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作 者:YANGJia-Ding ZHAOHa-Lin ZHANGTong-Hui YUNJian-Fei
出 处:《Acta Botanica Sinica》2004年第9期1009-1014,共6页Acta Botanica Sinica(植物学报:英文版)
摘 要:Under non-stress condition, effects of exogenous nitric oxide (NO) on chlorophyll fluorescence parameters in detached leaves and leaf discs of potato (Solanum tuberosum L.) were surveyed. Results showed that the maximal quantum efficiency (Fv/Fm) and the effective quantum efficiency (ΦPSⅡ)of photosystem Ⅱ (PSⅡ) were reduced by exogenous NO under illumination (150μmol.m^-2·s^-1, 25℃). This influence was related not only to the concentration of sodium nitroprusside (SNP, a NO donor) solution, but also to the active duration of NO on leaf tissue. Results with leaf discs showed that the effects of SNP on ΦPSⅡ could be prevented by bovine hemoglobin (a powerful NO scavenger), while amixture of NO2^- and NO3^-(the decomposition product of NO or its donor SNP) had much less influence on ΦPSⅡ than SNP, indicating that effects of exogenous SNP on PSⅡ photochemical activity was mainly due to NO generation. Under light (150μmol·m^-2·s^-1, 25℃) for 4h or longer period, the non-photochemical quenching (NPQ) in SNP-soaked leaves was statistically similar to that in H2O-soaked control, but ΦPSⅡ and the proportion of open reaction centers (measured as qP) were lower than control, respectively. After 25min dark-adaptation, the maximal fluorescence (Fm) in SNP treatment (8 and 12h illumination duration) was significantly lower than the control, while the initial fluorescence (Fo) in SNP and H2O-treated leaves had no significant difference. Therefore this indicated that under the present experimental condition, the NO-affected site might not be the PSⅡ reaction centers. On the donor side of PSⅡ, NO putatively influenced the light-harvesting capacity of leaves under light; on the acceptor side, NO-affected sites were some components of electron transport chain after QA, i.e.NO enhanced the reductive degree of reaction centers through blocking the electron transport after QA, thus reducing the photochemical activitv of PSⅡ.
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