Sunlight damage to cellular DNA : focus on oxidatively generated lesions.

Registro completo de metadados
MetadadosDescriçãoIdioma
Autor(es): dc.creatorSchuch, André Passaglia-
Autor(es): dc.creatorMoreno, Natália Cestari-
Autor(es): dc.creatorSchuch, Natielen Jacques-
Autor(es): dc.creatorMenck, Carlos Frederico Martins-
Autor(es): dc.creatorGarcia, Camila Carrião Machado-
Data de aceite: dc.date.accessioned2025-08-21T15:48:49Z-
Data de disponibilização: dc.date.available2025-08-21T15:48:49Z-
Data de envio: dc.date.issued2017-11-27-
Data de envio: dc.date.issued2017-11-27-
Data de envio: dc.date.issued2017-
Fonte completa do material: dc.identifierhttp://www.repositorio.ufop.br/handle/123456789/9182-
Fonte completa do material: dc.identifierhttps://doi.org/10.1016/j.freeradbiomed.2017.01.029-
Fonte: dc.identifier.urihttp://educapes.capes.gov.br/handle/capes/1024739-
Descrição: dc.descriptionThe routine and often unavoidable exposure to solar ultraviolet (UV) radiation makes it one of the most significant environmental DNA-damaging agents to which humans are exposed. Sunlight, specifically UVB and UVA, triggers various types of DNA damage. Although sunlight, mainly UVB, is necessary for the production of vitamin D, which is necessary for human health, DNA damage may have several deleterious consequences, such as cell death, mutagenesis, photoaging and cancer. UVA and UVB photons can be directly absorbed not only by DNA, which results in lesions, but also by the chromophores that are present in skin cells. This process leads to the formation of reactive oxygen species, which may indirectly cause DNA damage. Despite many decades of investigation, the discrimination among the consequences of these different types of lesions is not clear. However, human cells have complex systems to avoid the deleterious effects of the reactive species produced by sunlight. These systems include antioxidants, that protect DNA, and mechanisms of DNA damage repair and tolerance. Genetic defects in these mechanisms that have clear harmful effects in the exposed skin are found in several human syndromes. The best known of these is xeroderma pigmentosum (XP), whose patients are defective in the nucleotide excision repair (NER) and translesion synthesis (TLS) pathways. These patients are mainly affected due to UV-induced pyrimidine dimers, but there is growing evidence that XP cells are also defective in the protection against other types of lesions, including oxidized DNA bases. This raises a question regarding the relative roles of the various forms of sunlight-induced DNA damage on skin carcinogenesis and photoaging. Therefore, knowledge of what occurs in XP patients may still bring important contributions to the understanding of the biological impact of sunlight-induced deleterious effects on the skin cells.-
Formato: dc.formatapplication/pdf-
Idioma: dc.languageen-
Direitos: dc.rightsaberto-
Direitos: dc.rightsThis is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/BY-NC-ND/4.0/). Fonte: o próprio artigo.-
Palavras-chave: dc.subjectUltraviolet radiation-
Palavras-chave: dc.subjectDNA lesions-
Palavras-chave: dc.subjectDNA repair-
Palavras-chave: dc.subjectPhotoaging-
Palavras-chave: dc.subjectSkin cancer-
Título: dc.titleSunlight damage to cellular DNA : focus on oxidatively generated lesions.-
Aparece nas coleções:Repositório Institucional - UFOP

Não existem arquivos associados a este item.