DNA Repair Mechanisms are a complex, interconnected series of cellular biochemical pathways responsible for identifying and correcting damage to the deoxyribonucleic acid (DNA) molecule, thereby preserving the integrity of the human genome. These processes are essential for preventing mutations that can lead to cellular senescence, malignant transformation, or accelerated aging. In the context of hormonal health, the efficiency of these mechanisms is directly influenced by nutrient status and endocrine signaling, particularly by sex hormones which can modulate the expression of key repair enzymes. Maintaining robust repair capacity is a critical component of cellular longevity and disease prevention.
Origin
The scientific understanding of DNA repair began in the mid-20th century with the realization that DNA, despite its stability, is constantly subjected to damaging agents and requires active maintenance. The concept gained prominence with the discovery of specific enzymatic pathways, such as nucleotide excision repair and base excision repair, which earned the Nobel Prize in Chemistry in 2015. This field has now become central to longevity science, recognizing that the cumulative failure of these mechanisms is a hallmark of biological aging.
Mechanism
The mechanisms operate through several distinct pathways, each specialized for a different type of DNA lesion. For instance, base excision repair corrects minor chemical alterations, while nucleotide excision repair handles larger structural distortions caused by UV light or chemical adducts. Double-strand breaks, the most severe damage, are managed by homologous recombination or non-homologous end joining. These pathways involve a sequence of recognition, excision of the damaged segment, synthesis of new DNA, and ligation, all orchestrated by a sophisticated network of cellular proteins and enzymes.
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