Ethylene evolution and antioxidant defence mechanism in Cicer arietinum roots in the presence of nitrate and aminoethoxyvinylglycine

The plants of chickpea (Cicer arietinum L.) cv. HC-1 were raised in earthen pots filled with 5 kg washed river sand under natural conditions of the sc reen house. Forty to forty-five days after sowing, the roots were exposed t o 10, 20 and 40 mM NO3- through rooting medium with the aim for studying NO 3- induced changes in ethylene production and root functioning. Aminoethoxy vinylglycine (AVG, 5 mu M), an ethylene biosynthesis inhibitor, was added a fter 24 h of NO3- treatments. Three days after the treatments, NO3- applied at 10 mM induced a significant increase in 1-amino cyclopropane-1-carboxyl ic acid (ACC) content (49 %) and in vivo ACC oxidase activity (100 %) which were associated with an increase in ethylene production (25 %) and with an important increase in both H2O2 (60 %) and malondialdehyde (MDA, 1 270 %). In contrast, supply of NO3- at 40 mM resulted in an important increase in ethylene production (400 %) by inducing significant enhancement of ACC cont ent (123 %), ACC oxidase activity (128 %) and with simultaneous increase of H2O2 (160 %) and MDA (1 900 %). The reversible membrane alteration showed a linear correlation with ethylene production. This was confirmed by a shar p decline in NO3- induced ethylene evolution by AVG. An oxidative damage by NO3- to the defence mechanism was evident from the increase in H2O2 conten t which is apparent from the decrease in activities of superoxide dismutase (EC 1.15.1.1), catalase (EC 1.11.1.6), ascorbate peroxidase (EC 1.11.1.11) and glutathione reductase (EC 1.11.1.9) to 23-67, 39-43, 33-55 and 26-45 % , respectively. The AVG treatment showed partial recovery in the activities of these enzymes and decrease in H2O2 content (17-32 %). It is inferred th at ethylene evolution due to NO3- is the key marker interfering with the fu nctioning of roots along with the weakening of antioxidant defence mechanis m. (C) 2000 Editions scientifiques et medicales Elsevier SAS.