Abstract

Hydrogen peroxide, a central modulator of stress signal transduction pathways, activates multiple defense responses that reinforce resistance to various abiotic and biotic stresses in plants. The present study examines the potential biochemical mechanisms of hydrogen peroxide pre-treatment-induced drought tolerance in mustard ( Brassica juncea L.) seedlings by analyzing numerous vital components of methylglyoxal and reactive oxygen species detoxification systems. Eight-day-old seedlings were pre-treated with low concentration (50 µM) of hydrogen peroxide for 24 h prior to the imposition of drought stress (20% PEG-6000) for 48 h. Hydrogen peroxide pre-treatment enhanced the membrane stability of leaf tissues under drought stress, as revealed from greatly reduced malondealdehyde content. The level of endogenous hydrogen peroxide contents in exogenous hydrogen peroxide pre-treated drought stressed-seedlings was markedly lower than those of the seedlings subjected to drought stress without hydrogen peroxide pre-treatment. A declination in the activities of ascorbate peroxidase, catalase and glyoxalase II were observed in response to drought stress whereas dehydroascorbate reductase, glutathione peroxidase and glyoxalase I activities significantly increased. The content of ascorbate, reduced glutathione and oxidized glutathione increased significantly whereas glutathione/glutathione disulphide ratio decreased in drought-stressed seedlings. Surprisingly, hydrogen peroxide pre-treated drought-stressed seedlings maintained a significantly higher ascorbate peroxidase, glutathione reductase, catalase, glutathione S-trasnferase, and glyoxalase II activities and glutathione/glutathione disulphide ratio when compared with the seedlings subjected to drought stress without hydrogen peroxide pre-treatment. Our results indicated that hydrogen peroxide primed a defense response in the seedlings that could trigger the activation of both ROS and MG detoxification pathways and enabled the seedlings tolerance to drought-induced oxidative damage.

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