This review discusses the molecular mechanisms of ultraviolet radiation (UVR)-induced DNA damage and repair. UVR, particularly UV-B (280–315 nm), causes various DNA lesions such as cyclobutane pyrimidine dimers (CPDs), 6-4 photoproducts (6-4PPs), and their Dewar isomers, as well as DNA strand breaks. To counteract these lesions, organisms have developed highly conserved repair mechanisms, including photoreactivation, base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (MMR). Additionally, double-strand break repair, SOS response, cell-cycle checkpoints, and programmed cell death (apoptosis) are also operative in various organisms. UVR-induced DNA damage leads to various types of lesions, including CPDs, 6-4PPs, and oxidative damage. These lesions can cause structural distortions in DNA, affecting important cellular processes such as DNA replication and transcription. The repair mechanisms, including photoreactivation, BER, and NER, are essential for maintaining genomic integrity and preventing mutagenesis, tumorigenesis, and cell death. Photoreactivation is a light-dependent repair process that directly monomerizes the cyclobutane ring of CPDs using visible/blue-light energy. This process is carried out by photolyase enzymes, which are found in various organisms. However, photolyase activity is absent or nonfunctional in placental mammals like humans. Excision repair involves the removal of abnormal or damaged bases through two major subpathways: base excision repair (BER) and nucleotide excision repair (NER). BER is responsible for repairing base lesions caused by hydrolytic deamination, alkylating agents, ionizing radiation, and UV radiation via reactive oxygen species. NER is critical for repairing UV-induced DNA lesions such as CPDs and 6-4PPs, which cause helical distortion of the DNA double helix. NER is highly conserved in eukaryotes and involves a complex set of proteins that recognize and remove these lesions. The repair mechanisms, including photoreactivation, BER, and NER, are essential for maintaining genomic integrity and preventing the harmful effects of UVR. These mechanisms are particularly important in plants, which have developed various strategies to protect themselves from UVR, including the use of flavonoids and phenolic compounds, as well as DNA repair by photoreactivation. The study of these mechanisms provides insights into the molecular processes that allow organisms to survive and adapt to UVR exposure.This review discusses the molecular mechanisms of ultraviolet radiation (UVR)-induced DNA damage and repair. UVR, particularly UV-B (280–315 nm), causes various DNA lesions such as cyclobutane pyrimidine dimers (CPDs), 6-4 photoproducts (6-4PPs), and their Dewar isomers, as well as DNA strand breaks. To counteract these lesions, organisms have developed highly conserved repair mechanisms, including photoreactivation, base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (MMR). Additionally, double-strand break repair, SOS response, cell-cycle checkpoints, and programmed cell death (apoptosis) are also operative in various organisms. UVR-induced DNA damage leads to various types of lesions, including CPDs, 6-4PPs, and oxidative damage. These lesions can cause structural distortions in DNA, affecting important cellular processes such as DNA replication and transcription. The repair mechanisms, including photoreactivation, BER, and NER, are essential for maintaining genomic integrity and preventing mutagenesis, tumorigenesis, and cell death. Photoreactivation is a light-dependent repair process that directly monomerizes the cyclobutane ring of CPDs using visible/blue-light energy. This process is carried out by photolyase enzymes, which are found in various organisms. However, photolyase activity is absent or nonfunctional in placental mammals like humans. Excision repair involves the removal of abnormal or damaged bases through two major subpathways: base excision repair (BER) and nucleotide excision repair (NER). BER is responsible for repairing base lesions caused by hydrolytic deamination, alkylating agents, ionizing radiation, and UV radiation via reactive oxygen species. NER is critical for repairing UV-induced DNA lesions such as CPDs and 6-4PPs, which cause helical distortion of the DNA double helix. NER is highly conserved in eukaryotes and involves a complex set of proteins that recognize and remove these lesions. The repair mechanisms, including photoreactivation, BER, and NER, are essential for maintaining genomic integrity and preventing the harmful effects of UVR. These mechanisms are particularly important in plants, which have developed various strategies to protect themselves from UVR, including the use of flavonoids and phenolic compounds, as well as DNA repair by photoreactivation. The study of these mechanisms provides insights into the molecular processes that allow organisms to survive and adapt to UVR exposure.