NDLI: Rescue of cells from apoptosis increases DNA repair in UVB exposed cells: implications for the DNA damage response

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Toxicology Research Vol - 4 Issue - 2

Toxicology Research Vol - 4 Issue - 1

Toxicology Research Vol -3

Toxicology Research Vol -2

Toxicology Research Vol -1

Rescue of cells from apoptosis increases DNA repair in UVB exposed cells: implications for the DNA damage response

Content Provider	Royal Society of Chemistry (RSC)
Author	Evans, Mark D. Young, Antony R. Abbas, Hussein H. K. Cooke, Marcus S. Delinassios, George J. Mistry, Vilas Macip, Salvador Karbaschi, Mahsa
Copyright Year	2015
Abstract	Classically, the nucleotide excision repair (NER) of cyclobutane pyrimidine dimers (CPD) is a lengthy process (t1/2 > 48 h). Using the T4 endonuclease V-modified comet assay, we uniquely found a far more rapid repair of UVA-induced CPD (t1/2 = 4.5 h) in human skin keratinocytes. The repair of UVB-induced CPD began to slow within 1 h of irradiation, causing damage to persist for over 36 h. A similar trend was noted for the repair of oxidatively-modified purine nucleobases. Supportive of this differential repair, we noted an up-regulation of key genes associated with NER in UVA-irradiated cells, whereas the same genes were down regulated in UVB-irradiated cells. There were no significant differences in cell viability between the two treatments over the first 6 h post-irradiation, but after 24 h apoptosis had increased significantly in the UVB-irradiated cells. The role of apoptosis was confirmed using a pan-caspase inhibitor, which increased CPD repair, similar to that seen with UVA. These data indicate that the cellular ‘decision’ for apoptosis/DNA repair occurs far earlier than previously understood, and that the induction of apoptosis leads to lesion persistence, and not vice versa. This also highlights a new, potential increased carcinogenic risk from UVA-induced DNA damage as, rather than undergoing apoptosis, high levels of damage are tolerated and repaired, with the attendant risk of mutation.
Starting Page	725
Ending Page	738
Page Count	14
File Format	HTM / HTML PDF
ISSN	2045452X
Volume Number	4
Issue Number	3
Journal	Toxicology Research
DOI	10.1039/c4tx00197d
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	Enzyme inhibitor Ultraviolet DNA repair Comet assay Pyrimidine dimer DNA Purine Cyclobutane Thyroid hormones Lesion Mutation Endonuclease Apoptosis
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Toxicology

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Rescue of cells from apoptosis increases DNA repair in UVB exposed cells: implications for the DNA damage response

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Rescue of cells from apoptosis increases DNA repair in UVB exposed cells: implications for the DNA damage response