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首页> 外文会议>Asian Society for Mitochondrial Research and Medicine >Mitochondrion-Targeted Photosensitizer Enhances the Photodynamic Effect-Induced Mitochondrial Dysfunction and Apoptosis
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Mitochondrion-Targeted Photosensitizer Enhances the Photodynamic Effect-Induced Mitochondrial Dysfunction and Apoptosis

机译：线粒体靶向光敏剂增强了光动力学效应诱导的线粒体功能障碍和凋亡

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Recently, the mitochondrion has been considered as a novel pharmacological target for anticancer therapy due to its crucial role involved in arbitrating cell apoptosis. We have previously demonstrated that 488-nm laser irradiation induced a specific mitochondrial reactive oxygen species (mROS) formation and apoptotic death. In this study, we used a second generation of photosensitizers, the benzoporphyrin-derivative monoacid ring A (BPD-MA). We investigated specifically mechanisms at the mitochondrial level for BPD-MA coupled with 690-nm laser irradiation, the photodynamic effect (PDE) of BPD-MA, using conventional and laser scanning imaging microscopy in intact C6 glioma cells. We demonstrated BPD-MA localized mainly in the mitochondrial area. The phototoxicity induced by 1～10 J 690-nm laser irradiation was minor as compared to that induced by 488-nm laser irradiation. Unlike other mitochondrion-targeted photosensitizers, the dark toxicity induced by BPD-MA (0.05～5 mg/mL, effective doses used for the PDE) was relatively low. Nevertheless, the PDE of BPD-MA using 0.5 mg/mL coupled with 5J 690- nm irradiation induced profound and rapid (< 1 min) mitochondrial swelling, mROS formation, and severe plasma membrane blebing as compared to that induced by 488-nm laser irradiation (< 10 min). Later, the PDE of BPD-MA resulted in positive propidium iodide cell-death stain and positive TUNEL apoptotic nuclear stain and DNA laddering. Finally, the PDT of BPD-MA also instantaneously promoted the mitochondrion to diminish its covalent binding with a mitochondrial marker, MitoTracker Green. We conclude that the PDT of BPD-MA targeted primarily and compellingly the mitochondrion to induce effective mitochondria-mediated apoptosis and thus may serve as a powerful photosensitizer for clinical cancer therapy.
机译：最近，由于其在仲裁细胞凋亡中涉及至关重要的作用，对线粒体被认为是一种新的药理靶标。我们之前已经证明，488nm激光辐照诱导特定的线粒体反应性氧物质（MRO）形成和凋亡死亡。在这项研究中，我们使用第二代光敏剂，苯并卟啉 - 衍生物单酸环A（BPD-MA）。我们研究了在完整的C6胶质瘤细胞中使用常规和激光扫描成像显微镜的BPD-MA与690nm激光照射，光动力学效应（PDE）的线粒体水平的机制。我们展示了主要在线粒体区域的BPD-MA。与488-nm激光照射诱导的相比，由1〜10J690-nm激光照射诱导的光毒性较小。与其他线粒体靶向的光敏剂不同，BPD-MA（0.05〜5mg / ml，用于PDE的有效剂量）诱导的暗毒性相对较低。然而，与488-NM激光诱导相比，使用0.5mg / ml的BPD-MA的PDE使用0.5mg / ml耦合，与5J 690-nm辐照诱导的深层和快速（<1分钟）线粒体溶胀，MRO形成和严重的血浆膜渗流辐照（<10分钟）。后来，BPD-MA的PDE导致正碘化丙啶细胞死亡染色和正动脉凋亡核污染和DNA梯子。最后，BPD-MA的PDT也瞬间促进了线粒体以减少其与线粒体标记物，MitotRacker Green的共价结合。我们得出结论，BPD-MA的PDT主要靶向，迫使线粒体诱导有效的线粒体介导的细胞凋亡，因此可以作为临床癌症治疗的强大光敏剂。

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