Molecular mechanisms of ultraviolet radiation-induced DNA damage and repair

Laboratory of Photobiology and Molecular Microbiology, Centre of Advanced Study in Botany, Banaras Hindu University, Varanasi 221005, India.
Journal of nucleic acids 01/2010; 2010:592980. DOI: 10.4061/2010/592980
Source: PubMed


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.

Download full-text


Available from: Rajeshwar P Sinha
  • Source
    • "Several processes are affected by UV irradiance. For instance, UVB induces a reduction in the metabolism of heterotrophic bacteria (e.g., Amado et al., 2015), as well as aquatic primary producers, such as cyanobacteria, mainly due to DNA damage (Buma et al., 2001; Helbling et al., 2001; Rastogi et al., 2010). Furthermore, detrimental effects by UVA on phytoplankton have been observed on primary production, pigment degradation and changes in nitrogen metabolism (Kim and Watanabe, 1994; Döhler and Buchmann, 1995; Palffy and Voros, 2006). "
    [Show abstract] [Hide abstract]
    ABSTRACT: Cyanobacteria are aquatic photosynthetic microorganisms. While of enormous ecological importance, they have also been linked to human and animal illnesses around the world as a consequence of toxin production by some species. Cylindrospermopsis raciborskii, a filamentous nitrogen-fixing cyanobacterium, has attracted considerable attention due to its potential toxicity and ecophysiological adaptability. We investigated whether C. raciborskii could be affected by ultraviolet (UV) radiation. Non-axenic cultures of C. raciborskii were exposed to three UV treatments (UVA, UVB, or UVA + UVB) over a 6 h period, during which cell concentration, viability and ultrastructure were analyzed. UVA and UVA + UVB treatments showed significant negative effects on cell concentration (decreases of 56.4 and 64.3%, respectively). This decrease was directly associated with cell death as revealed by a cell viability fluorescent probe. Over 90% of UVA + UVB- and UVA-treated cells died. UVB did not alter cell concentration, but reduced cell viability in almost 50% of organisms. Transmission electron microscopy (TEM) revealed a drastic loss of thylakoids, membranes in which cyanobacteria photosystems are localized, after all treatments. Moreover, other photosynthetic- and metabolic-related structures, such as accessory pigments and polyphosphate granules, were damaged. Quantitative TEM analyses revealed a 95.8% reduction in cell area occupied by thylakoids after UVA treatment, and reduction of 77.6 and 81.3% after UVB and UVA + UVB treatments, respectively. Results demonstrated clear alterations in viability and photosynthetic structures of C. raciborskii induced by various UV radiation fractions. This study facilitates our understanding of the subcellular organization of this cyanobacterium species, identifies specific intracellular targets of UVA and UVB radiation and reinforces the importance of UV radiation as an environmental stressor.
    Full-text · Article · Oct 2015 · Frontiers in Microbiology
  • Source
    • "In addition, both UVB and UVA radiation can also induce apoptosis by increasing the expression of the cell surface receptor Fas, which leads to the clustering of Fas and the activation of the Fas/caspase 8 pathway (Bang et al., 2003, 2002). Therefore, apoptosis works to secure genomic integrity, avoiding the segregation of the UV-affected chromosome by the elimination of damaged cells (Rastogi et al., 2010). Furthermore, choosing of oviposition sites protected from sunlight helps to reduce the exposure of embryos to UV levels below the lethal dose, thus reducing considerably the environmental risk imposed by solar UVB radiation (Palen and Schindler, 2010). "
    [Show abstract] [Hide abstract]
    ABSTRACT: The increased incidence of solar ultraviolet B (UVB) radiation has been proposed as an environmental stressor, which may help to explain the enigmatic decline of amphibian populations worldwide. Despite growing knowledge regarding the UV-induced biological effects in several amphibian models, little is known about the efficacy of DNA repair pathways. In addition, little attention has been given to the interplay between these molecular mechanisms with other physiological strategies that avoid the damage induced by sunlight. Here, DNA lesions induced by environmental doses of solar UVB and UVA radiation were detected in genomic DNA samples of treefrog tadpoles (Hypsiboas pulchellus) and their DNA repair activity was evaluated. These data were complemented by monitoring the induction of apoptosis in blood cells and tadpole survival. Furthermore, the tadpoles' ability to perceive and escape from UV wavelengths was evaluated as an additional strategy of photoprotection. The results show that tadpoles are very sensitive to UVB light, which could be explained by the slow DNA repair rates for both cyclobutane pyrimidine dimers (CPDs) and pyrimidine (6,4) pyrimidone photoproducts (6,4PPs). However, they were resistant to UVA, probably as a result of the activation of photolyases during UVA irradiation. Surprisingly, a sensory mechanism that triggers their escape from UVB and UVA light avoids the generation of DNA damage and helps to maintain the genomic integrity. This work demonstrates the genotoxic impact of both UVB and UVA radiation on tadpoles and emphasizes the importance of the interplay between molecular and sensory mechanisms to minimize the damage caused by sunlight.
    Full-text · Article · Oct 2015 · Journal of Experimental Biology
  • Source
    • "B) Os dois principais fotoprodutos induzidos pela absorção de luz UV pela molécula de DNA são os dímeros de pirimidina ciclobutano (CPD) e os fotoprodutos 6-4 pirimidina-pirimidona (6-4PPs). Estruturas moleculares foram adaptadas da revisão de Rastogi, et al 2010. C) A replicação de dímeros pode resultar em mutações pontuais. "

    Preview · Article · Jun 2015
Show more