Avaliação dos efeitos da exposição isolada e simultânea ao laser vermelho de baixa potência e LED ultravioleta A

Abstract

Exposure to non-ionizing radiation from low-power sources can trigger the process of photobiomodulation (PBM), which has been used for therapeutic purposes in the treatment of wounds, pain, and inflammation. PBM is initiated by the absorption of these radiations by endogenous photoacceptors, which promotes changes in biological processes at the molecular, cellular, and systemic levels. These changes are generally associated with beneficial effects, but may involve modifications in molecules such as DNA, which would trigger specific repair mechanisms. Nevertheless, studies investigating the harmful effects of specific radiation, such as low-power red laser and ultraviolet A (UVA) light emitting diodes (LED), remain scarce. In this context, the present study aimed to evaluate the effects of these radiations, in isolation and in combination, on DNA damage and the modulation of cellular repair pathways. For this purpose, pUC19 plasmids and Saccharomyces cerevisiae cultures were used to investigate the occurrence of single and double strand breaks in DNA, changes in cell viability and proliferation, as well as the expression of genes related to the base excision repair (BER), nucleotide excision repair (NER), telomere maintenance and non-homologous recombination pathways. The cells evaluated included proficient and deficient lines in the BER pathway. Exposure to radiation was performed at different fluences: 10.6 and 21.2 J/cm² for red laser (660 nm) and 3.0 and 6.0 J/cm² for UVA LED (390 nm). The results demonstrated that, at the fluences evaluated, isolated or simultaneous exposure to laser and LED did not alter cell viability and proliferation and did not alter the electrophoretic profile. However, there was significant modulation in the expression of the genes APN1 (BER), RAD10 (NER), STN1 and TEN1 (telomere maintenance) when exposed to UVA LED and simultaneously to laser and UVA LED. It is concluded that PBM, under the conditions tested, did not cause lethal damage to the evaluated models, but was able to reduce the expression of genes associated with genomic stability. These findings suggest the participation of DNA repair and telomere maintenance mechanisms in PBM and that new therapeutic protocols can be proposed aiming at genomic stability.