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Review
. 2020 Oct 1;21(19):7264.
doi: 10.3390/ijms21197264.

Focus on UV-Induced DNA Damage and Repair-Disease Relevance and Protective Strategies

Mateusz Kciuk  1   2 , Beata Marciniak  2 , Mariusz Mojzych  3 , Renata Kontek  2
Affiliations
Review

Focus on UV-Induced DNA Damage and Repair-Disease Relevance and Protective Strategies

Mateusz Kciuk et al. Int J Mol Sci. .

Abstract

The protective ozone layer is continually depleting due to the release of deteriorating environmental pollutants. The diminished ozone layer contributes to excessive exposure of cells to ultraviolet (UV) radiation. This leads to various cellular responses utilized to restore the homeostasis of exposed cells. DNA is the primary chromophore of the cells that absorbs sunlight energy. Exposure of genomic DNA to UV light leads to the formation of multitude of types of damage (depending on wavelength and exposure time) that are removed by effectively working repair pathways. The aim of this review is to summarize current knowledge considering cellular response to UV radiation with special focus on DNA damage and repair and to give a comprehensive insight for new researchers in this field. We also highlight most important future prospects considering application of the progressing knowledge of UV response for the clinical control of diverse pathologies.

Keywords: DNA damage; DNA repair; ROS; UV radiation; photoproducts.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Common ultraviolet (UV)-induced photoproducts. Cyclobutane-pyrimidine dimers (CPDs) comprise 75% of photodamage, while 6-4 photoproducts (6-4PPs) constitute 25% of photodamage. Derivatives of two thymine bases were shown in the figure.
Figure 2
Figure 2
Formation of cytosine photohydrate (6-hydroxy-5,6-dihydrocytosine) as a result of photohydration reaction.
Figure 3
Figure 3
Purine photoproducts: adenine dimer, Pörschke photoproduct, thymine-adenine photoadduct, 4,6-diamino-5-guanidinopyrimidine (DGPY), and 8-(5-aminoimidazol-4-yl)adenine (8-AIA).
Figure 4
Figure 4
Oxidized DNA bases: formamidopyrimidine derivative of adenine (Fapy-A), 7,8 dihydro-8-oxoguanine (8-oxo-G), and thymine glycol. Modifications of the proper base structures by ROS were highlighted with the red boxes.
Figure 5
Figure 5
Ataxia telangiectasia and Rad3-related protein (ATR) and ataxia telangiectasia mutated (ATM)-mediated DNA damage response (DDR) pathways activated upon DNA damage. The details are discussed in text.
Figure 6
Figure 6
Downstream signaling cascade activated by ATR and ATM via CHK1/2 dependent phosphorylation events. A detailed description of the pathway can be found in the text.
Figure 7
Figure 7
Photoreactivation reaction: the exposure to UV light leads to the formation of cyclobutane-pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs) removed by photolyase enzyme in the light-dependent manner.
Figure 8
Figure 8
Excision repair pathways for the repair of UV damage include UV-damage endonuclease (UVDE)–mediated repair (UVER), nucleotide excision repair (NER) composed of Uvr proteins in prokaryotes and XP proteins in eukaryotes, and base excision repair (BER) for the repair of UV-induced oxidative damage.
Figure 9
Figure 9
NHEJ and HR double strand break repair. The details of the repair processes were placed in the main text above.
See this image and copyright information in PMC

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