Pt（II）-卟啉靶向线粒体细胞色素C氧化酶的光动力学治疗
Targeting cytochrome C oxidase in mitochondria with Pt(II)-porphyrins for Photodynamic Therapy
摘要：
线粒体是活细胞的动力室，在那里合成化学“能量货币”三磷酸腺苷（ATP）。一系列膜蛋白质复合物I至IV（即电子传递链）的氧化磷酸化是质子穿过线粒体内膜的电化学电势差或质子动力（PMF）的来源。PMF是通过电子传递链的复合物V，即通过FoF 1-ATP合酶产生ATP所必需的。在光动力疗法（PDT）中破坏细胞色素C氧化酶（COX;复合物IV）是通过阳离子光敏剂Pt（II）-TMPyP实现的。电子显微镜显示线粒体christae的破坏作为PDT的主要步骤。时间分辨磷光测量鉴定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，COX的破坏不仅可能干扰ATP的合成，但可以加速细胞色素C释放到胞质溶胶诱导凋亡。
英文摘要：
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 FoF1-ATP 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.
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