User:Kaiya78/Photocarcinogen
The type of UV radiation determines the characteristics of photocarcinogenesis. For example, UVA radiation characteristically gives rise to reactive oxygen species (ROS) whereas UVB radiation correlates with CPD lesions. DNA absorption of UV radiation primarily leads to CPD and 6-4 lesions. The neighboring pyrimidines form a cyclobutane pyrimidine dimer in a CPD lesion. DNA absorption of UV radiation can also lead to TC, CC, and TT lesions but with much less frequency. The failure of DNA repair mechanisms to fix such lesions notably characterizes photocarcinogenesis. [1]
In addition, UV radiation often increases the production of cytokines such as interleukin-10 which indirectly hinder antigen presentation in cells. Moreover, UV radiation frequently leads to mutations in the tumor suppressor gene p53 in photocarcinogenesis. [2]
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- ^ Black, H.S.; deGruijl, F.R.; Forbes, P.D.; Cleaver, J.E.; Ananthaswamy, H.N.; deFabo, E.C.; Ullrich, S.E.; Tyrrell, R.M. (1997-08-XX). "Photocarcinogenesis: an overview". Journal of Photochemistry and Photobiology B: Biology. 40 (1): 29–47. doi:10.1016/S1011-1344(97)00021-3.
{{cite journal}}: Check date values in:|date=(help) - ^ Valejo Coelho, Margarida Moura; Matos, Tiago R.; Apetato, Margarida (2016-09-XX). "The dark side of the light: mechanisms of photocarcinogenesis". Clinics in Dermatology. 34 (5): 563–570. doi:10.1016/j.clindermatol.2016.05.022.
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