THE APPARENT PRODUCTION OF SUPEROXIDE AND HYDROXYL RADICALS BY HEMATOPORPHYRIN AND LIGHT AS SEEN BY SPIN-TRAPPING
THE APPARENT PRODUCTION OF SUPEROXIDE AND HYDROXYL RADICALS BY HEMATOPORPHYRIN AND LIGHT AS SEEN BY SPIN-TRAPPING
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DOI：
10.1016/0014-5793(80)81288-9
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发表时间：
1980-01-01
期刊：
影响因子：
3.5
通讯作者：
OBERLEY, LW
中科院分区：
文献类型：
--
作者：
BUETTNER, GR;OBERLEY, LW
已知血卟啉具有光动力特性。生物分子或细胞暴露于血卟啉和可见光可能会导致损伤 [1]，甚至可能致命 [2]。这种失活作用在癌细胞中似乎比在相应的正常细胞中更大[3]。这被认为部分是由于血卟啉在恶性组织中比在大多数其他组织中积累更多14-71。有证据表明，血卟啉和光的细胞毒性作用是单线态氧光敏产生的结果，单线态氧是分子氧的一种短暂的、高度反应性的状态(8-101，然而，血卟啉与生物分子的相互作用可能是通过一种激进的机制而不是通过一种简单的机制进行的。单线态氧机制[111]有证据表明，暴露于血卟啉和红光的细胞系统中羟基自由基的产生可以在非质子溶剂中产生超氧自由基[1131]，但在水存在的情况下没有观察到自由基的形成[131][141]中报道了血卟啉的光敏产生，但仅在NADH或NADPH存在的情况下。因此，需要彻底研究这种反应的自由基机制的重要性。在[1.5-l 71]中，我们提出了一种新的恶性肿瘤模型。该模型的本质如下：肿瘤细胞的锰超氧化物歧化物数量减少，但同时它们能够产生大量的超氧化物自由基。我们相信，恶性细胞和正常细胞之间的这种差异可以用于治疗癌症。
Hematoporphyrin is known to have photodynamic properties. The exposure of biomolecules or cells to hematoporphyrin and visible light can result in damage [l] and can even be lethal [2]. This inactivating effect appears to be greater in cancer cells than in corresponding normal cells [3]. This is thought to be due in part to the greater acc~ ulation of hematoporphyrin in malignant tissue than in most other tissues 14-71.There is evidence that the cytotoxic action of hematoporphyrin and light is the result of the photosensitized production of singlet oxygen, a short-lived, hi@ ly reactive state of molecular oxygen (8-101, However, the interaction of hematoporphyrin with biomolecules may proceed by a radical mechanism rather than by a singlet oxygen mechanism [111. In [121 evidence indicating the production of hydroxyl radical in cell systems exposed to hematopo~ hyr~ and red light appeared. He~ topo~ hy~ could produce superoxide radical in aprotic solvents 1131, but no free radical formation in the presence of water was observed [131. The photosensitized production of superoxide by hematoporphyrin has been reported in [141 but only in the presence of NADH or NADPH. Thus, the significance of a radical mechanism for this reaction needs to be thoroughly investigated. In [1.5-l 71 we proposed a new model for malignancy. The essence of the model is as follows: Tumor cells have diminished amounts of the mang~ ese~ onta~~ g superoxide dismuta~, but at the same time they are capable of produc~ g significant amounts of superoxide radical. We believe this difference between malignant and normal cells can be exploited in the treatment of cancer. Agents