UV-induced DNA damage and repair mechanisms are critical for organisms to survive increasing UV radiation due to ozone depletion. UV radiation causes DNA lesions such as cyclobutane-pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs), which are major mutagenic and cytotoxic lesions. Cells have developed various repair mechanisms, including photoreactivation by photolyase, base excision repair (BER), nucleotide excision repair (NER), mutagenic repair, recombinational repair, cell-cycle checkpoints, apoptosis, and alternative repair pathways. These mechanisms help counteract DNA damage caused by UV or other stressors. Ozone depletion, primarily due to chlorofluorocarbons (CFCs), has increased UV-B radiation reaching Earth's surface, leading to significant DNA damage in organisms. UV-B and UV-A radiation can damage DNA, with UV-B being more harmful. DNA damage has both cytotoxic and genotoxic effects, potentially leading to mutations and cell death. Organisms have developed UV-absorbing pigments to mitigate DNA damage, but complete protection is not possible. UV-induced DNA damage includes CPDs and 6-4PPs, which distort DNA structure and interfere with transcription and replication. CPDs are more abundant and cytotoxic, while 6-4PPs may have more severe mutagenic effects. Dewar isomers of 6-4PPs are formed by photoisomerization. These lesions can block transcription and replication, leading to mutations and cell death if not repaired. DNA repair mechanisms ensure accurate genetic transmission and survival. These mechanisms include photoreactivation, BER, NER, and others, which help repair DNA damage and prevent mutations. Understanding these mechanisms is crucial for addressing the impacts of increased UV radiation on organisms.UV-induced DNA damage and repair mechanisms are critical for organisms to survive increasing UV radiation due to ozone depletion. UV radiation causes DNA lesions such as cyclobutane-pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs), which are major mutagenic and cytotoxic lesions. Cells have developed various repair mechanisms, including photoreactivation by photolyase, base excision repair (BER), nucleotide excision repair (NER), mutagenic repair, recombinational repair, cell-cycle checkpoints, apoptosis, and alternative repair pathways. These mechanisms help counteract DNA damage caused by UV or other stressors. Ozone depletion, primarily due to chlorofluorocarbons (CFCs), has increased UV-B radiation reaching Earth's surface, leading to significant DNA damage in organisms. UV-B and UV-A radiation can damage DNA, with UV-B being more harmful. DNA damage has both cytotoxic and genotoxic effects, potentially leading to mutations and cell death. Organisms have developed UV-absorbing pigments to mitigate DNA damage, but complete protection is not possible. UV-induced DNA damage includes CPDs and 6-4PPs, which distort DNA structure and interfere with transcription and replication. CPDs are more abundant and cytotoxic, while 6-4PPs may have more severe mutagenic effects. Dewar isomers of 6-4PPs are formed by photoisomerization. These lesions can block transcription and replication, leading to mutations and cell death if not repaired. DNA repair mechanisms ensure accurate genetic transmission and survival. These mechanisms include photoreactivation, BER, NER, and others, which help repair DNA damage and prevent mutations. Understanding these mechanisms is crucial for addressing the impacts of increased UV radiation on organisms.