Frank McFarlane Burnet named this theory in Hayflick's honor. in his book entitled Intrinsic Mutagenesis, published in 1974. The concept of the Hayflick limit helped scientists study the effects of cell aging in human body, the development of a cell from the embryonic stage to the moment of death, including the effect of shortening the length of the ends of chromosomes, called telomeres.
In 1961, Hayflick began working at the Wistar Institute, where during his observations he saw that human cells do not divide indefinitely. Hayflick and Paul Moorhead described this phenomenon in a monograph entitled “Serial Cultivation of Human Diploid Cell Strains.” Hayflick's work at the Wistar Institute was intended to provide a nutrient solution for scientists conducting experiments at the institute, but Hayflick was also engaged in his own research into the effects of viruses in cells. In 1965, Hayflick outlined the concept of the Hayflick limit in more detail in a monograph entitled “Limited Lifespan of Human Diploid Cell Strains in an Artificial Environment.”
Hayflick came to the conclusion that a cell can only complete mitosis, that is, the process of reproduction through division, forty to sixty times, after which death occurs. This conclusion applied to all types of cells, whether adult or germ cells. Hayflick put forward a hypothesis according to which the minimum replicative capacity of a cell is associated with its aging and, accordingly, with the aging process of the human body.
In 1974, Hayflick co-founded the National Institute on Aging in Bethesda, Maryland.
This institution is a branch of the US National Institutes of Health. In 1982, Hayflick also became vice chairman of the American Society of Gerontology, founded in 1945 in New York. Subsequently, Hayflick worked to popularize his theory and refute Carrel's theory of cellular immortality.
Refutation of Carrel's theory
Alexis Carrel, French surgeon who worked with tissue in the early twentieth century chicken heart, believed that cells are capable of endlessly reproducing by division. Carrel claimed that he was able to achieve division of chicken heart cells in a nutrient medium - this process continued for more than twenty years. His experiments with chicken heart tissue strengthened the theory of endless cell division. Scientists have repeatedly tried to repeat Carrel’s work, but their experiments never confirmed Carrel’s “discovery.”
Criticism of Hayflick's theory
In the 1990s, some scientists, such as Harry Rubin of the University of California, Berkeley, argued that the Hayflick limit applied exclusively to damaged cells. Rubin speculated that cell damage could be caused by the cells being exposed to a different environment from their original environment in the body, or by scientists exposing the cells to conditions in the laboratory.
Further research into the phenomenon of aging
Despite the criticism, other scientists have used Hayflick's theory as the basis for further research into the phenomenon of cellular aging, especially telomeres, which are the ends of chromosomes. Telomeres protect chromosomes and reduce mutations in DNA. In 1973, the Russian scientist A. Olovnikov applied Hayflick's theory of cell death in his studies of the ends of chromosomes that do not reproduce themselves during mitosis. According to Olovnikov, the process of cell division ends as soon as the cell can no longer reproduce the ends of its chromosomes.
A year later, in 1974, Burnet called Hayflick's theory the Hayflick limit, using the name in his paper, Intrinsic Mutagenesis. At the center of Burnet's work was the assumption that aging is an intrinsic factor in the cells of various life forms, and that their life activity corresponds to a theory known as the Hayflick limit, which sets the time of death of an organism.
Elizabeth Blackburn of the University of San Francisco and her colleague Jack Szostak, a fellow at Harvard Medical School in Boston, Massachusetts, turned to the Hayflick limit theory in their studies of telomere structure in 1982, when they succeeded in cloning and isolating telomeres.
In 1989, Greider and Blackburn took the next step in studying the phenomenon of cell aging by discovering an enzyme called telomerase (an enzyme of the transferase group that controls the size, number and nucleotide composition of chromosome telomeres). Greider and Blackburn found that the presence of telomerase helps body cells avoid programmed death.
In 2009, Blackburn, D. Szostak and K. Greider received the Nobel Prize in Physiology or Medicine with the wording “for the discovery of the mechanisms of chromosome protection by telomeres and the enzyme telomerase.” Their research was based on the Hayflick limit.
10.12.2016
Hayflick limit or limit is a limit on the number of divisions of somatic cells, named after its discoverer Leonard Hayflick. In 1961, Hayflick observed how human cells dividing in cell culture die after about 50 divisions and show signs of aging as they approach this limit.
For most human cells, the Hayflick limit is 52 divisions.
The progress of the experiment by Leonard Hayflick and Paul Moorhead.
Fibroblasts were taken - connective tissue cells of the body that synthesize the extracellular matrix. Fibroblasts secrete precursors of collagen and elastin proteins, as well as mucopolysaccharides. During embryogenesis, fibroblasts arise from stem cells of mesenchymal origin. They play an important role in wound healing; their main function is the synthesis of components of the intercellular substance: proteins (collagen and elastin).
Equal parts of normal male and female fibroblasts were mixed, differing in the number of cell divisions undergone (male - 40 divisions, female - 10 divisions) so that the fibroblasts could be distinguished from each other in the future. In parallel, a control was placed with male 40-day fibroblasts. When the control unmixed population of male cells stopped dividing, the mixed experimental culture contained only female cells, because all male cells have already died. Based on this, Hayflick concluded that normal cells have a limited ability to divide, unlike cancer cells, which are immortal.
It has been hypothesized that a so-called "mitotic clock" is located inside every cell, based on the following observations:
1. Normal human fetal fibroblasts in culture are capable of doubling the population only a limited number of times.
2. Cells that have undergone cryogenic treatment “remember” how many times they divided before freezing.
Biological meaning of the phenomenon.
Currently, the dominant point of view associates the Hayflick limit with the manifestation of a mechanism for suppressing tumor formation that arose in multicellular organisms. In other words, tumor suppressor mechanisms, such as replicative senescence and apoptosis, are undoubtedly useful in early ontogenesis and adulthood, but indirectly cause aging - they limit life expectancy as a result of the accumulation of dysfunctional senescent cells or excessive death of functional ones.
The main one is the accumulation of random gene damage during cell replication. Each cell division involves environmental factors, such as smoke, radiation, chemicals known as hydroxyl free radicals, and cell breakdown products, that interfere with the accurate reproduction of DNA in the next generation of cells. There are many DNA repair enzymes in the body that monitor the copying process and correct transcription problems as they occur, but they are not able to catch all errors. As cells replicate repeatedly, DNA damage accumulates, leading to improper protein synthesis and improper functioning. These functional errors are, in turn, the cause of diseases characteristic of aging, such as arteriosclerosis, heart disease and malignant tumors.
This boundary has been found in cultures of all fully differentiated cells of both humans and other multicellular organisms. The maximum number of cell divisions varies depending on the type of cell and varies even more depending on the organism to which the cell belongs. The Hayflick limit is associated with a reduction in the size of telomeres, sections of DNA at the ends of chromosomes. As is known, the DNA molecule is capable of replication before each cell division. At the same time, the telomeres at its ends are shortened after each cell division. Telomeres shorten very slowly - several (3-6) nucleotides per cell cycle, that is, for the number of divisions corresponding to the Hayflick limit, they will shorten by only 150-300 nucleotides. Thus, the shorter the DNA “telomeric tail”, the more divisions it has undergone, which means the older the cell.
There is an enzyme called telomerase in the cell, the activity of which can ensure the lengthening of telomeres, which also extends the life of the cell. Cells in which telomerase functions (sex cells, cancer cells) are immortal. In ordinary (somatic) cells, of which the body mainly consists, telomerase “does not work”, so telomeres are shortened with each cell division, which ultimately leads to its death within the Hayflick limit, because another enzyme is DNA polymerase unable to replicate the ends of a DNA molecule.
Currently, an epigenetic theory of aging has been proposed, which explains telomere erosion primarily by the activity of cellular recombinases activated in response to DNA damage caused mainly by age-related depression of mobile genome elements. When, after a certain number of divisions, telomeres disappear completely, the cell freezes at a certain stage of the cell cycle or starts a program of apoptosis - a phenomenon of gradual cell destruction discovered in the second half of the 20th century, manifested in a decrease in cell size and minimization of the amount of substance entering the intercellular space after its destruction.
The existence of methods with stem cells is questioned by some researchers, for example, Professor S.V. Savelyev. There is an opinion that this is simply an ideological justification for the existence of a highly profitable industry for maintaining patients in a state of coma-2, so that there is an argument for the patient’s relatives about the possibility of his rehabilitation.
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