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What is the role of telomeres in oxidative damage and aging?

One of the key factors contributing to aging is oxidative damage. Oxidative damage occurs when reactive oxygen species (ROS), such as free radicals, accumulate in cells and cause damage to cellular components, including DNA. This damage can lead to mutations, genomic instability, and ultimately, cellular dysfunction.

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Telomeres are particularly vulnerable to oxidative damage due to their repetitive DNA sequences and the presence of guanine-rich regions. Guanine is highly susceptible to oxidation, and oxidative damage can result in the shortening and erosion of telomeres.

As telomeres shorten over time, cells enter a state of replicative senescence, where they lose their ability to divide and function properly. This process is known as cellular aging. Shortened telomeres can also trigger a DNA damage response, leading to cellular senescence or apoptosis (cell death).

Furthermore, oxidative stress can accelerate telomere shortening by increasing the activity of telomerase, an enzyme responsible for telomere length maintenance. Telomerase activity is normally low in most somatic cells but is upregulated in response to oxidative stress. While increased telomerase activity can temporarily counteract telomere shortening, it can also promote the survival and proliferation of damaged cells, potentially contributing to age-related diseases, such as cancer.

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In summary, telomeres play a crucial role in protecting the genome from oxidative damage. However, oxidative stress can lead to telomere shortening and accelerate cellular aging. Understanding the interplay between telomeres, oxidative damage, and aging is essential for unraveling the mechanisms underlying the aging process and developing strategies to promote healthy aging.

Keywords: oxidative, damage, telomeres, cellular, shortening, telomere, stress, activity, telomerase