Lee Chung Soo, Han Eun Sook, Lee Won Bok
Department of Pharmacology, College of Medicine, Chung-Ang University, Seoul, South Korea.
Neurochem Res. 2003 Dec;28(12):1833-41. doi: 10.1023/a:1026119708124.
Phenelzine, deprenyl, and antioxidants (SOD, catalase, ascorbate, or rutin) reduced the loss of cell viability in differentiated PC12 cells treated with 250 microM MPP+, whereas N-acetylcysteine and dithiothreitol did not inhibit cell death. Phenelzine reduced the condensation and fragmentation of nuclei caused by MPP+ in PC12 cells. Phenelzine and deprenyl prevented the MPP+-induced decrease in mitochondrial membrane potential, cytochrome c release, formation of reactive oxygen species, and depletion of GSH in PC12 cells. Phenelzine revealed a scavenging action on hydrogen peroxide and reduced the hydrogen peroxide-induced cell death in PC12 cells, whereas deprenyl did not depress the cytotoxic effect of hydrogen peroxide. Both compounds reduced the iron and EDTA-mediated degradation of 2-deoxy-D-ribose degradation. The results suggest that phenelzine attenuates the MPP+-induced viability loss in PC12 cells by reducing the alteration of mitochondrial membrane permeability that seems to be mediated by oxidative stress.
苯乙肼、司来吉兰和抗氧化剂（超氧化物歧化酶、过氧化氢酶、抗坏血酸或芦丁）可减少用250微摩尔MPP⁺处理的分化PC12细胞的细胞活力丧失，而N - 乙酰半胱氨酸和二硫苏糖醇则不能抑制细胞死亡。苯乙肼可减少MPP⁺在PC12细胞中引起的细胞核凝聚和碎片化。苯乙肼和司来吉兰可防止MPP⁺诱导的PC12细胞线粒体膜电位降低、细胞色素c释放、活性氧的形成以及谷胱甘肽的消耗。苯乙肼对过氧化氢具有清除作用，并减少了过氧化氢诱导的PC12细胞死亡，而司来吉兰并未抑制过氧化氢的细胞毒性作用。两种化合物均减少了铁和EDTA介导的2 - 脱氧 - D - 核糖降解。结果表明，苯乙肼通过减少似乎由氧化应激介导的线粒体膜通透性改变，减轻了MPP⁺诱导的PC12细胞活力丧失。
