Summary
It is well established that UV radiation present in sunlight is a potent human carcinogen. UV radiation is termed a “complete carcinogen” because it causes skin cancers without additional initiators or promoters. The mutagenic and carcinogenic effects of UV light can be attributed to the induction of DNA damage and errors in repair and replication. Fortunately, cells are equipped with a variety of mechanisms that constantly monitor and repair most of the damage inflicted by UV light. Nucleotide excision repair system prevents the DNA damages from leading to DNA mutations, and finally, to skin carcinogenesis. In this process, the p53 gene plays a pivotal role by causing cell cycle arrest to gain some time for DNA repair, or inducing cell death by apoptosis when the DNA damages are too severe to repair. Tanning leads to the reduction of DNA damage by protecting the nuclei from UV irradiation. UV-induced immunosuppression, on the other hand, seems to promote skin carcinogenesis. Besides UVB radiation, UVA also plays a substantial role in photoaging by inducing the formation of reactive oxygen species. However, in contrast to UVA, UVB is more active in inducing mutations in tumor suppressor genes and oncogenes and in skin carcinogenesis. Finally, therapeutic UV exposure for the treatment of skin disorders causes unwarranted clinical side effects. A better understanding of the interaction between UV radiation and the skin should lead to harnessing the beneficial aspects of UV irradiation and minimize the harmful effects.