Abstract

Ultraviolet (UV) radiation is a potent environmental mutagen that causes DNA damage, significantly contributing to skin cancer development. The most common forms of UV-induced DNA damage are pyrimidine dimers, particularly thymine-thymine dimers, which distort the DNA structure and impede cellular processes like replication and transcription. To mitigate the consequences of UV-induced lesions, cells have evolved sophisticated repair mechanisms, primarily nucleotide excision repair (NER), which removes bulky DNA adducts, and base excision repair (BER), which handles oxidative DNA damage. The timely recognition and efficient repair of these lesions are crucial to maintaining genomic stability and preventing mutations that could lead to carcinogenesis. This review explores the interplay between UVinduced DNA damage recognition, the activation of repair pathways, and the impact on cancer risk. It discusses the key proteins and enzymes involved in detecting UV-induced lesions, the role of NER in resolving pyrimidine dimers, and the secondary involvement of BER and direct reversal mechanisms. We also examine how defective DNA repair systems, particularly those associated with genetic disorders like xeroderma pigmentosum, heighten the risk of skin cancers. Furthermore, we explore how aging, excessive UV exposure, and genetic mutations influence the efficiency of repair processes and contribute to an increased cancer risk. Understanding these intricate mechanisms is essential for developing preventive strategies and therapeutic interventions aimed at enhancing DNA repair capacity and reducing UV-related cancer incidence. This review emphasizes the importance of targeted therapies and public health measures that could enhance DNA repair and minimize the mutagenic effects of UV radiation.