TY - JOUR
T1 - 2,4-dichlorophenoxyacetic acid-induced leaf senescence in mung bean (Vigna radiata L. Wilczek) and senescence inhibition by co-treatment with silver nanoparticles
AU - Karuppanapandian, Thirupathi
AU - Wang, Hong Wei
AU - Prabakaran, Natarajan
AU - Jeyalakshmi, Kandhavelu
AU - Kwon, Mi
AU - Manoharan, Kumariah
AU - Kim, Wook
PY - 2011/2
Y1 - 2011/2
N2 - 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 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 (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 100μM 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.
AB - 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 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 (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 100μM 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.
KW - 2,4-Dichlorophenoxyacetic acid
KW - Ethylene
KW - Leaf senescence
KW - Mung bean
KW - Nuclear DNA fragmentation
KW - Silver nanoparticles
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UR - http://www.scopus.com/inward/citedby.url?scp=78751700997&partnerID=8YFLogxK
U2 - 10.1016/j.plaphy.2010.11.007
DO - 10.1016/j.plaphy.2010.11.007
M3 - Article
C2 - 21144762
AN - SCOPUS:78751700997
VL - 49
SP - 168
EP - 177
JO - Plant Physiology and Biochemistry
JF - Plant Physiology and Biochemistry
SN - 0981-9428
IS - 2
ER -