In the worlds of cancer and aging research, the word telomeres is the new buzz word. This article, “Will Telomeres Alter The Way We Look At Aging And Cancer”, looks at how telomeres research is having an impact on the way we think about aging and cancer. There are additional links to telomeres resources at the end of this this post.
Contained in the core or nucleus of the cell, your genes can be found on twisted, double-stranded molecules of DNA called chromosomes. Towards the ends of the chromosomes are usually stretches of DNA called telomeres, which in turn shield our own genetic data, make it easy for cells to split, and keep some secrets to how we age and acquire cancer.
Telomeres have already been in comparison with the plastic tips on shoelaces simply because they prevent chromosome tips from wearing and adhering to each other, which might scramble a being’s genetic information to bring about cancer, other health conditions or death.
Yet, if a cell divides, the telomeres get shorter. Whenever they get short, the cell will not be able to divide and becomes inactive or “senescent” or dies. The process is associated with aging, cancer along with a greater risk of death. So telomeres in addition have been compared to a bomb fuse.
Just what are telomeres?
Similar to the rest of a chromosome and its genes, telomeres are sequences of DNA – sequence of chemical information. Like other DNA, these are made of four nucleic acid bases: G for guanine, A for adenine, T for thymine and C for cytosine.
Telomeres come from repeating chains of TTAGGG on a single strand of DNA bound to AATCCC on the other side strand. Thus, one section of telomere is a “repeat” created from six “base sets.”
In cells within human blood, the duration of telomeres ranges from 8,000 base pairs at birth to 3,000 base pairs as people age and as little as 1,500 in elderly people. (A complete chromosome has approximately 150 million base sets.) Whenever a cell divides, a typical person loses thirty to two hundred base sets on the ends of the particular cell’s telomeres.
Cells normally can divide only about fifty to seventy times, with telomeres getting progressively shorter till the cells become senescent, die or experience genetic damage that could cause cancer.
Telomeres usually do not shorten with age in tissues like heart muscle where cells don’t continuously divide.
Exactly why do chromosomes have telomeres?
Without telomeres, the principle area of the chromosome – the part containing genes essential for life – would get shorter every time a cell splits. So telomeres allow cells to separate without dropping genes. Cell splitting is needed so we can grow brand new skin, blood, bone along with other cells when needed.
With no telomeres, chromosome ends could fuse together in addition to degrade the cell’s genetic blueprint, making the cell malfunction, become cancerous or die. Because broken DNA is dangerous, a cell has the power to sense and repair chromosome damage. With no telomeres, the ends of chromosomes would appear like broken DNA, and the cell would try to fix something that wasn’t broken. That also will make them stop dividing and over time die.
Why do telomeres get shorter whenever a cell divides?
Before any cell could split , the chromosomes within it are duplicated in order that each one of the two new cells contains identical genetic substance. A chromosome’s 2 strands of DNA must unwind and separate. An enzyme (DNA polymerase) then starts to make two fresh lengths of DNA to fit each of the two unwound strands. It does this along with the support of short pieces of RNA. When each fresh corresponding strand is completed, it’s a bit shorter compared to original strand due to the room needed at the end by this small part of RNA. It is just like a person that paints himself into a corner and cannot paint the corner.
Does indeed anything combat telomere shortening?
The enzyme called telomerase adds bases to the ends of telomeres. In fresh cells, telomerase keeps telomeres from wearing down too much. But as cells divide over and over again, there isn’t enough telomerase, so the telomeres grow reduced and also the cells grow older.
Telomerase stays active in sperm and eggs, which are passed from one generation to the next. If reproductive cells did not contain telomerase to keep up the capacity of their telomeres, any living thing with these types of cells soon would become extinct.
What role do telomeres play in cancer?
As a cell starts to become cancerous, it splits more often, and its particular telomeres become short quicker. If its telomeres get way too short, the cell may perish. It could possibly escape this fate by being a cancer cell as well as activating an enzyme called telomerase, which in turn inhibits the telomeres from becoming even shorter.
Research has found shortened telomeres in several cancers, such as pancreatic, bone, prostate, bladder, lung, kidney, and neck and head.
Computing telomerase can be a completely new way to diagnose cancer. If scientists can be able to stop telomerase, they may be capable of beat cancer by causing cancer cells in order to get older and perish . Within a experiment, researchers blocked telomerase activity in human breast and cancer of prostate cells growing inside the laboratory, prompting the tumor cells to die. But there are risks. Blocking telomerase could impair fertility, wound healing, and output of blood cells and disease fighting capability cells.
Think about telomeres along with the aging process?
Geneticist Richard Cawthon and colleagues at the University of Utah found shorter telomeres are connected with shorter lives. Among people older than 60, individuals with shorter telomeres were three times more prone to die from cardiovascular disease and eight times more prone to die from infectious disease.
While telomere shortening has been connected to the process of aging, it is not yet known whether shorter telomeres are a sign of aging – like gray hair – or actually bring about aging.
Should telomerase makes cancer cells immortal, could it prevent normal cells from aging? Could we extend lifespan by preserving or restoring the size of telomeres with telomerase? If so, does that increase a risk the telomerase will also cause cancer?
Scientists aren’t yet sure. Nevertheless they are already able to make use of telomerase to make human cells keep dividing far beyond their normal limit in laboratory experiments, and the cells don’t become cancerous.
If telomerase might be used routinely to “immortalize” human cells, it could 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, as well as skin cells for people with severe burns and wounds. Efforts to test new drugs and gene therapies also will be helped by a limitless availability of normal human cells grown inside 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 just a few years. No one yet knows why. But it’s evidence that telomeres alone don’t dictate lifespan.
Cawthon’s analysis found that whenever individuals are divided into 2 groups based on telomere size, the 50 percent with longer telomeres survives 5 years more time than those with shorter telomeres. That suggests lifespan might be improved five-years by improving the amount of telomeres in individuals with shorter ones.
Individuals with longer telomeres continue to experience telomere shortening while they age. How many years might be added onto our lifetime by completely preventing telomere shortening? Cawthon believes ten years and perhaps 30 years.
After a person becomes older than 60, their chance of dying doubles with every 8 years that pass. So a 68-year-old has 2 times the potential risk of death within a year in comparison with a 60-year-old. Cawthon’s research discovered that variations in telomere size included only four percent of this difference. And while intuition informs us seniors have a higher risk of loss of life, only yet another 6 percent is due solely to chronological age. Whenever telomere length, chronological age and gender are blended (women live longer than men), those factors account for thirty seven% in the variation in the threat of passing away over the age of 60. So what on earth causes the additional 63 percent?
A primary cause of aging is “oxidative stress.” It’s the harm to DNA, proteins and lipids (fatty substances) caused by oxidants, that are highly reactive substances containing oxygen. These oxidants are produced normally when we breathe, as well as result from inflammation, infection and use of alcohol and cigarettes. In one study, scientists exposed worms to two substances that reduce the effects of oxidants, and then the worms’ lifespan increased an average forty four percent.
Another element in aging is “glycation.” It happens when glucose sugar from what we eat binds to alot of your DNA, proteins and lipids, leaving them unable to do their jobs. The issue becomes worse as we grow older, causing body tissues to malfunction, causing illness and death. This might explain why research in a variety of laboratory animals indicate that restricting calorie intake extends lifespan.
It is possible oxidative stress, glycation, telomere shortening and chronological age – in addition to various genes – all interact to cause aging.
Are you ready for possibilities for human immortality?
The lifespan of humanity has elevated considerably ever since the 1600s, when the lifespan of humans was 30 years. By 1998, the life expectancy of the average American was 76. The reasons included sewers along with other sanitation measures, antibiotics, clean water, refrigeration, vaccines along with other medical efforts to stop children and babies from dying, diet improvements and also improved healthcare.
A number of scientists believe that average life expectancy will continue to rise, although few believe the typical will grow past ninety. But a few predict quite lengthier lifespans are probable.
Cawthon says should all processes of getting older could possibly be removed along with oxidative stress damage could be fixed, “one scientific estimate says that people may well live one thousand years.”
Telomeres may actually alter the way we look at aging and cancer.