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缺铁如何扰乱生菜叶片光系统 I 中的电子流?

How does iron deficiency disrupt the electron flow in photosystem I of lettuce leaves?

机构信息

Groupe de Recherche en Biologie Végétale (GRBV), Université du Québec à Trois-Rivières, Trois-Rivières, Québec G9A 5H7, Canada; Unité de Physiologie et de Biochimie de la Tolérance au Sel chez les Plantes, Faculté des Sciences de Tunis, Campus Universitaire, 1060, Tunisia.

出版信息

J Plant Physiol. 2013 Nov 1;170(16):1400-6. doi: 10.1016/j.jplph.2013.05.004. Epub 2013 Jun 6.

DOI:10.1016/j.jplph.2013.05.004
PMID:23747063
Abstract

The changes observed photosystem I activity of lettuce plants exposed to iron deficiency were investigated. Photooxidation/reduction kinetics of P700 monitored as ΔA820 in the presence and absence of electron transport inhibitors and acceptors demonstrated that deprivation in iron decreased the population of active photo-oxidizable P700. In the complete absence of iron, the addition of plant inhibitors (DCMU and MV) could not recover the full PSI activity owing to the abolition of a part of P700 centers. In leaves with total iron deprivation (0μM Fe), only 15% of photo-oxidizable P700 remained. In addition, iron deficiency appeared to affect the pool size of NADP(+) as shown by the decline in the magnitude of the first phase of the photooxidation kinetics of P700 by FR-light. Concomitantly, chlorophyll content gradually declined with the iron concentration added to culture medium. In addition, pronounced changes were found in chlorophyll fluorescence spectra. Also, the global fluorescence intensity was affected. The above changes led to an increased rate of cyclic electron transport around PSI mainly supported by stromal reductants.

摘要

研究了缺铁胁迫下生菜植株光系统 I 活性的变化。在存在和不存在电子传递抑制剂和受体的情况下,通过监测 P700 的光氧化/还原动力学ΔA820,结果表明,缺铁会降低可光氧化 P700 的活性群体。在完全没有铁的情况下,由于 P700 中心的一部分被废除,添加植物抑制剂(DCMU 和 MV)不能恢复完整的 PSI 活性。在完全缺铁的叶片(0μM Fe)中,只有 15%的可光氧化 P700 仍然存在。此外,缺铁似乎影响 NADP(+)的池大小,如 FR-光下 P700 光氧化动力学第一阶段幅度的下降所示。同时,叶绿素含量随着培养基中添加的铁浓度逐渐下降。此外,还发现叶绿素荧光光谱发生了明显变化。此外,全局荧光强度也受到影响。上述变化导致 PSI 周围的环式电子传递速率增加,主要由基质还原剂支持。

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