2,4-dichlorophenoxyacetic acid-induced leaf senescence in mung bean (Vigna radiata L. Wilczek) and senescence inhibition by co-treatment with silver nanoparticles

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 (AgNO3) 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 500 μM 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 (H2O2) and superoxide radicals (O2·−). 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 Ca2+-dependent DNase. Supplementation with 100 μM AgNO3 or AgNPs inhibited 2,4-D-induced leaf senescence. The present results suggest that increased oxidative stress (O2·− and H2O2) 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.

Research highlights► 2,4-D-induced leaf senescence in mung bean is marked by a defined phenotypic anomaly. ► Administration of Ag+ ions inhibits auxin-induced senescence in mung bean leaves. ► Onset of 2,4-D-induced leaf senescence is marked by overproduction of ROS. ► 2,4-D-induced leaf senescence is marked by condensed chromatin and nDNA degradation. ► Auxin-induced senescence was mediated by the activation of Ca2+-dependent DNase.