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. 2020 Nov 4;11(11):1304. doi: 10.3390/genes11111304

Figure 1.

Figure 1

The common DNA lesions induced by UV-A (315–400 nm), UV-B (280–315 nm) and UV-C (100–280 nm), the action spectrum for generalized DNA damage from 200–400 nm (solid line) and the absorption spectrum for DNA with the maximum at 260 nm (dotted line). Cyclobutane pyrimidine dimers (CPDs), 7,8-dihydro-2′-deoxyguanosine (8-oxo-dG) and single strand breaks (SSBs) are formed upon UV-A, UV-B and UV-C radiation. CPDs can undergo photoreversion to undamaged bases upon UV-C radiation (a). UV-B and UV-C are responsible for the formation of (6-4) pyrimidine–pyrimidone photoproducts (6-4 PPs) and double strand breaks (DSBs). The role of UV-A in the direct formation of DSBs is controversial. While under a biologically relevant intensity of UV-A formation of 6-4 PPs does not occur, upon absorption of UV-A, 6-4 PPs can isomerize to Dewar isomers (b). Under UV-A, isolated 6-4 PPs can act as photosensitizers leading, to production of CPDs and SSBs.