UV radiation is selectively absorbed by DNA, mainly in the UV-B and the UV-C regions. Excitation of DNA leads to typical photoproducts, the most important being pyrimidine dimers and the so-called 6-4-photoproduct. The yield of strand breaks is very low directly after exposure, but they may be formed indirectly upon further incubation. Although DNA absorbs only weakly in the UV-A region, it may be damaged indirectly via endogenous photosensitisers. Photoproducts are subject to repair processes which are genetically determined. Photoreactivation splits selectively pyrimidine dimers but it is limited to lower eukaryotes and does not occur in mammalian cells. Nucleotide excision repair acts on various types of damage. UVinduced damage manifests itself also at the level of chromosomes. Chromatid-type aberrations are more frequent with UV irradiation than chromosomal aberrations. The action spectrum for their formation demonstrates that an indirect mechanism plays an important role in the UV-A region. Also micronuclei are found after broadband UV exposure which are presumably due to indirectly formed double-strand breaks. UV radiation is a strong inducer of sister-chromatid exchanges, in contrast to ionising radiation, where the yields are low. This suggests that strand breaks play only a minor role.