文献类型： 外文期刊
作者： Xu, H. X. 1 ; Weng, X. Y. 2 ; Yang, Y. 2 ;
作者机构： 1.Zhejiang Univ, Coll Life Sci, State Key Lab Plant Physiol & Biochem, Hangzhou 310058, Zhejiang, Peoples R China
2.Zhejiang Univ, Coll Life Sci, State Key Lab Plant Physiol & Biochem, Hangzhou 310058, Zhejiang, Peoples R China; Zhejiang Acad Agr Sci, Inst Hort, Hangzhou 310021, Zhejiang, Peoples R China
关键词： oryza sativa;photosynthetic characteristics;phosphorus deficiency;chlorophyll fluorescence;photoprotective mechanism
期刊名称：RUSSIAN JOURNAL OF PLANT PHYSIOLOGY （ 影响因子：1.481； 五年影响因子：1.608 ）
ISSN： 1021-4437
年卷期： 2007 年 54 卷 6 期
页码：
收录情况： SCI
摘要： The effects of phosphorus deficiency on the photosynthetic characteristics were studied in rice seedlings (Oryza sativa L.) every 8 days after treatment. P deficiency caused a significant reduction in the net photosynthesis rate (P-N) in rice plants. During the first 16 days of P deficiency, the maximurn efficiency of PSII photochemistry (F-v/F-m), the effective PSII quantum yield (phi(PSII)), the electron transport rate (ETR) as well as photochemical quenching (qP) in the P-limited rice plants kept close to the control, but the excitation energy capture efficiency of PSII reaction centers (F'(v)/F'(m)) was significantly declined in the P-deficient rice leaves. Meanwhile, in the stressed leaves, we also found a significant increase in nonphotochemical quenching (NPQ) as well as in the activities of superoxide dismutase (SOD) and ascorbate peroxidase (APX). It was indicated that a series of photoprotective mechanisms had been initiated in rice plants in response to short-term P deficiency. Therefore, PSII functioning was not affected significantly under such stress. As P deficiency continued, the excess excitation energy was accumulated in excess of the capacity of photoprotection systems. When the rice suffered from P deficiency more than 16 days, phi(PSII), ETR, and qP were decreased more rapidly than that in the control plants, although NPQ still kept higher in the stressed plants. These results were also consistent with the data on the distribution of excitation energy. The excess energy induced the generation of reactive oxygen species, which might lead to the further damage to PSII functioning
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