More on Oxidative Stress, Telomeres, and Aging

In recent years researchers have been sketching a convincing picture of causal links between shortened telomeres, damaged mitochondria, rising oxidative stress, and the degenerations of aging. This is important because researchers are on the verge of being able to both manipulate telomere length and repair or replace damaged mitochondria. Here are some introductory posts from the archives:

Following on from that, a paper that adds a little more to the pile of evidence by demonstrating a correlation between different forms of genes associated with oxidative stress, shortened telomeres, and measurable symptoms of aging:

Oxidative stress, telomere length and biomarkers of physical aging in a cohort aged 79 years from the 1932 Scottish Mental Survey

Telomere shortening is a biomarker of cellular senescence and is associated with a wide range of age-related disease. Oxidative stress is also associated with physiological aging and several age-related diseases. Non-human studies suggest that variants in oxidative stress genes may contribute to both telomere shortening and biological aging. We sought to test whether oxidative stress-related gene polymorphisms contribute to variance in both telomere length and physical biomarkers of aging in humans.

Telomere lengths were calculated for 190 (82 men, 108 women) participants aged 79 years and associations with 384 SNPs, from 141 oxidative stress genes, identified 9 significant SNPS, of which those from 5 genes [had] robust associations with physical aging biomarkers, respiratory function or grip strength. Replication of associations in a sample of 318 (120 males, 198 females) participants aged 50 years confirmed significant associations for two of the five SNPs on telomere length.

These data indicate that oxidative stress genes may be involved in pathways that lead to both telomere shortening and physiological aging in humans. Oxidative stress may explain, at least in part, associations between telomere shortening and physiological aging.

Which leads nicely into the role of mitochondrial damage in rising levels of oxidative stress with age, thereby reinforcing the evidence for accumulated mitochondrial damage as the important root cause of telomere shortening. All the more reason to support research aimed at repairing that damage.


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