PROGRAMMED CELL DEATH IN PLANTS: PROTECTIVE EFFECT OF MITOCHONDRIA-TARGETED QUINONES
Ubiquinone or plastoquinone covalently linked to synthetic decyltriphenylphosphonium (DTPP+) or rhodamine cations prevented programmed cell death (PCD) induced by chitosan or CN<sup>-</sup> as seen by destruction of the cell nuclei. CN<sup>-</sup> induced the destruction of nuclei in both epidermal cells (EC) and guard cells (GC) of leaf epidermis of pea (Pisum sativum L.), whereas chitosan was effective only in EC. The half-maximum concentrations for protective effects of quinone derivatives were within the pico- and nanomolar range. The protective effect of the quinones was abolished by a protonophoric uncoupler and decreased by tetraphenylphosphonium cations. CN-induced PCD was strengthened by the quinone derivatives at concentrations above 10<sup>-8</sup>-10<sup>-7</sup> M. DTPP+ derivatives of quinones, unlike plastoquinone linked to the rhodamine cation (SkQR1), suppressed menadione-induced H<sub>2</sub>O<sub>2</sub> generation in the cells. The CN-induced destruction of GC nuclei was abolished by DTPP<sup>+</sup> derivatives in the dark, but not in the light. SkQR1 produced a protective effect on this process both in the dark and in the light, and its effect was similar to that of rhodamine 6G in the light. The data show that mitochondria are involved in PCD in plants