Hideg Eva, Kós Péter B, Vass Imre
Institute of Plant Biology , Biological Research Center, 6726 Szeged, Temesvári. krt. 62, Hungary.
Physiol Plant. 2007 Sep;131(1):33-40. doi: 10.1111/j.1399-3054.2007.00913.x.
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 micromol m(-2) s(-1)) photosynthetically active radiation (PAR) induced singlet oxygen production as detected by quenching of 3-[N-(beta-diethylaminoethyl)-N-dansyl]aminomethyl-2,2,5,5-tetramethyl-2,5-dihydro-1H-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 micromol 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).
在本研究中,我们探究了由孟加拉玫瑰红的光动力效应产生的化学单线态氧在破坏烟草叶片光系统II(PSII)复合体中的作用,其中通过用林可霉素浸润抑制了依赖蛋白质合成的修复过程。如通过对同时浸润了林可霉素和孟加拉玫瑰红的叶片中3-[N-(β-二乙氨基乙基)-N-丹磺酰基]氨基甲基-2,2,5,5-四甲基-2,5-二氢-1H-吡咯荧光猝灭所检测到的,30分钟暴露于低强度(150微摩尔·米-2·秒-1)光合有效辐射(PAR)诱导了单线态氧的产生。这种光照处理导致了PSII的光抑制,这通过PSII反应中心光化学产量和D1蛋白量的显著损失得以揭示。当叶片中不存在孟加拉玫瑰红时,相同的低强度PAR不会诱导这些光损伤症状。然而,当PSII上的激发压力增加到1500微摩尔·米-2·秒-1时,也观察到了PSII的不可逆光损伤,表明体内应用的林可霉素处理足以抑制蛋白质修复。我们的结果表明,单线态氧能够直接对PSII造成氧化损伤,正如先前提出的那样,并反驳了其最近假设的仅抑制PSII蛋白质修复的作用(Nishiyama等人,2006年)。