Within the nucleus of a cell, our genes are arranged along twisted, double-stranded DNA molecules, called chromosomes. At the ends of the chromosomes there are DNA fragments called telomeres that protect our genetic data, make it possible to break the cells and keep some secrets about how we age and cancer.
The telomeres have been compared to the plastic edges on the shoe laces because they keep the ends of the chromosomes from breaking and sticking to one another, which would destroy or blend the genetic information of an organism.
However, every time a cell is divided, Telomeres become shorter. When it’s too soon, the cell can no longer be divided. It is inactive or dies. This process is associated with aging, cancer and the highest risk of death. Thus, the Telomeres have also been compared with a bomb tube.
What are Telomeres?
Like the rest of the chromosome, including its genes, the telomeres are DNA sequence chains of chemical code. Like all DNAs, they are made up of four nucleic acid bases: G for guanine, A for adenine, T for thymine, and C for cytosine.
Telomeres consist of repeated sequences of TTAGGG in a clone associated with AATCGG in the other clone. Thus, a part of the Telomer is a “repetition” consisting of six “base pairs”.
In white blood cells, the length of Telomeres varies from 8,000 pairs of bases in neonates to 3,000 pairs in adults and 1,500 in elderly. (An entire chromosome has about 150 million base pairs.) Each time it is divided, an average cell loses 30 to 200 pairs of bases from the ends of its telomere.
Cells normally can only be separated about 50 to 70 times, with telomeres gradually decreasing until the cells become noticeable or die.
Telomeres are not abbreviated in tissues where cells are not continuously divided, such as the heart muscle.
Why chromosomes have Telomeres?
Without Telomeres, the main part of the chromosome, that is, the part with genes necessary for life, would become shorter whenever a cell is divided. Thus, telomeres allow cells to break down without losing genes. Cell division is essential for the development of new skin, blood, bone and other cells.
Without Telomeres, the ends of the chromosomes could merge and corrupt the genetic pattern of the cell, possibly causing dysfunction, cancer or cell death. Because broken DNA is dangerous, a cell has the ability to perceive and repair damage to the chromosome.
Without Telomeres, the ends of the chromosomes would look like broken DNA, and the cell would try to correct something that had not been broken. This would make them stop dividing and eventually die.
Why Do Telomeres become shorter every time a cell is divided?
Before a cell can be divided, it copies its chromosomes so that both new cells have the same genetic material. In order to copy, the two DNA clones of the chromosome must be unraveled and separated. An enzyme (DNA polymerase) reads the existing clones for the construction of two new clones. It initiates the procedure by means of short RNA fragments. When every new fitting part is complete, it is a little smaller than the original part due to the space required at the end for this small piece of RNA. It’s like someone who is painting himself at a corner and can not paint the corner.
Telomerase triggers the reduction of Telomerase
An enzyme called Telomerase adds bases to the end of the Telomer. In young cells, Telomerase keeps Telomer from decreasing too much. But as the cells are repeatedly divided, there is not enough Telomerase, so that Telomeres become shorter and the cells get older.
Telomerase remains active in sperm and eggs, which are transferred from one generation to the next. If the reproductive cells did not have Telomerase to maintain the length of their Telomeres, any organism with such cells could not exist.
As a cell begins to become cancerous, it is divided more often, and its telomeres become very small. If its telomeres are too small, the cell may die. Often, these cells escape from death by making more of the enzyme telomerase, which prevents telomeres from becoming even smaller.
Many cancers have reduced Telomeres, including the pancreas, bone, prostate, bladder, lung, kidney and head and neck.
Measuring Telomerase may be a way to detect cancer. And if scientists can learn how to stop Telomerase, they could fight cancer by making cancer cells die. In one experiment, the researchers blocked the action of Telomerase in human breast and prostate cancer cells developed in the laboratory, prompting neoplastic cells to die. But there are dangers. Release of Telomerase could affect fertility, wound healing, and the production of blood and immune cells.
Telomeres and aging
Geneticist Richard Cawthon and his associates at Utah University found shorter Telomere linked to shorter lives. Among people over the age of 60, people with shorter Telomeres were three times more likely to die from heart disease and eight times more likely to die from infectious diseases.
While the reduction of Telomeres has been linked to the aging process, it is not yet known whether shorter Telomeres are just an indication of aging such as gray hair or actually contribute to aging.
If Telomerase makes the cancer cells immortal, could it prevent aging of normal cells? Can we extend the lifespan by maintaining or restoring the length of Telomeres with Telomerase?
If so, will this increase the risk of getting cancer?
Scientists are not yet sure. But they managed to use Telomerase in the lab to keep human cells dividing well beyond their normal limit and the cells are not cancerous.
If we used Telomerase to “immortalize” human cells, we may be able to produce massive cells for transplantation, including insulin-producing cells to treat diabetes, muscle cells for treatment of muscular dystrophy, cartilage cells for certain types of arthritis, and skin cells for Healing severe burns and sores. An unlimited supply of normal human cells developed in the lab would also help efforts to test new drugs and gene therapies.
What is The Role Of Tumors In Aging?
Some long-lasting species such as humans have telomere that are much smaller than species like mice, which only live for a few years. No one knows why. But it is evidence that only Telomeres do not dictate life.
Cawthon’s study found that when people are divided into two groups based on the length of the telomere, half with larger telomeres live on average five years longer than those with smaller telomeres. This study shows that lifespan could increase five years by increasing the length of Telomeres in people with shorter.
People with longer Telomeres still show a decrease in Telomerase as they grow older. How many years could be added to our lifetime, by completely disrupting the reduction of Telomere?
Cawthon believes 10 years and maybe 30 years.
After the age of 60, the risk of death is doubled every 8 years. Thus, a 68 year-old is twice as likely to die within a year as compared to a 60 year time. Cawthon’s study found that the differences in the length of Telomeres accounted for only 4% of this difference. And while our intuition tells us that older people have a higher risk of dying, only 6% is solely due to chronological age. When the length of Telomeres, chronological age and gender are combined (women live longer than men), these factors account for 37% of the risk of death over 60 years of age. So what causes the other 63%?
A major cause of aging is “oxidative stress”. It is the damage of DNA, proteins and lipids (fats) caused by oxidants, which are very active substances containing oxygen. These oxidants are normally produced when we breathe and also result from inflammation, contamination and consumption of alcohol and cigarettes. In a study, scientists exposed worms to two substances that neutralize oxidants and the life span of worms increased by an average of 44%.
Another factor in aging is “glycosylation.” This happens when glucose, the main sugar we use as energy, binds to one of our DNA, proteins and lipids, leaving them unable to do their job. The problem is getting worse as we get older, causing dysfunction of body tissues, resulting in disease and death. Glycosylation may explain why animal studies indicate that limiting calorie intake extends the life span.
The most likely, oxidative stress, glycosylation, reduction in the number of telomeres and chronological aging all together contribute to aging.
Telomeres and other diseases
People with a disease called congenial dystartosis have telomeres that decrease much faster than normal. These people endure premature aging and death. They are at greater risk of life-threatening infections, leukemia and other forms of blood cancer, intestinal disorders, cirrhosis of the liver and pulmonary fibrosis, a lethal pulmonary artery. They are also more likely to have gray hair, baldness, poor wound healing, skin stains, intestinal disorders, bone softening, and learning difficulties.
The conclusion is that Telomeres can play a role in all of these conditions because they all include tissues in which cells often gets divided. There are also some elements linking the shorter Trichomes with Alzheimer’s disease, arterial hypertension, high blood pressure and type II diabetes.
What are the perspectives of human immortality?
Human life has increased significantly since 1600, when the average life was 30 years. By 2012, the average US life expectancy was almost 79.
Reasons for this increase include sewers and other sewage systems, antibiotics, clean water, cooling, vaccines and other medical efforts to prevent the death of children and babies and the treatment of infections and acute cases of diseases .
Some scientists predict that the average life expectancy will continue to rise, although many doubt that the average will always be much higher than 90 years. But some say that long life is possible.
Surveys also show that life expectancy can reach 150 years, and even more recent research has shown that there is no longer a life expectancy.
Cawthon says that if all aging processes could be eliminated and oxidative stress damage could be restored, “an estimate is that people could live for 1,000 years.”
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