NDLI: Programmed cell death in plants: Protective effect of mitochondrial-targeted quinones

Content Provider	Springer Nature Link
Author	Vasil’ev, L. A. Dzyubinskaya, E. V. Kiselevsky, D. B. Shestak, A. A. Samuilov, V. D.
Copyright Year	2011
Abstract	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.
Starting Page	1120
Ending Page	1130
Page Count	11
File Format	PDF
ISSN	00062979
Journal	Biochemistry (Moscow)
Volume Number	76
Issue Number	10
e-ISSN	16083040
Language	English
Publisher	SP MAIK Nauka/Interperiodica
Publisher Date	2011-10-12
Publisher Place	Dordrecht
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	programmed cell death mitochondrial-targeted quinones mitochondria chitosan reactive oxygen species pea Biomedicine general Microbiology Biochemistry Bioorganic Chemistry
Content Type	Text
Resource Type	Article
Subject	Biochemistry Biophysics Geriatrics and Gerontology

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