PORPHYRIN ION RADICAL METABOLITES AND THEIR REACTIONS

尿卟啉I在先天性心脏病患者体内组织中的蓄积 红系卟啉症患者，可以经历一种酶促反应- 适当的电子还原为卟啉阴离子自由基时 降低辅因是存在的。我们已经证明了厌氧 含有NADPH和尿卟啉1的微粒体孵育给出了一个 一种卟啉阴离子自由基的电子自旋共振光谱。 抑制剂研究表明NADPH-细胞色素P-450还原酶 是电子供体。这个自由基经历了二级衰变。 由于自由基的非酶歧化作用。有氧 微粒体孵育也被研究为减少 氧气转化为超氧化物通过监测氧气消耗和自旋- 捕捉超氧化物。这些实验证明， 卟啉自由基向分子氧的电子转移 确实发生了，但由于自由基阴离子的形成速度很慢，所以没有 基础水平以上的耗氧量可以在 微体孵化。尿卟啉I的光还原研究 还对好氧和厌氧培养进行了研究。类似 结果是用光敏素II，一种光激活的 抗肿瘤药物。各种卟啉的氧化为 对过氧化物酶引发的阳离子自由基也进行了研究。 由于辣根过氧化物酶的酶中间体化合物 我，本身就是一种卟啉IX阳离子自由基，这项工作将有 对电子转移和卟啉代谢的影响。

Uroporphyrin I, which accumulates in body tissues of congenital erythropoietic porphyria patients, can undergo an enzymatic one- electron reduction to the porphyrin anion radical when a suitable reducing cofactor is present. We have demonstrated that anaerobic microsomal incubations containing NADPH and uroporphyrin 1 give an electron spin resonance spectrum of a porphyrin anion free radical. Inhibitor studies indicate that NADPH-cytochrome P-450 reductase is the electron donor. This radical undergoes a second-order decay due to nonenzymatic disproportionation of the radical. Aerobic microsomal incubations were also investigated for the reduction of oxygen to superoxide by monitoring oxygen consumption and the spin- trapping of superoxide. These experiments demonstrated that electron transfer from the porphyrin radical to molecular oxygen does occur, but due to the slow formation of the radical anion, no oxygen consumption above the basal level could be detected in the microsomal incubations. The photoreduction of uroporphyrin I in aerobic and anaerobic incubations was also investigated. Similar results have been obtained with photofrin II, a photo-activated antitumor agent. The oxidation of a variety of porphyrins to cation free radicals by peroxidases also has been investigated. Since the enzyme intermediate of horseradish peroxidase, compound I, is itself a porphyrin IX cation radical, this work will have implications for electron transfer as well as porphyrin metabolism.