We are all concerned about aging and how it will affect us. There has been research done on telomeres and their affect of aging and cancer. There are additional resources at the end of this article.
Within the heart or nucleus of a cell, our genes are situated on twisted, double-stranded molecules of DNA called chromosomes. Towards the ends of the chromosomes are sections of DNA called telomeres, which safeguard each of our genetic data files, allow cells to divide, and hold some encoded information how you age and get cancer.
Telomeres are already compared to the plastic tip covers on shoelaces since they prevent chromosome tips from tearing and sticking with one another, which would scramble an organism’s genetic information to result in cancer, other health problems or death.
Yet, every time a cell divides, the telomeres become shorter. Should they get short, the cell no longer can divide and ceases to be active or “senescent” or dies. This process is part of aging, cancer and a higher risk of death. So telomeres in addition have been compared with a bomb fuse.
What exactly are telomeres?
Just like the remainder of a chromosome as well as its genes, telomeres are chains of DNA – chains of chemical information. Like other DNA, these are constructed from 4 nucleic acid bases: G for guanine, A for adenine, T for thymine and C for cytosine.
Telomeres are constructed with repeating chains of TTAGGG on a single strand of DNA attached to AATCCC on the other side strand. Thus, one component of telomere is a “repeat” created from 6 “base pairs.”
In human blood cells, the duration of telomeres ranges from 8,000 base pairs at birth to 3,000 base sets as people age and as few as 1,500 in seniors. (A full chromosome has about 150 million base pairs.) Whenever a cell divides, the average person loses thirty to two hundred base sets from the ends of the cell’s telomeres.
Cells typically can split no more than 50 to 70 times, with telomeres getting progressively shorter until the cells become senescent, die or experience genetic damage that will cause cancer.
Telomeres usually do not shorten as we grow older in tissues like heart muscle where cells don’t continuously divide.
Why do chromosomes have telomeres?
Without telomeres, the principle area of the chromosome – the section containing genes required for life – would get shorter each time a cell separates. So telomeres allow cells to separate without the loss of genes. Cell division is required so you can grow completely new skin, blood, bone as well as other cells as required.
Without having telomeres, chromosome ends could fuse together and degrade the cell’s genetic blueprint, making the cell malfunction, become cancerous or die. Because damaged DNA is dangerous, a cell has the ability to sense and repair chromosome damage. Devoid of telomeres, the ends of chromosomes would appear like broken DNA, and the cell would try to fix something which wasn’t broken. That also will make them stop dividing and over time die.
Exactly why do telomeres get shorter whenever a cell splits?
Prior to a cell can split , the chromosomes inside of it are duplicated to ensure that both of the two new cells contains the same genetic substance. A chromosome’s two strands of DNA must unwind and split. An enzyme (DNA polymerase) then starts to make 2 brand new lengths of DNA to fit each one of the 2 unwound strands. It lets you do this with the help involving short bits of RNA. When each new matching string is finished, it is a bit shorter compared to original strand due to the room needed right at the end by this small section of RNA. It is like someone who paints themself into a corner and can’t paint the corner.
Will anything at all deal with telomere shortening?
The enzyme named telomerase adds bases to the ends of telomeres. In fresh cells, telomerase keeps telomeres from wearing down a lot of. But as cells divide repeatedly, there is not enough telomerase, therefore the telomeres grow smaller and also the cells grow older.
Telomerase continues to be active in sperm and eggs, that are passed from one generation to another. If reproductive cells wouldn’t possess telomerase to keep up the length of their telomeres, any organism with this kind of cells soon would not exist.
Is there a role that telomeres play in cancer?
When a cell starts to become cancerous, it splits more often, and its particular telomeres become much shorter. If its telomeres get short, the cell may cease to live. It can escape this fate by becoming a cancer cell and activating an enzyme called telomerase, which usually prevents the telomeres from becoming even shorter.
Numerous studies have found shortened telomeres in a great many cancers, which includes pancreatic, bone, prostate, bladder, lung, kidney, and head and neck.
Calculating telomerase may be a completely new strategy to detect cancer. If perhaps scientists can learn how to cease telomerase, they could be capable of combat cancer by causing cancer cells in order to age as well as perish . In a single experiment, researchers impeded telomerase activity in human breast and cancer of the prostate cells growing within the laboratory, prompting the tumor cells to die. But you will discover risks. Blocking telomerase could impair fertility, wound healing, and output of blood cells and defense mechanisms cells.
What about telomeres and aging?
Geneticist Richard Cawthon and colleagues at the University of Utah found shorter telomeres are associated with shorter lives. Among people older than 60, those with shorter telomeres were three times more likely to die from heart disease and eight times more likely to die from infectious disease.
While telomere shortening has been linked to the aging process, it is not yet known whether shorter telomeres are just a sign of aging – like gray hair – or actually contribute to aging.
If telomerase makes cancer cells immortal, could it prevent normal cells from aging? Could we extend lifespan by preserving or restoring the length of telomeres with telomerase? If so, does that raise a risk the telomerase also will cause cancer?
Scientists are not yet sure. But they have been able to use telomerase to make human cells keep dividing far beyond their normal limit in laboratory experiments, and the cells do not become cancerous.
If telomerase could be used routinely to “immortalize” human cells, it would be theoretically possible to mass produce any human cell for transplantation, including insulin-producing cells to cure diabetes patients, muscle cells for muscular dystrophy, cartilage cells for people with certain kinds of arthritis, and skin cells for people with severe burns and wounds. Efforts to test new drugs and gene therapies also would be helped by an unlimited supply of normal human cells grown in the laboratory.
How big a role do telomeres play in aging?
Some long-lived species like humans have telomeres that are much shorter than species like mice, which live only a few years. Nobody yet knows why. But it’s evidence that telomeres alone do not dictate lifespan.
Cawthon’s study found that when people are broken into a couple of groups depending on telomere extent, the 50 percent with longer telomeres lives five years more compared to those with shorter telomeres. That suggests lifetime could possibly be increased five years by increasing the length of telomeres in people who have shorter ones.
People who have longer telomeres nevertheless experience telomere shortening as they age. How many years could possibly be added to our life-span by completely preventing telomere shortening? Cawthon believes a decade and maybe 3 decades.
After a person is over the age of 60, their risk of dying doubles with every eight years that pass. So a 68-year-old has double the potential risk of passing away inside a calendar year compared to a person sixty years old. Cawthon’s research discovered that differences in telomere length accounted for only four percent of the difference. Even though intuition tells us the elderly possess a greater risk of dying, only another 6% corresponds simply to chronological age. When telomere length, chronological age and gender are mixed (women live longer than men), those factors are the reason for thirty seven percent in the variance in your probability of passing away after 60 years old. So what on earth causes the additional sixty three%?
A significant cause of aging is “oxidative stress.” It is the injury to DNA, proteins and lipids (fatty substances) brought on by oxidants, which are highly reactive substances containing oxygen. These oxidants are produced usually when we breathe, as well as result from inflammation, infection and consumption of alcohol and cigarettes. In one study, scientists exposed worms to two substances that reduce the effects of oxidants, and the worms’ lifespan increased almost 44 percent.
Another factor in aging is “glycation.” It takes place when glucose sugar from what we eat binds to some of your DNA, proteins and lipids, leaving them not able to do their jobs. The problem becomes worse even as we grow older, causing body tissues to fail to function properly, leading to illness and death. This may explain why studies in numerous laboratory animals indicate that restricting calories extends lifespan.
It’s possible oxidative stress, glycation, telomere shortening and chronological age – along with various genes – all interact to cause aging.
What are the prospects for human life extension?
Human lifespan has increased considerably since the 1600s, when the average lifespan was 30 years. By 1998, the average U S life expectancy was 76. The reasons included sewers and other sanitation measures, antibiotics, water that is clean, refrigeration, vaccines and other medical efforts to prevent youngsters from dying, diet improvements and better health care.
Several scientists believe that the average life expectancy will continue to improve, although many do not believe the typical will exceed ninety. But a few predict significantly lengthier lifespans are feasible.
Cawthon says if all processes of getting older could be taken away and oxidative stress damage could be fixed, “one estimate is people could live 1,000 years.”