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Nitric Oxide Improves Internal Iron Availability in Plants

机译：一氧化氮可提高植物体内的铁利用率

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Iron deficiency impairs chlorophyll biosynthesis and chloroplast development. In leaves, most of the iron must cross several biological membranes to reach the chloroplast. The components involved in the complex internal iron transport are largely unknown. Nitric oxide (NO), a bioactive free radical, can react with transition metals to form metal-nitrosyl complexes. Sodium nitroprusside, an NO donor, completely prevented leaf interveinal chlorosis in maize (Zea mays) plants growing with an iron concentration as low as 10 μm Fe-EDTA in the nutrient solution. S-Nitroso-N-acetylpenicillamine, another NO donor, as well as gaseous NO supply in a translucent chamber were also able to revert the iron deficiency symptoms. A specific NO scavenger, 2-(4-carboxy-phenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, blocked the effect of the NO donors. The effect of NO treatment on the photosynthetic apparatus of iron-deficient plants was also studied. Electron micrographs of mesophyll cells from iron-deficient maize plants revealed plastids with few photosynthetic lamellae and rudimentary grana. In contrast, in NO-treated maize plants, mesophyll chloroplast appeared completely developed. NO treatment did not increase iron content in plant organs, when expressed in a fresh matter basis, suggesting that root iron uptake was not enhanced. NO scavengers 2-(4-carboxy-phenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide and methylene blue promoted interveinal chlorosis in iron-replete maize plants (growing in 250 μm Fe-EDTA). Even though results support a role for endogenous NO in iron nutrition, experiments did not establish an essential role. NO was also able to revert the chlorotic phenotype of the iron-inefficient maize mutants yellow stripe1 and yellow stripe3, both impaired in the iron uptake mechanisms. All together, these results support a biological action of NO on the availability and/or delivery of metabolically active iron within the plant.
机译：缺铁会损害叶绿素的生物合成和叶绿体的发育。在叶子中，大多数铁必须穿过多个生物膜才能到达叶绿体。复杂的内部铁运输涉及的组件在很大程度上是未知的。一氧化氮（NO）是一种具有生物活性的自由基，可以与过渡金属反应形成金属-亚硝酰基配合物。硝普钠（NO供体）完全防止了营养液中铁浓度低至10μmFe-EDTA的玉米（Zea mays）植物叶片间叶绿化。另一个NO供体S-亚硝基-N-乙酰青霉胺以及半透明腔室中的气态NO供应也能够恢复缺铁症状。一种特定的NO清除剂2-（4-羧基-苯基）-4,4,5,5-四甲基咪唑啉-1-氧基1-3氧化物阻止了NO供体的作用。还研究了NO处理对缺铁植物光合作用的影响。来自缺铁玉米植物的叶肉细胞的电子显微照片显示，质体几乎没有光合叶片和粗粒。相反，在NO处理的玉米植株中，叶肉叶绿体似乎完全发育。当以新鲜物质为基础表达时，NO处理不会增加植物器官中的铁含量，这表明根铁的吸收没有增加。 NO清除剂2-（4-羧基-苯基）-4,4,5,5-四甲基咪唑啉-1-氧基-3-氧化物和亚甲基蓝促进了铁充足的玉米植物中的小叶绿化（在250μmFe-EDTA中生长） 。尽管结果支持内源性NO在铁营养中的作用，但实验并没有确立必要的作用。 NO还能够还原铁效率低的玉米低铁突变体黄色条纹1和黄色条纹3的绿素表型。总之，这些结果支持NO对植物内代谢活性铁的可用性和/或传递的生物学作用。

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