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首页> 美国卫生研究院文献>Antioxidants Redox Signaling >Cancer Phototherapy via Selective Photoinactivation of Respiratory Chain Oxidase to Trigger a Fatal Superoxide Anion Burst
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Cancer Phototherapy via Selective Photoinactivation of Respiratory Chain Oxidase to Trigger a Fatal Superoxide Anion Burst

机译：通过选择性光灭活呼吸链氧化酶触发致命的超氧阴离子爆炸的癌症光疗。

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>Aims: Here, we develop a novel cancer treatment modality using mitochondria-targeting, high-fluence, low-power laser irradiation (HF-LPLI) in mouse tumor models and explore the mechanism of mitochondrial injury by HF-LPLI. >Results: We demonstrated that the initial reaction after photon absorption was photosensitization of cytochrome c oxidase (COX), to inhibit enzymatic activity of COX in situ and cause respiratory chain superoxide anion (O2−•) burst. We also found that HF-LPLI exerted its main tumor killing effect through mitochondrial O2−• burst via electron transport chain (ETC). These phenomena were completely absent in the respiration-deficient cells and COX knockdown cells. With a carefully selected irradiation protocol, HF-LPLI could efficaciously destroy tumors. The inhibition of enzymatic activity of COX and generation of O2−• by HF-LPLI in vivo were also detected. >Innovation: It is the first time that the mechanism involved in the interaction between light and its photoacceptor under HF-LPLI treatment is clarified. Our results clearly indicate that HF-LPLI initiates its effects via targeted COX photoinactivation and that the tumor-killing efficacy is dependent of the subsequent mitochondrial O2−• burst via ETC. >Conclusion: Based on both in vitro and in vivo results, we conclude that HF-LPLI can selectively photoinactivate respiratory chain oxidase to trigger a fatal mitochondrial O2−• burst, producing oxidative damage on cancer cells. This study opens up the possibilities of applications of HF-LPLI as a mitochondria-targeting cancer phototherapy. Antioxid. Redox Signal. 20, 733–746.
机译：>目标：在这里，我们在小鼠肿瘤模型中使用线粒体靶向，高通量，低功率激光照射（HF-LPLI）开发了一种新型的癌症治疗方法，并探索了HF导致线粒体损伤的机制-LPLI。 >结果：我们证明了光子吸收后的初始反应是细胞色素C氧化酶（COX）的光敏化，以抑制COX的原位酶活性并引起呼吸链超氧阴离子（O2 -•< / sup>）。我们还发现，HF-LPLI通过经由​​电子传输链（ETC）的线粒体O2 -•爆发而发挥了主要的杀伤作用。这些现象在呼吸缺陷细胞和COX抑制细胞中完全不存在。通过精心选择的辐照方案，HF-LPLI可以有效地破坏肿瘤。还检测到HF-LPLI在体内抑制了COX的酶活性并产生了O2 -•。 >创新：这是首次阐明在HF-LPLI处理下光与其光受体之间相互作用的机制。我们的结果清楚地表明，HF-LPLI通过有针对性的COX光灭活来启动其作用，并且杀伤肿瘤的功效取决于随后通过ETC发生的线粒体O2 -•爆发。 >结论：基于体内和体外结果，我们得出结论，HF-LPLI可以选择性地使呼吸链氧化酶光失活，从而触发致命的线粒体O2 -•爆发，产生氧化性对癌细胞的损害。这项研究开辟了将HF-LPLI用作靶向线粒体的癌症光疗的可能性。抗氧化。氧化还原信号。 20，733–746。

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