RESUMO
Radiations emitted by low power radiation sources have been applied for therapeutic proposals due to their capacity of inactivating bacteria and cancer cells in photodynamic therapy and stimulating tissue cells in photobiomodulation. Exposure to these radiations could increase cell proliferation in bacterial cultures under stressful conditions. Cells in infected or not infected tissue injuries are also under stressful conditions and photobiomodulation-induced regenerative effect on tissue injuries could be related to effects on stressed cells. The understanding of the effects on cells under stressful conditions could render therapies based on photobiomodulation more efficient as well as expand them. Thus, the objective of this review was to update the studies reporting photobiomodulation on prokaryotic and eukaryotic cells under stress conditions. Exposure to radiations emitted by low power radiation sources could induce adaptive responses enabling cells to survive in stressful conditions, such as those experienced by bacteria in their host and by eukaryotic cells in injured tissues. Adaptive responses could be the basis for clinical photobiomodulation applications, either considering their contraindication for treatment of infected injuries or indication for treatment of injuries, inflammatory process resolution, or tissue regeneration.
Assuntos
Bactérias/citologia , Bactérias/efeitos da radiação , Células Eucarióticas/efeitos da radiação , Terapia com Luz de Baixa Intensidade , Estresse Fisiológico/efeitos da radiação , HumanosRESUMO
PURPOSE: We analysed the lethal and mutagenic interactions between γ-rays, cisplatin (Pt) and etoposide (E), three agents used in tumour chemoradiotherapy. Corresponding results at cellular and molecular levels could provide additional elements on involved mechanisms and, on antitumour activity and toxicity in combined cancer treatments. MATERIALS AND METHODS: The yeast Saccharomyces cerevisiae SC7K(lys2-3) (auxotrophic for lysine) was used as eukaryotic model. Exponential growing cells were exposed to the mentioned agents, as single and combined treatments. Lethal and mutation interaction equations were determined as a function of doses according to quantitative models. DNA double-strand breaks were evaluated immediately after treatments, through pulsed-field electrophoresis and laser densitometry. RESULTS: All three agents induced significant mutant frequency. The γâ+Pt + E combination determined maximal lethal and mutagenic synergism, followed by γâ+âPt and γâ+âE combinations. Meanwhile, Ptâ+âE combination showed lethal additivity and very low mutagenic synergism. Ptâ+âE double combination determined moderate DNA degradation. DNA degradation after γ-exposure, was similar to that of γâ+âPt, γâ+âE and γâ+âPtâ+âE combinations. CONCLUSIONS: Synergistic lethal and mutagenic interactions indicate crosstalk between non-homologous end joining, homologous recombination and postreplicative repair pathways. Ptâ+âE additivity indicate independence of involved repair pathways. Furthermore, the quantification of interactive events may be an additional suitable tool in tumour therapy planning.
Assuntos
Cisplatino/farmacologia , Etoposídeo/farmacologia , Células Eucarióticas/efeitos dos fármacos , Células Eucarióticas/efeitos da radiação , Raios gama , Mutagênicos/metabolismo , Saccharomyces cerevisiae/metabolismo , Antineoplásicos/metabolismo , Antineoplásicos/farmacologia , Cisplatino/metabolismo , Quebras de DNA de Cadeia Dupla/efeitos dos fármacos , Quebras de DNA de Cadeia Dupla/efeitos da radiação , Reparo do DNA/efeitos dos fármacos , Reparo do DNA/efeitos da radiação , Etoposídeo/metabolismo , Células Eucarióticas/metabolismo , Modelos Biológicos , Mutagênicos/toxicidade , Saccharomyces cerevisiae/citologia , Saccharomyces cerevisiae/genéticaRESUMO
Cyclobutane pyrimidine dimers (CPDs) are directly involved in signaling for UV-induced apoptosis in mammalian cells. Failure to remove these lesions, specially those located at actively expressing genes, is critical, as cells defective in transcription coupled repair have increased apoptotic levels. Thus, the blockage of RNA synthesis by lesions is an important candidate event triggering off active cell death. In this work, wild-type and XPB mutated Chinese hamster ovary (CHO) cells expressing a marsupial photolyase, that removes specifically CPDs from the damaged DNA, were generated, in order to investigate the importance of this lesion in both RNA transcription blockage and apoptotic induction. Photorepair strongly recovers RNA synthesis in wild-type CHO cell line, although the resumption of transcription is decreased in XPB deficient cells. This recovery is accompanied by the prevention of cells entering into apoptosis. These results demonstrate that marsupial photolyase has access to CPDs blocking RNA synthesis in vivo, and this may be affected by the presence of a mutated XPB protein.