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首页> 外文会议>Optical methods for tumor treatment and detection: Mechanisms and techniques in photodynamic therapy XIX >Targeting cytochrome C oxidase in mitochondria with Pt(II)-porphyrins for Photodynamic Therapy
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Targeting cytochrome C oxidase in mitochondria with Pt(II)-porphyrins for Photodynamic Therapy

机译：用Pt（II）-卟啉靶向线粒体中的细胞色素C氧化酶进行光动力治疗

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Mitochondria are the power house of living cells, where the synthesis of the chemical "energy currency" adenosine triphosphate (ATP) occurs. Oxidative phosphorylation by a series of membrane protein complexes I to IV, that is, the electron transport chain, is the source of the electrochemical potential difference or proton motive force (PMF) of protons across the inner mitochondrial membrane. The PMF is required for ATP production by complex V of the electron transport chain, I.e. by F_0F_1ATP synthase. Destroying cytochrome C oxidase (COX; complex IV) in Photodynamic Therapy (PDT) is achieved by the cationic photosensitizer Pt(II)-TMPyP. Electron microscopy revealed the disruption of the mitochondrial christae as a primary step of PDT. Time resolved phosphorescence measurements identified COX as the binding site for Pt(II)-TMPyP in living HeLa cells. As this photosensitizer competed with cytochrome C in binding to COX, destruction of COX might not only disturb ATP synthesis but could expedite the release of cytochrome C to the cytosol inducing apoptosis.
机译：线粒体是活细胞的动力源，化学“能量货币”三磷酸腺苷（ATP）的合成发生在这里。一系列膜蛋白复合物I至IV（即电子传输链）的氧化磷酸化是质子跨线粒体内膜的电化学势差或质子动力（PMF）的来源。 PMF是通过电子传输链的络合物V产生ATP所必需的。通过F_0F_1ATP合酶。通过阳离子光敏剂Pt（II）-TMPyP实现光动力疗法（PDT）中的细胞色素C氧化酶（COX；复合物IV）的破坏。电子显微镜显示线粒体克里斯塔氏菌的破坏是PDT的主要步骤。时间分辨的磷光测量确定了COX为活HeLa细胞中Pt（II）-TMPyP的结合位点。由于这种光敏剂与细胞色素C竞争结合COX，因此破坏COX不仅会干扰ATP的合成，而且会加速细胞色素C向细胞质的释放，从而诱导细胞凋亡。

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