* To whom correspondence should be addressed.
Received April 23, 2011; Revision received May 23, 2011
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 H2O2 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.
KEY WORDS: programmed cell death, mitochondrial-targeted quinones, mitochondria, chitosan, reactive oxygen species, pea