Ultraviolet radiation–induced lesions, generated by UV-B (280–320nm wavelength) or UV-A
(320–400nm wavelength), result from DNA damage, which is converted to mutations during
cellular repair processes. UB-B and UV-A generate different types of DNA damage and DNA
repair mechanisms (reviewed in Reference 113). Irradiation with UV-B produces cyclobutane
pyrimidine dimers that are repaired by nucleotide excision repair. If left unrepaired,
C?T and CC?TT base transitions occur. UVA- induced DNA damage produces mostly oxidative
lesions via photosensitization mechanisms and is repaired by base excision repair.
UV-B and UV-A also produce different effects on the immune system and elicit different transcriptional
and inflammatory responses. While the specific mechanisms by which UV radiation
induces basal cell or squamous cell carcinomas or melanoma are not clear, a number of signal
transduction pathways are affected that can either lead to apoptosis or to increased cell proliferation.
UV irradiation activates receptor tyrosine kinases and other cell surface receptors. It also enhances phosphorylation by ligand-independent mechanisms via inhibition of protein tyrosine phosphatase activity. Liganddependent cell surface receptor activation can also occur by activation of autocrine or paracrine
release of growth factors from keratinocytes, melanocytes, or neighboring fibroblasts. It is clear, however, that better animal models are needed to clearly define the mechanisms by which UV light causes human cancer. OXYGEN FREE RADICALS, AGING, AND CANCER The diseases of aging include cardiovascular disease, decline in function of the immune system, brain dysfunction,
