Rengel Z, Zhang W-H
Soil Science and Plant Nutrition, School of Earth and Geographical Sciences, The University of Western Australia, 35 Stirling Highway, Crawley WA 6009, Australia.
Department of Horticulture, Viticulture & Oenology, Waite Campus, Adelaide University, PMB #1, Glen Osmond SA 5064, Australia.
New Phytol. 2003 Aug;159(2):295-314. doi: 10.1046/j.1469-8137.2003.00821.x.
This review is concentrating on the role of aluminium (Al)-calcium (Ca) interactions in Al toxicity syndrome in plants. Disruption of cytoplasmic Ca homeostasis has been suggested as a primary trigger of Al toxicity. Aluminium causes an increase in cytosolic Ca activity, potentially disrupting numerous biochemical and physiological processes, including those involved in the root growth. The source of Ca for the increase in cytosolic Ca activity under Al exposure is partly extracellular (likely to be due to the Al-resistant portion of the flux through depolarization-activated Ca channels and fluxes through Ca -permeable nonselective cation channels in the plasma membrane) as well as intracellular (increased cytosolic Ca activity enhances the activity of Ca release channels in the tonoplast and the endoplasmic reticulum membrane). The effect on increased cytosolic Ca activity of possible Al-related inhibition of the plasma membrane and endo-membrane Ca -ATPases and Ca exchangers (CaX) that sequester Ca out of the cytosol is insufficiently documented at present. The relationship between Al toxicity, cytoplasmic Ca homeostasis and cytoplasmic pH needs to be elucidated. Technical improvements that would allow measurements of cytosolic Ca activity within the short time after exposure to Al (seconds or shorter) are eagerly awaited. Contents I. Introduction 296 II. Symptoms of aluminium toxicity 296 III. Calcium - aluminium interactions 297 IV. The role of electrical properties of the plasma membrane in calcium-aluminium interactions 306 V. Oxidative stress 307 VI. Callose 308 VII. Cytoskeleton 308 VIII. Conclusions 309 Acknowledgements 309 References 309.
本综述聚焦于铝（Al）-钙（Ca）相互作用在植物铝毒综合征中的作用。细胞质钙稳态的破坏被认为是铝毒的主要触发因素。铝会导致胞质钙活性增加，可能会扰乱众多生化和生理过程，包括那些与根系生长相关的过程。铝暴露下胞质钙活性增加的钙来源部分是细胞外的（可能是由于通过去极化激活钙通道的通量中抗铝部分以及通过质膜中钙通透非选择性阳离子通道的通量），还有细胞内的（胞质钙活性增加会增强液泡膜和内质网膜中钙释放通道的活性）。目前关于铝可能对质膜和内膜钙ATP酶以及将钙隔离在胞质溶胶外的钙交换器（CaX）产生的抑制作用对胞质钙活性增加的影响，记录尚不充分。铝毒、细胞质钙稳态和细胞质pH之间的关系有待阐明。人们急切期待能在接触铝后短时间内（几秒或更短时间）测量胞质钙活性的技术改进。内容 一、引言296 二、铝毒症状296 三、钙-铝相互作用297 四、质膜电性质在钙-铝相互作用中的作用306 五、氧化应激307 六、胼胝质308 七、细胞骨架308 八、结论309 致谢309 参考文献309
