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Mechanism of Effect of Oxidative Stress on Telomere Length Uncovered
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Mechanism of Effect of Oxidative Stress on Telomere Length Uncovered

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Highlights
  • The ability of a cell to divide is controlled by the ends of the chromosomes called the telomeres
  • The length of the telomere decreases with age and increases in cancers
  • Oxidative stress does not affect the telomere of the cell directly but damages the DNA precursors that are used to form telomeres.


Researchers from the University of Pittsburgh have found that oxidative stress damages DNA precursors required to form telomeres. Their research was published in the Nature Structural and Molecular Biology.

The genetic material of each human cell consists of 23 pairs of chromosomes. The chromosomes transmit information correctly to the newly formed cells during cell division. Incorrect transmission of information results in genetic defects.

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The building blocks of the chromosomes are referred to as nucleotides. The ends of the chromosomes have short DNA sequences of repeated nucleotides called telomeres. The telomeres protect the chromosomes, and ensure correct transmission of information. The enzyme telomerase maintains the telomeres.

As a person ages, the size of the telomere reduces. This reduces the dividing capacity of the cell. Finally, it becomes so short that the cell stops dividing. This is the reason why the body cannot repair damage to tissues like the brain in older age, and leads to aging-related progressive disease like Alzheimer's disease.
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On the other hand, an increase in the length of the telomeres promotes cell division. This could be a mechanism behind the formation of cancers. Therefore, when it comes to telomeres, an ideal length is essential and either too long or too short can be detrimental.

Researchers from the University of Pittsburgh evaluated the changes caused by oxidative stress on telomeres. Oxidative stress results from inflammatory processes in the body, and sometimes due to environmental factors. The free radicals produced during the process can attack DNA and produce defects in the genes. Oxidative stress has been implicated as a reason behind several disease conditions like Alzheimer's disease, Parkinson's disease, cancers and atherosclerosis.

The researchers found that oxidative stress does not directly affect the telomeres. However, it damages DNA precursors required to form the telomeres. When such a damaged DNA is added to the te lomere, it does not allow further lengthening of the telomere.

The results of this study have its implications in cancer. Since cancerous cells have excessive telomerase activity, if the DNA precursors are oxidized, it could restrict the length of the telomere and stop the growth of cancer cells.

Further research in the field could provide clues to alternate treatments of cancers.

References :
  1. Fouquerel E et al. Oxidative guanine base damage regulates human telomerase activity. Nature Structural & Molecular Biology (2016) doi:10.1038/nsmb.3319
Source: Medindia

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