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23-12-2010 | Dermatology | Article

UVA does not activate DNA damage response pathways


Free abstract

MedWire News: DNA double-stranded breaks (DSBs) are not formed by ultraviolet (UV)A, suggest study findings showing that UVA does not activate the Fanconi anemia (FA)/BRCA DNA damage response pathway responsible for recombination repair.

"Although UVA induces only a smaller amount of DNA photoproducts than UVB, lack of recombination repair at those sites may result in the formation of chromosome aberrations that have been shown to be generated by UVA," say Thomas Rünger (Boston University School of Medicine, Massachusetts, USA) and colleagues.

To investigate the possible formation of DNA DSBs by UVA, the researchers studied the activation of the FA/BRCA pathway and of RAD51 in primary skin fibroblasts following exposure to various doses of UVA.

Physiological doses of UVB (100, 200, or 300 J m-2), but not UVA, induced time- and dose-dependent FANCD2 protein monoubiquitination and formation of FANCD2 nuclear foci, which are both indicative of FA/BRCA pathway activation.

Furthermore, no formation of gamma-H2AX foci - a site of DNA damage with repair or stalled replication forks - was observed with UVA, even at high doses of 400 kJ/m2. "These data strongly indicate that UVA does not generate a detectable number of DNA DSBs," say the authors.

To further verify the findings, Rünger and team assessed the formation of DNA DSBs using neutral single-cell electrophoresis. DNA DSBs were generated with infrared and UVB radiation, but not with UVA.

The team says the findings suggest that recombination repair is not involved in the processing of UVA-induced DNA damage, and that DNA lesions commonly thought to require DNA recombination are not being formed in a significant number by UVA.

"The lack of FA/BRCA pathway activation with UVA may result in altered translesional DNA synthesis. This is in line with our recently proposed hypothesis that photoproducts generated by pure UVA may be more mutagenic than those generated by UVB or mixed UVA and UVB because of a lack of protective DNA damage responses," say the researchers.

The findings are published in the Journal of Investigative Dermatology.

MedWire ( is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2010

By Ingrid Grasmo