2014 Volume 36 Issue 3 Pages 111-117
Photogenotoxicity is generally defined as the ability of chemicals to induce genotoxic effects under ultraviolet (UV) and/or visible light. The potential of chemically-induced epigenetic alterations in the nucleus to affect the genotoxicity of UV has been discussed in this review. UV induces the formation of pyrimidine dimers and is, therefore, considered to be genotoxic. Pyrimidine dimers are effectively repaired by nucleotide excision repair (NER), a process in which the relaxation of nucleosome interactions is considered necessary. Histone modifications such as acetylation are a cause of the change of nucleosome interactions, and previous studies and reviews demonstrated that these modifications altered the generation as well as repair of DNA damage. We previously reported that the hyperacetylation of histones enhanced sensitivity to UV light and suppressed NER. Some chemicals, metals, pesticides, and hormones have been shown to acetylate histone residues. The dysregulation of histone modifications caused by these chemicals may affect the formation of pyrimidine dimers following exposure to UV light as well as repair ability, which suggests the new concept of “photogenotoxicity”.