Tewari Rajesh Kumar, Hadacek Franz, Sassmann Stefan, Lang Ingeborg
Department of Terrestrial Ecosystem Research (TER), Faculty of Life Sciences, University of Vienna, Althanstrasse 14, 1090 Vienna, Austria.
Environ Exp Bot. 2013 Jul;91(100):74-83. doi: 10.1016/j.envexpbot.2013.03.006.
Using iron-deprived (-Fe) chlorotic as well as green iron-deficient (5 μM Fe) and iron-sufficient supplied (50 μM Fe) leaves of young hydroponically reared plants, we explored iron deficiency effects on triggering programmed cell death (PCD) phenomena. Iron deficiency increased superoxide anion but decreased hydroxyl radical (•OH) formation (TBARS levels). Impaired photosystem II efficiency led to hydrogen peroxide accumulation in chloroplasts; NADPH oxidase activity, however, remained on the same level in all treatments. Non-autolytic PCD was observed especially in the chlorotic leaf of iron-deprived plants, to a lesser extent in iron-deficient plants. It correlated with higher DNAse-, alkaline protease- and caspase-3-like activities, DNA fragmentation and chromatin condensation, hydrogen peroxide accumulation and higher superoxide dismutase activity. A significant decrease in catalase activity together with rising levels of dehydroascorbic acid indicated a strong disturbance of the redox homeostasis, which, however, was not caused by •OH formation in concordance with the fact that iron is required to catalyse the Fenton reaction leading to •OH generation. This study documents the chain of events that contributes to the development of non-autolytic PCD in advanced stages of iron deficiency in leaves.
我们使用水培培育的幼嫩植物缺铁（-Fe）黄化叶以及绿色缺铁（5 μM铁）和铁充足供应（50 μM铁）的叶片，探究缺铁对引发程序性细胞死亡（PCD）现象的影响。缺铁增加了超氧阴离子，但减少了羟基自由基（•OH）的形成（丙二醛水平）。光合系统II效率受损导致叶绿体中过氧化氢积累；然而，NADPH氧化酶活性在所有处理中保持在相同水平。非自溶性PCD尤其在缺铁植物的黄化叶中观察到，在缺铁植物中程度较轻。它与较高的脱氧核糖核酸酶、碱性蛋白酶和类半胱天冬酶-3活性、DNA片段化和染色质浓缩、过氧化氢积累以及较高的超氧化物歧化酶活性相关。过氧化氢酶活性显著降低以及脱氢抗坏血酸水平升高表明氧化还原稳态受到强烈干扰，然而，这并非由•OH形成引起，这与铁是催化导致•OH生成的芬顿反应所必需的事实一致。本研究记录了在叶片缺铁晚期导致非自溶性PCD发展的一系列事件。
