What are Telomeres?
Telomeres are ribonucleoprotein complexes that are found at the ends of chromosomes. Telomeres play a role in cellular health, inherent cellular processes, metabolism, and cell cycle regulation. Telomerase is a specialized enzyme with reverse transcriptase, Terc, and dyskerin as catalytic components. Dyskeratosis congenita, aplastic anemia, myelodysplastic syndromes, and leukemias are all caused by mutations in the telomere or any component of the telomerase enzyme.
With aging, telomere length decreases. Telomere shortening causes senescence, apoptosis, or neoplastic transformation of somatic cells, impacting an individual’s health and longevity. Shorter telomeres have been linked to an increased risk of illness and a worse chance of survival. Specific lifestyle variables can either enhance or reduce the rate of telomere shortening. Better dietary and physical activity choices can slow the pace of telomere shortening or perhaps avoid excessive telomere attrition, resulting in a delay in the start of age-related illnesses and a longer lifetime.
Function of Telomere
Telomeres, DNA–protein complexes at the ends of chromosomes, safeguard the genome from degradation and chromosome fusion. Telomeric DNA is linked with telomere-binding proteins, and a loop structure controlled by TRF2 shields the ends of human chromosomes from exonucleolytic destruction, and may also stimulate telomeric DNA synthesis by a mechanism akin to homologous recombination’s “gap-filling.”
Telomere shortening occurs during DNA replication and can lead to chromosomal breakdown and cell death if left unchecked. Telomerase activity, or the ability to lengthen telomeres, is found in germline and some hematopoietic cells, whereas somatic cells have low or undetectable levels of this activity, and their telomeres shorten with replication.
Effect of stress on Telomeres
The release of glucocorticoid hormones by the adrenal gland is linked to stress. These hormones have been found to lower antioxidant protein levels, potentially leading to increased oxidative DNA damage and telomere shortening.
Telomere and aging
Telomere shortening has been linked to aging, mortality, and illnesses associated with age. In both humans and mice, normal aging is linked to telomere shortening, and research on genetically engineered animal models shows causal connections between telomere erosion and aging. However, it is unclear whether short telomeres are simply a sign of aging or if they play a role in the development of the aging process.
The length of a child’s telomeres is influenced by the father’s age, which has evolutionary consequences. Telomeres on leukocytes shrink with age, whereas telomeres on sperm lengthen. Shorter telomeres are thought to have lower energy costs (due to less replication), but they also have immune system-related and another aging- and disease-related costs, so the effect of paternal age on telomere length could be an adaptation to help the child fit into the environment they’re born into.
Sources and references: Telomeres, lifestyle, cancer, and aging by Masood A. Shammas https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3370421/