The range of photon energies in solar radiation and the diverse cell a
nd molecular targets in skin allow for participation of oxygen radical
s and oxidative stress at several levels in the development of skin ca
ncer: DNA damage and mutation, membrane damage, and intracellular sign
alling. The intense UVA component of sunlight (315-400 nm) is of parti
cular interest because of deep penetration, generation of oxidative da
mage and having a mutational spectrum which overlaps that of the more
carcinogenic UVB (280-315 nm). Many UV-induced mutagenic and signallin
g events are now understood at the molecular level, and significant pr
otection from UV carcinogenesis has been obtained with antioxidants in
experimental animals. There is little evidence to suggest, however, t
hat similar results have been achieved in humans although the converse
effect has been established, of elevated skin cancer risk following s
imultaneous exposure to sunlight and precursors of the pro-oxidant par
aquat. The present difficulty in translating these findings to prevent
human skin cancer may arise from deficiencies in the models used and
incomplete information about the specific responses of the target cell
s relevant to solar UV.