Are Telomeres The Key To Aging And Cancer?
Inside the nucleus of a cell, our genes are arranged along twisted, double-stranded molecules of DNA called chromosomes. At the ends of the chromosomes are stretches of DNA called telomeres, which protect our genetic data, make it possible for cells to divide, and hold some secrets to how we age and get cancer.
Telomeres have been compared with the plastic tips on shoelaces, because they keep chromosome ends from fraying and sticking to each other, which would destroy or scramble an organism’s genetic information.
Yet, each time a cell divides, the telomeres get shorter. When they get too short, the cell can no longer divide; it becomes inactive or “senescent” or it dies. This shortening process is associated with aging, cancer, and a higher risk of death. So telomeres also have been compared with a bomb fuse.
Like the rest of a chromosome, including its genes, telomeres are sequences of DNA — chains of chemical code. Like all DNA, they are made of four nucleic acid bases: G for guanine, A for adenine, T for thymine, and C for cytosine.
Telomeres are made of repeating sequences of TTAGGG on one strand paired with AATCCC on the other strand. Thus, one section of telomere is a “repeat” made of six “base pairs.”
In white blood cells, the length of telomeres ranges from 8,000 base pairs in newborns to 3,000 base pairs in adults and as low as 1,500 in elderly people. (An entire chromosome has about 150 million base pairs.) Each time it divides, an average cell loses 30 to 200 base pairs from the ends of its telomeres.
Cells normally can divide only about 50 to 70 times, with telomeres getting progressively shorter until the cells become senescent or die.
Telomeres do not shorten in tissues where cells do not continually divide, such as heart muscle.
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