UV-induced DNA damage plays a key role in the initiation phase of skin cancer. 
When left unrepaired or when damaged cells are not eliminated by apoptosis, DNA 
lesions express their mutagneic properties, leading to the activation of 
proto-oncogene or the inactivation of tumor suppression genes. The chemical 
nature and the amount of DNA damage strongly depend on the wavelength of the 
incident photons. The most energetic part of the solar spectrum at the Earth's 
surface (UVB, 280-320 nm) leads to the formation of cyclobutane pyrimidine 
dimers (CPDs) and pyrimidine (6-4) pyrimidone photoproducts (64PPs). Less 
energetic but 20-times more intense UVA (320-400 nm) also induces the formation 
of CPDs together with a wide variety of oxidatively generated lesions such as 
single strand breaks and oxidized bases. Among those, 8-oxo-7,8-dihydroguanine 
(8-oxoGua) is the most frequent since it can be produced by several mechanisms. 
Data available on the respective yield of DNA photoproducts in cells and skin 
show that exposure to sunlight mostly induces pyrimidine dimers, which explains 
the mutational signature found in skin tumors, with lower amounts of 8-oxoGua 
and strand breaks. The present review aims at describing the basic 
photochemistry of DNA and discussing the quantitative formation of the different 
UV-induced DNA lesions reported in the literature. Additional information on 
mutagenesis, repair and photoprotection is briefly provided.