Physiological Aspects of UV-Excitation of DNA

Abstract

Solar ultraviolet (UV) radiation, mainly UV-B (280-315 nm), is one of the most potent genotoxic agents that adversely affects living organisms by altering their genomic stability. DNA through its nucleobases has absorption maxima in the UV region and is therefore the main target of the deleterious radiation. The main biological relevance of UV radiation lies in the formation of several cytotoxic and mutagenic DNA lesions such as cyclobutane pyrimidine dimers (CPDs), 6-4 photoproducts (6-4PPs), and their Dewar valence isomers (DEWs), as well as DNA strand breaks. However, to counteract these DNA lesions, organisms have developed a number of highly conserved repair mechanisms such as photoreactivation, excision repair, and mismatch repair (MMR). Photoreactivation involving the enzyme photolyase is the most frequently used repair mechanism in a number of organisms. Excision repair can be classified as base excision repair (BER) and nucleotide excision repair (NER) involving a number of glycosylases and polymerases, respectively. In addition to this, double-strand break repair, SOS response, cell-cycle checkpoints, and programmed cell death (apoptosis) are also operative in various organisms to ensure genomic stability. This review concentrates on the UV-induced DNA damage and the associated repair mechanisms as well as various damage detection methods.

Only IL‐1β release is inflammasome‐dependent upon ultraviolet B irradiation although IL‐18 is also secreted

“…Ultraviolet B (UVB; 290‐315 nm) is the most harmful type of ultraviolet radiation to which human tissues are exposed to every day 11 . The photons present in UVB are directly absorbed by DNA; UVB not only can cause direct mutagenic and cytotoxic damage in cells, but it also induces the production of ROS, which indirectly damages DNA 11‐13 . Although negligible amounts of UVB reach the retina in adults, 14,15 we have utilized it in our experimental model in order to mimic a DNA‐damaged environment in human retinal pigment epithelium (RPE) cells.…”

Sensitivity of two Nostoc species harbouring diverse habitats to ultraviolet-B radiation

“…Consequently, increased levels of UVR (280-400 nm) reach the Earth's surface, and harvesting of solar radiation for photosynthesis exposes cyanobacteria to UV B (280-315 nm) and UV A (315-400 nm) radiations. The high energetic UV B radiation has the greatest poten tial for cell damage caused by both direct effects on DNA and proteins as they absorb maximally in the UV region and indirect effects via the production of reac tive oxygen species [17][18][19][20][21]. Morphogenesis, pigmen tation, motility and orientation, nitrogen and CO 2 fix ation, phycobiliproteins, enzymatic activity pro teome, genome and photosynthesis are well known targets of short wavelength UV B radiation that even tually affect the growth and survival of organisms [22].…”

Screening and partial purification of photoprotective pigment scytonemin from cyanobacterial crusts dwelling on the historical monuments in and around Varanasi, India

“…7 In contrast, UV-A (315-400 nm) radiation is not absorbed directly by the native DNA, but still induce DNA damage either by producing a secondary photoreaction of existing DNA photoproducts or via indirect photosensitizing reactions. 8,9 Several defense strategies have been evolved in cyanobacteria to counteract the damaging effects of UV, such as migration, mat formation, synthesis of antioxidants, presence of specific active repair mechanisms and UV-absorbing compounds. 10,11 The UV-absorbing/ screening compounds such as mycosporine-like amino acids (MAAs) 12 and scytonemin have received fair attention for their potential role in UV photoprotection.…”