Abstract
DNA is one of the prime molecules, and its stability is of utmost importance for proper functioning and existence of all living systems. Genotoxic chemicals and radiations exert adverse effects on genome stability. Ultraviolet radiation (UVR) (mainly UV-B: 280–315 nm) is one of the powerful agents that can alter the normal state of life by inducing a variety of mutagenic and cytotoxic DNA lesions such as cyclobutane-pyrimidine dimers (CPDs), 6-4 photoproducts (6-4PPs), and their Dewar valence isomers as well as DNA strand breaks by interfering the genome integrity. To counteract these lesions, organisms have developed a number of highly conserved repair mechanisms such as photoreactivation, base excision repair (BER), nucleotide excision repair (NER), and mismatch repair (MMR). Additionally, double-strand break repair (by homologous recombination and nonhomologous end joining), SOS response, cell-cycle checkpoints, and programmed cell death (apoptosis) are also operative in various organisms with the expense of specific gene products. This review deals with UV-induced alterations in DNA and its maintenance by various repair mechanisms.
Highlights
The stratospheric ozone layer is continuously depleting due to the release of atmospheric pollutants such as chlorofluorocarbons (CFCs), chlorocarbons (CCs), and organobromides (OBs)
Solar UV radiation is responsible for a wide range of biological effects including alteration in the structure of protein, DNA, and many other biologically important molecules, chronic depression of key physiological processes, and acute physiological stress leading to either reduction in growth and cell division, pigment bleaching, N2 fixation, energy production, or photoinhibition of photosynthesis in several organisms [3, 9, 10]
DNA damage results in (i) misincorporation of bases during replication process, (ii) hydrolytic damage, which results in deamination of bases, depurination, and depyrimidination [36], (iii) oxidative damage, caused by direct interaction of ionizing radiations (IR) with the DNA molecules, as well as mediated by UV radiation-induced free radicals or reactive oxygen species [37, 38], and (iv) alkylating agents that may result in modified bases [36, 39]
Summary
The stratospheric ozone layer is continuously depleting due to the release of atmospheric pollutants such as chlorofluorocarbons (CFCs), chlorocarbons (CCs), and organobromides (OBs). Certain UV-absorbing pigments are produced by a number of organisms as a first line of defense; they are unable to avoid UV-radiation completely from reaching DNA in superficial tissue [28,29,30,31,32]. As a second line of defense several organisms have developed a number of specific and highly conserved repair mechanisms such as photoreactivation, excision repair, mismatch repair (MMR), double strand break (DSB) repair and certain other mechanisms like damage tolerance (dimer bypass), SOS (save our soul) response, checkpoint activation, and programmed cell death (PCD) or apoptosis (Figure 1) that efficiently remove DNA lesions ensuring the genomic integrity [22]. We discuss the molecular mechanisms of UV-induced DNA damage and repair mechanism (s) operative in various organisms
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