土壤干旱下玉米叶细胞膜脂过氧化和膜磷脂脱酯化反应以及膜超微结构的变化

Changes of Lipid Peroxidation, Reasterification of Phosphatide and Ultrastructure of Membrane in Leaf Cells of Maize under Soil Drought Condition

玉米开花期土壤干旱可使叶细胞中的超氧物歧化酶(SOD)活性降低,丙二醛(MDA)含量增加;酸性磷酸酯酶活性增强,可溶性磷含量增加.随干旱加强,MDA含量增加与亚麻酸含量降低呈极显著负相关,亚油酸含量增加与亚麻酸含量降低呈极显著负相关,酸性磷酸酯酶活性与膜脂脂肪酸不饱和度的变化呈相反的趋势.电镜观察发现,干旱加强,质膜、叶绿体膜系统受损加重,起初(ψ_L=-0.41MPa)质膜,叶绿体被膜膨散,尔后断裂,重度干旱(ψ_L=-1.83MPa)几乎解体.叶绿体片层结构随干旱加强,排列混乱,且间质片层对干旱较敏感.同时,细胞内脂类小滴增多增大.表明干旱下增加的活性氧启动了膜脂过氧化和膜磷脂的脱酯化反应.推测活性氧伤害膜的“原初机制”可能是干旱下活性氧含量增加首先启动了膜脂过氧化,导致膜脂脂肪酸不饱和度降低,对为膜束缚的酸性磷酸酯酶起明显的增溶溶解,进而促进膜磷脂脱酯化反应,加速了膜结构与功能的破坏.

Soil drought during flowering period of maize resulted in decrease of SOD (superoxide dismutase) activities and increase of MDA (malonaldehyde) contents in leaf cells, acid phosphatase activities and soluble phosphotus contents elevated. There was significant negative correlationship between MDA and linolenic acid contents, and also between linoleic acid and linolenic acid contents. Compared with the changes of the index of unsaturated fatty acid, acid phosphatase activities changed in an opposite direction. Observation through electron microscope revealed that plasma membrane and chloroplast membrane were injured seriously as the drought developed. At first, the plasma membrane and chloroplast membrane swelled (ΨL =-0.41MPa), then fractured and then almost disintergrated under serious drought condition (ΨL = -1.83MPa). The chloroplast lamellae arranged disorderly as the drought developed, and the stroma lamellae was also sensitive to drought. The fat droplets in cells increased and became larger, indicating that more active oxygen started the lipid peroxidation and phosphatide densterification of membrane. It was inferred that the primary mechanism of membrane injury caused by actvie oxygen might be as follows. Moer active oxygen contents under drought condition started the lipid peroxidation of membrane which resulted in decrease of unsaturated fatty acid, enhanced dissolution of acid phosphatase binded to membrane causing lipid densterification of membrane and accelerating damage of membrane in structure and function.