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Photosystem II damage induced by chemically generated singlet oxygen in tobacco leaves
Author(s) -
Hideg Éva,
Kós Péter B.,
Vass Imre
Publication year - 2007
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1111/j.1399-3054.2007.00913.x
Subject(s) - singlet oxygen , rose bengal , photoinhibition , photosystem ii , chemistry , photochemistry , chlorophyll fluorescence , photosensitizer , quenching (fluorescence) , oxygen , photosynthesis , biophysics , fluorescence , biochemistry , biology , organic chemistry , physics , quantum mechanics
In the present work, we investigated the role of chemically generated singlet oxygen, produced by photodynamic effect of rose bengal, in damaging the PSII complex in tobacco leaves in which protein synthesis‐dependent repair was inhibited by infiltration with lincomycin. A 30‐min exposure to low‐intensity (150 μmol m −2 s −1 ) photosynthetically active radiation (PAR) induced singlet oxygen production as detected by quenching of 3‐[ N ‐(β‐diethylaminoethyl)‐ N ‐dansyl]aminomethyl‐2,2,5,5‐tetramethyl‐2,5‐dihydro‐1 H ‐pyrrole fluorescence in leaves infiltrated with both lincomycin and rose bengal. This light treatment caused photoinhibition of PSII, as revealed by the marked loss both of the photochemical yield and the amount of D1 protein in PSII reaction center. When rose bengal was not present in the leaves, these symptoms of photodamage were not induced by the same low‐intensity PAR. However, when excitation pressure on PSII was increased to 1500 μmol m −2 s −1 , irreversible photodamage of PSII was also observed, showing that the lincomycin treatment applied in vivo was sufficiently inhibiting protein repair. Our results show that singlet oxygen is able to cause oxidative damage in PSII directly, as suggested earlier and argue against its recently hypothesized role exclusive to inhibiting PSII protein repair (Nishiyama et al. 2006).