Department of Plant Sciences, Centre for Excellence in Genomic Sciences, School of Biological Sciences, Madurai Kamaraj University, Madurai 625021, India.
Plant Physiol Biochem. 2011 Feb;49(2):168-77. doi: 10.1016/j.plaphy.2010.11.007. Epub 2010 Nov 19.
Leaf senescence induced by 2,4-dichlorophenoxyacetic acid (2,4-D) and senescence inhibition caused by supplementation with silver (Ag(+)) ions in the form of silver nitrate (AgNO(3)) or silver nanoparticles (AgNPs) were investigated in 8-day-old mung bean (Vigna radiata L. Wilczek) seedlings. Inhibition of root and shoot elongation were observed in mung bean seedlings treated with 500μM 2,4-D. Concomitantly, the activity of 1-aminocyclopropane-1-carboxylic acid synthase was significantly induced in leaf tissue. Leaf senescence induced by 2,4-D was closely associated with lipid peroxidation as well as increased levels of cytotoxic hydrogen peroxide (H(2)O(2)) and superoxide radicals (O(2)(·-)). Despite decreased catalase activity, the activities of peroxidase, superoxide dismutase, monodehydroascorbate reductase, dehydroascorbate reductase, and glutathione reductase were increased during 2,4-D-induced leaf senescence. Further, the levels of reduced ascorbate, oxidized ascorbate, and reduced glutathione were markedly decreased, whereas the level of oxidized glutathione increased. 2,4-D-induced leaf senescence in mung bean was accompanied by an increase in positive terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling, nuclear DNA fragmentation, and the activity of a 15-kDa Ca(2+)-dependent DNase. Supplementation with 100μM AgNO(3) or AgNPs inhibited 2,4-D-induced leaf senescence. The present results suggest that increased oxidative stress (O(2)(·-) and H(2)O(2)) led to senescence in mung bean leaves. Furthermore, significantly induced antioxidative enzymes are not sufficient to protect mung bean cells from 2,4-D-induced harmful ROS.
用 2,4-二氯苯氧乙酸(2,4-D)诱导叶片衰老,并通过补充硝酸银(Ag(+))离子(以硝酸银或银纳米粒子的形式)来抑制衰老,研究了 8 天大的绿豆(Vigna radiata L. Wilczek)幼苗。用 500μM 2,4-D 处理绿豆幼苗时,观察到根和茎伸长受到抑制。同时,叶片组织中 1-氨基环丙烷-1-羧酸合酶的活性显著诱导。2,4-D 诱导的叶片衰老与脂质过氧化以及细胞毒性过氧化氢(H(2)O(2))和超氧自由基(O(2)(·-))水平升高密切相关。尽管过氧化氢酶活性降低,但过氧化物酶、超氧化物歧化酶、单脱氢抗坏血酸还原酶、脱氢抗坏血酸还原酶和谷胱甘肽还原酶的活性在 2,4-D 诱导的叶片衰老过程中增加。此外,还原型抗坏血酸、氧化型抗坏血酸和还原型谷胱甘肽的水平显著降低,而氧化型谷胱甘肽的水平增加。2,4-D 诱导的绿豆叶片衰老伴随着末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记、核 DNA 片段化和 15kDa Ca(2+)-依赖性 DNase 活性的增加。补充 100μM AgNO(3)或 AgNPs 抑制 2,4-D 诱导的叶片衰老。本研究结果表明,氧化应激增加(O(2)(·-)和 H(2)O(2))导致绿豆叶片衰老。此外,显著诱导的抗氧化酶不足以保护绿豆细胞免受 2,4-D 诱导的有害 ROS 的伤害。