Can skin cancer in humans be prevented by alleviation of oxidative stress?

Summary

The range of photon energies in solar radiation and the diverse cell and molecular targets in skin allow for participation of oxygen radicals and oxidative stress at several levels in the development of skin cancer: DNA damage and mutation, membrane damage, and intracellular signalling. The intense UVA component of sunlight (315–400 nm) is of particular interest because of deep penetration, generation of oxidative damage and having a mutational spectrum which overlaps that of the more carcinogenic UVB (280–315 nm). Many UV-induced mutagenic and signalling events are now understood at the molecular level, and significant protection from UV carcinogenesis has been obtained with antioxidants in experimental animals. There is little evidence to suggest, however, that similar results have been achieved in humans although the converse effect has been established, of elevated skin cancer risk following simultaneous exposure to sunlight and precursors of the pro-oxidant paraquat. 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 cells relevant to solar UV.