Ascenso Andreia, Pedrosa Tiago, Pinho Sónia, Pinho Francisco, de Oliveira José Miguel P Ferreira, Cabral Marques Helena, Oliveira Helena, Simões Sandra, Santos Conceição
Instituto de Investigação do Medicamento (iMed.ULisboa), Faculdade de Farmácia, Universidade de Lisboa, Avenida Professor Gama Pinto, 1649-003 Lisboa, Portugal ; Departamento de Biologia, Laboratório de Biotecnologia e Citómica, CESAM, Universidade de Aveiro, Campus Universitário de Santiago, 3810-193 Aveiro, Portugal.
Departamento de Biologia, Laboratório de Biotecnologia e Citómica, CESAM, Universidade de Aveiro, Campus Universitário de Santiago, 3810-193 Aveiro, Portugal.
Oxid Med Cell Longev. 2016;2016:8214631. doi: 10.1155/2016/8214631. Epub 2015 Nov 17.
Lycopene has been reported as the antioxidant most quickly depleted in skin upon UV irradiation, and thus it might play a protective role. Our goal was to investigate the effects of preexposure to lycopene on UV-B-irradiated skin cells. Cells were exposed for 24 h to 10 M lycopene, and subsequently irradiated and left to recover for another 24 h period. Thereafter, several parameters were analyzed by FCM and
RT-PCR: genotoxicity/clastogenicity by assessing the cell cycle distribution; apoptosis by performing the Annexin-V assay and analyzing gene expression of apoptosis biomarkers; and oxidative stress by ROS quantification. Lycopene did not significantly affect the profile of apoptotic, necrotic and viable cells in nonirradiated cells neither showed cytostatic effects. However, irradiated cells previously treated with lycopene showed an increase in both dead and viable subpopulations compared to nonexposed irradiated cells. In irradiated cells, lycopene preexposure resulted in overexpression of BAX gene compared to nonexposed irradiated cells. This was accompanied by a cell cycle delay at S-phase transition and consequent decrease of cells in G0/G1 phase. Thus, lycopene seems to play a corrective role in irradiated cells depending on the level of photodamage. Thus, our findings may have implications for the management of skin cancer.
据报道，番茄红素是紫外线照射后皮肤中最易快速消耗的抗氧化剂，因此它可能发挥保护作用。我们的目标是研究预先暴露于番茄红素对紫外线B照射的皮肤细胞的影响。将细胞暴露于10μM番茄红素24小时，随后进行照射，并再恢复24小时。此后，通过流式细胞术（FCM）和逆转录聚合酶链反应（RT-PCR）分析了几个参数：通过评估细胞周期分布来检测遗传毒性/致断裂性；通过进行膜联蛋白-V检测并分析凋亡生物标志物的基因表达来检测凋亡；通过活性氧（ROS）定量来检测氧化应激。番茄红素对未照射细胞中的凋亡、坏死和活细胞的分布没有显著影响，也未显示出细胞生长抑制作用。然而，与未预先处理的照射细胞相比，预先用番茄红素处理的照射细胞中死亡和活细胞亚群均增加。在照射细胞中，与未预先处理的照射细胞相比，预先暴露于番茄红素导致BAX基因过表达。这伴随着在S期转换时的细胞周期延迟以及随后G0/G1期细胞数量的减少。因此，根据光损伤程度，番茄红素似乎在照射细胞中发挥纠正作用。因此，我们的发现可能对皮肤癌的治疗具有重要意义。
