Faculty of Biology, Lomonosov Moscow State University, Russia.
Biochemistry (Mosc). 2011 Oct;76(10):1120-30. doi: 10.1134/S0006297911100051.
Ubiquinone or plastoquinone covalently linked to synthetic decyltriphenylphosphonium (DTPP(+)) or rhodamine cations prevent programmed cell death (PCD) in pea leaf epidermis induced by chitosan or CN(-). PCD was monitored by recording the destruction of cell nuclei. CN(-) induced the destruction of nuclei in both epidermal cells (EC) and guard cells (GC), whereas chitosan destroyed nuclei in EC not in GC. The half-maximum concentrations for the protective effects of the quinone derivatives were within the pico- and nanomolar range. The protective effect of the quinones was removed by a protonophoric uncoupler and reduced by tetraphenylphosphonium cations. CN(-)-Induced PCD was accelerated by the tested quinone derivatives at concentrations above 10(-8)-10(-7) M. Unlike plastoquinone linked to the rhodamine cation (SkQR1), DTPP(+) derivatives of quinones suppressed menadione-induced H(2)O(2) generation in the cells. The CN(-)-induced destruction of GC nuclei was prevented by DTPP(+) derivatives in the dark not in the light. SkQR1 inhibited this process both in the dark and in the light, and its effect in the light was similar to that of rhodamine 6G. The data on the protective effect of cationic quinone derivatives indicate that mitochondria are involved in PCD in plants.
泛醌或质体醌与合成的癸基三苯基膦（DTPP(+))或罗丹明阳离子共价连接，可防止几丁聚糖或 CN(-)诱导的豌豆叶片表皮程序性细胞死亡 (PCD)。通过记录细胞核的破坏来监测 PCD。CN(-)诱导表皮细胞 (EC) 和保卫细胞 (GC) 中的细胞核破坏，而几丁聚糖破坏 EC 中的细胞核而不破坏 GC 中的细胞核。醌衍生物的保护作用的半最大浓度在皮摩尔和纳摩尔范围内。质子载体解偶联剂去除了醌的保护作用，并被四苯基膦阳离子还原。醌衍生物在浓度高于 10(-8)-10(-7) M 时会加速 CN(-)诱导的 PCD。与与罗丹明阳离子连接的质体醌 (SkQR1) 不同，醌的 DTPP(+)衍生物抑制了细胞中 menadione 诱导的 H(2)O(2)生成。在黑暗中而非在光下，DTPP(+)衍生物可防止 CN(-)诱导的 GC 细胞核破坏。SkQR1 抑制了黑暗和光照下的这一过程，其在光照下的作用与罗丹明 6G 相似。阳离子醌衍生物的保护作用数据表明，线粒体参与了植物的 PCD。
