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dc.contributor.author Filgueira, Daza de Moraes Vaz Batista
dc.contributor.author Freitas, Diana Paula Salomão de
dc.contributor.author Votto, Ana Paula de Souza
dc.contributor.author Fillmann, Gilberto
dc.contributor.author Monserrat, José María
dc.contributor.author Monserrat, Laura Alicia Geracitano
dc.contributor.author Trindade, Gilma Santos
dc.date.accessioned 2010-10-06T18:48:52Z
dc.date.available 2010-10-06T18:48:52Z
dc.date.issued 2007
dc.identifier.citation FILGUEIRA, D. M. V. B. et al. . Photodynamic Action of Benzo[a]pyrene in K562 Cells. Photochemistry and Photobiology, v. 83, p. 1358-1363, 2007. pt_BR
dc.identifier.issn 1751-1097
dc.identifier.uri http://repositorio.furg.br/handle/1/119
dc.description.abstract Benzo[a]pyrene (BaP) is ubiquitously distributed in the environment, being considered the most phototoxic element among polycyclic aromatic hydrocarbon (PAHs). In presence of oxygen, PAHs can act as a photosensitizer by means of promoting photo-oxidation of biological molecules (photodynamic action, PDA). Thus, the present study analyzed the photodynamic action of BaP under UVA irradiation (BaP + UVA) and its oxidative effects on K562 cells. The evaluation of BaP kinetics showed that the highest intracellular concentration occurred after 18 h of incubation. Cell viability, reactive oxygen species (ROS) generation, lipid peroxidation, DNA damage (breaks and DNA–protein cross-link [DNAPC]) were assessed after exposure to BaP, UVA and BaP plus UVA irradiation (BaP + UVA). Cell viability was decreased just after exposure to BaP + UVA. Lipid peroxidation and DNA breaks increased after BaP + UVA exposure, while the DNAPC increased after BaP, UVA and BaP + UVA exposure, suggesting that BaP + UVA effects were a consequence of both type II (producing mainly singlet oxygen) and type I (producing others ROS) mechanisms of PDA. pt_BR
dc.language.iso eng pt_BR
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dc.title Photodynamic action of Benzo[a]pyrene in K562 Cells pt_BR
dc.type article pt_BR


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