The Role of UV Radiation in Chromosomal Mutations: Mechanisms, Impacts, and Implications for Genomic Stability

Abstract

Through both direct and indirect genotoxic pathways, ultraviolet (UV) radiation is a ubiquitous and powerful environmental mutagen that causes a broad range of chromosomal abnormalities. UV-B and UV-C exposure cause primary lesions like cyclobutane pyrimidine dimers (CPDs) and 6-4 photoproducts, but UV-A exposure causes oxidative damage through reactive oxygen species (ROS). These lesions cause structural abnormalities (deletions, duplications, and translocations) and numerical anomalies (aneuploidy) by interfering with DNA replication and chromosome segregation. In people with compromised DNA repair mechanisms, especially those with Cockayne Syndrome (CS) or Xeroderma Pigmentosum (XP), continuous DNA damage leads to chronic genomic instability and an increased risk of skin malignancies, such as melanoma, squamous cell carcinoma, and basal cell carcinoma. Oncogenes is made worse by mutational inactivation of tumour suppressor genes such as TP53 and PTEN. Public health hazards have increased due to increased UV-B exposure caused by environmental stresses, particularly ozone layer loss. An integrated strategy is needed to address this issue, integrating policy-driven public education and early screening initiatives with molecular diagnostics, gene-targeted medicines, and advancements in UV protection including wearable sensors and sophisticated sunscreens. In the face of continuous environmental change, such tactics are crucial to lowering the burden of mutations and maintaining genomic integrity.