Oxidative Stress-Induced Protein Damage Inhibits DNA Repair and Determines Mutation Risk and Therapeutic Efficacy.

ABSTRACT:

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The relationship between sun exposure and nonmelanoma skin cancer risk is well established. Solar UV (wavelength 280-400 nm) is firmly implicated in skin cancer development. Nucleotide excision repair (NER) protects against cancer by removing potentially mutagenic DNA lesions induced by UVB (280-320 nm). How the 20-fold more abundant UVA (320-400 nm) component of solar UV radiation increases skin cancer risk is not understood. Here it is demonstrated that the contribution of UVA to the effect of UV radiation on cultured human cells is largely independent of its ability to damage DNA. Instead, the effects of UVA reflect the induction of oxidative stress that causes extensive protein oxidation. Because NER proteins are among those damaged, UVA irradiation inhibits NER and

SUBMITTER: McAdam E 

PROVIDER: S-EPMC4955916 | biostudies-literature | 2016 Jul

REPOSITORIES: biostudies-literature