Division of somatic cells with no or little active telomerase leads to telomere shortening by 30-150 base pairs per cell division because of the inability to maintain the length of the 3’ overhang (single-stranded DNA). Thus, aging is the main cause of telomere shortening in somatic cells. Germ and stem cells, and most cancer cells have active telomerase and preserved telomere length through cell division [10, 11].
Oxidative stress, and inflammation are important causes of telomere shortening,and also implicated in cellular senescence and aging [35, 36]. Studies in mice with low- grade inflammation induced by knockout of the nfkb1 subunit of NF-kappa-6 indicated that systemic chronic inflammation can accelerate ageing via ROS-mediated exacerbation of telomere dysfunction and cell senescence . Reactive oxygen species (ROS) are probably involved in both the induction and stabilisation of cellular senescence. Senescent cells of the secretory phenotype induce tissue inflammation (SASP) by secreting inflammatory molecules and inducing increases ROS generation, which in turn can accelerate telomere shortening [35, 36]. Accordingly, endogenous antioxidants, such as superoxide dismutase, inhibit ageing processes and telomere shortening .