THE AGING PROCESS Part 4
AGING PROCESS AT THE CELLULAR LEVEL
In 1961, American anatomist and cellular biologist Leonard Hayflick showed that normal human somatic cells can divide and renew themselves in cell cultures about 50 times, then enter a senescence phase and stop dividing. This is known as the “Hayflick Limit.”
In real life, most of these cells undergo preprogrammed cell death (apoptosis) and are cleared from the body by autophagy. But some remain partly alive and dysfunctional, producing inflammatory molecules. These cells are harmful and are called “zombie” cells. They cause chronic low-grade inflammation, which is frequently seen in older people.
Studies of cancer cell division in cell culture have shown that cancer cells divide indefinitely. Further research identified a cap at the end of each chromosome called a "telomere." When normal cells divide, telomere length gets shorter with each division, and when telomeres become too short, cells stop dividing. But in cancer cells, telomere length remains constant. This raises an important question: what keeps telomere length constant in cancer cells? More studies on cancer cell culture media revealed a high concentration of an enzyme called transferase produced by cancer cells. The same enzyme is also present in normal cell cultures but at lower concentrations, and it is completely absent when cells stop dividing. This enzyme is thought to be the secret of longevity. If researchers isolate this enzyme and give it to people, they think it will abolish the cell-division limit and halt aging.
However, when researchers isolated this enzyme and gave it to laboratory animals, they remained younger and lived longer. But in the end, they all developed cancer. This suggests that the cell-division limit protects against cancer.
As I see it, living creatures and human beings are created to get old and die, instead of living very long and developing cancer and dying in misery.
But the aging process is much more complex and multifactorial than a simple enzyme. Even before the cells reach their senescence stage, tissue stem cell counts start to decline, DNA damage increases, and the quality of repairs declines; intracellular organelle functions start to decline, mitochondria no longer produce enough energy, energy metabolism waste products can no longer be cleared and start to accumulate in the cells, ribosomes start to produce defective proteins, and a low-grade inflammation sets in.
So, telomere length and cellular senescence appear to be the main biological markers of cellular aging.
The complexity of the aging process must be why every living creature in Nature, including humans, ages differently.
