Photochemical processes to cellular DNA damage by UV radiation of different wavelengths: biological consequences

Abstract

UV radiation of sunlight induces in cellular DNA of different organisms photochemical reactions, which may lead to the development of series biological responses to arising lesions, including apoptosis, mutagenesis, and carcinogenesis. The chemical nature and the amount of DNA lesions depend on the wavelength of UV radiation. Photons of UV radiation in the region B (UVB, 290–320 nm) cause the production of two main defects, namely, cyclobutane pyrimidine dimers and, with a less yield, pyrimidine (6-4) pyrimidone photoproducts; their formation is the result of the direct UVB photon absorption by DNA bases. Photons of UV radiation in the region A (UVA, 320–400 nm) induce only cyclobutane dimers that can be formed by triplet-triplet energy transfer from cellular chromophores, absorbing photons of this UV region, to DNA thymine bases. UVA is much more effective than UVB in the sensitized oxidatively lesion formation in DNA such as single strand breaks and oxidized bases; among those, 8-oxo-dihydroguanine is the most frequent since it can be produced from several oxidation processes. In recent years, multiple papers, reporting novel, more detailed information about molecular mechanisms of photochemical reactions underlying the formation of different lesions in DNA were published. The present review mainly aims at summarizing and analyzing data contained in these publications, particularly regarding oxidative reactions that are initiated by reactive oxygen species and radicals generated by potential endogenous photosensitizers such as pterins, riboflavin, protoporphyrin IX, NADH, and melanin. The role of specific DNA photoproducts in genotoxic processes induced in living systems by UV radiation of different wavelengths, including human skin carcinogenesis, is discussed.