In vivo deleterious effects specific to reactive oxygen species on photosystem I and II after photo-oxidative treatments of rice (Oryza sativa L.) leaves

Under various photo-oxidative conditions in the presence of methyl viologen (MV), diethyldithiocarbamic acid (DDC, a superoxide dismutase (SOD) inhibitor), and hydroxyurea (HU, an ascorbate peroxidase (APX) inhibitor), the causal relationships of the reactive oxygen species (ROS) with the photo-oxidative damages in photosystems in vivo were investigated in rice leaves. In the MV-treated leaves, damages were mainly observed in photosystern (PS) II with a decrease in the maximum photochemical capacity of PSII, F-v/F-m and the degradation of D1 protein, a core component of PSII. For PSI, the extent of P700 photo-oxidation, P700(+), decreased slightly but PsaA/B proteins, core components of PSI, were barely affected. In contrast, DDC, which is expected to produce O-center dot(2)-, caused a greater decrease in P700(+), while the decrease in F-v/F-m, was relatively small in the DDC-treated leaves. Interestingly, the deleterious effect of Won PSII was largely masked in the presence of DDC, but instead the decrease in P700(+) was more pronounced in the MV/DDC-treated leaves. The damages in PSII by the treatment of MV were mainly caused by the accumulated H2O2 rather than (OH)-O-center dot, because dimethylsuffoxide, a hydroxyl radical scavenger, did not protect against the decrease of F-v/F-m in the MV-treated leaves. Unexpectedly, the ROS responsible for the HU-induced photo-oxidative damages in PSII was (OH)-O-center dot rather than H2O2. However, the production of (OH)-O-center dot did not imply a significant increase in the level of cellular catalytic free metals. Moreover, it was possible to differentiate various photo-oxidative stresses in vivo based on the degradation pattern of D I protein. In the present study, it was further discussed, how different ROS were responsible for the differential damages in photosystems in vivo under various photo-oxidative conditions, and how the differential inhibition of protective machineries contributed to the production and accumulation of different ROS. (c) 2004 Elsevier Ireland Ltd. All rights reserved.