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机构地区:[1]华南师范大学生物光子学研究院激光生命科学研究所暨激光生命科学教育部重点实验室,广东广州510631
出 处:《激光生物学报》2012年第6期486-491,共6页Acta Laser Biology Sinica
基 金:教育部"长江学者与创新团队计划"创新团队项目(IRT0829);国家自然科学基金--广东联合基金重点项目(U0931005);国家高技术研究发展计划(863计划)课题(2007AA10Z204)
摘 要:镉是一种高度有毒的重金属,能够抑制植物生长,甚至导致死亡,但是其诱导细胞程序性死亡(PCD)的分子机制仍然不是很清楚。本文利用荧光探针分子成像和激光共聚焦扫描显微技术,以拟南芥叶肉细胞原生质体为材料,观察100μmol/L CdCl2诱导PCD过程中一氧化氮(NO)的产生和亚细胞定位。结果表明高浓度CdCl2能够明显降低细胞活力,100μmol/L CdCl2能够诱导大量NO产生,在处理12 h后NO产生达到峰值。亚细胞定位观察发现NO荧光首先和线粒体有共定位。随着处理时间的延长在叶绿体和胞质也观察到NO荧光。Cadmium ( Cd^2+) , a non-essential element, exhibits high levels of toxicity. Cd^2+ exposure could inhibit plant growth and even result in cell death. Yet the mechanisms of Cadmium-induced programmed cell death (PCD) re- main largely unknown. Using fluorescent probes molecular imaging and laser confocal scanning microscopy, the temporal and spatial characteristics of nitric oxide (NO) production during Cd^2+ -induced PCD in Arabidopsis protoplasts were in- vestigated in vivo and in real-time. Results demonstrated that high doses of Cd^2+ strongly decreased cell viability and in- duced large amount of NO. After 12 h treatment with 100μmol/L Cd^2+ the NO content reached a maximum. NO was first generated in the mitochondrial regions of protoplasts and subsequently in chloroplasts and even whole cell as the treating time went on.
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