苹果缺钙对果实钙组分、亚细胞分布与超微结构的影响

Effect of Calcium Deficiency in Apple (Malus pumila) Fruits on Calcium Fractions, Subcelluar Distribution and Ultrastructure of Pulp Cells

通过苹果幼果期果面喷钙获得试材,采用逐级提取法测定红富士和新红星两个品种贮藏过程中钙形态的变化;采用焦锑酸钾沉淀-透射电子显微镜观察方法,研究果实细胞中钙的亚细胞分布特点及其相应的超微结构变化。结果表明,随贮藏时间增加,红富士和新红星苹果果实水溶性钙和果胶钙含量下降,磷酸钙和草酸钙以及硅酸钙含量相应增加,与对照不喷钙比较,喷钙明显增加贮藏苹果果实各种形态钙的含量;品种间红富士苹果全钙及各种形态钙含量均显著高于新红星。钙均匀分布于细胞壁、细胞膜、液泡膜、核膜和核质,并在液泡内堆积;缺钙时核膜模糊或断裂,且钙颗粒分布不均,细胞分室作用消失,细胞质中出现大量含钙颗粒。贮藏过程中果实水溶性钙和果胶钙则向磷酸钙和草酸钙的无效化转变,以及由此引起的细胞膜系统结构和功能的损伤,是缺钙导致苹果果实生理失调的重要机理之一。

Two apple varieties, Red Fuji and Starkrimson, with different resistance to bitter pit were selected in thistudy. Calcium solution (Ca treatment) and water (CK) were sprayed three times to the surface of the young apple fruitsuring the early stage of fruit development. Forms of calcium in the apple fruit during storage were fractionated by sequentxtracting. Localization and distribution of calcium and the influence of calcium nutrition on cell ultrastructure were observedy transmission electron microscopy combined with in situ precipitation of calcium with an improved method of potassiumyroantimonate technique. The result indicated that calcium content in various forms in apple fruits from CK treatment wereelatively low, and spraying calcium solution on young fruit surface increased the contents of calcium in all forms in appleruits. In the course of storage, the contents of soluble calcium and pectic calcium declined and those in calcium phosphate calcium oxalate and silicic calcium forms increased. The calcium content of Red Fuji in all forms was higher than that oftarkrimson, which suggests that calcium accumulating capability of Red Fuji fruits is higher than that of Starkrimson.nder transmission electron microscopy, Ca containing antimonite precipitates (CaAP) was mainly distributed in cell wallonoplast, nuclear membrane and nucleoplasm, much more CaAP deposited in vacuole. Ca deficiency of apple fruits duringtorage leads to disappearance of compartmentation, decrease of CaAP in the positions indicated above, and entrance ofuch more CaAP to cytoplasm. The above results indicated that the transformation from soluble calcium and pectic formso calcium phosphate, oxalate forms and damage of cell membrane structuraly and functionally resulted from calciumdeficiency during storage were the crucial cause of metabolise disease.