ABSTRACT
Both heat and chilling caused reduction in membrane protein thiol level and increased accumulation of thiobarbituric acid reactive substances in 72 hr old germinating tissues (indicators of oxidative stress) and reduced germination and early growth performances. Calcium chelator EGTA [Ethylene glycol-bis(2-aminoethylether)-N,N,N´,N, tetra acetic acid] calcium channel blocker LaCl3 (Lanthanum chloride) and calmodulin inhibitor TFP (trifluroperazine) aggravated these effects of heat and chilling and added calcium reversed them. Imposition of heat and chilling stress during early germination also causes accumulation of reactive oxygen species (ROS) like O2 - and H2O2. Calcium treatment significantly reduced the accumulation of both the toxic ROS, while EGTA, LaCl3 and TFP treatment enhanced the accumulation. Activities of antioxidative enzymes catalase (CAT), ascorbate peroxidase (APOX) and glutathione reductase (GR) and total thiol content decreased significantly under both heat and chilling stress in germinating Amaranthus seedlings. Seedlings raised with Ca2+ treatment under heat and chilling stress exhibit higher activities of CAT, GR and APOX and total thiol level than the untreated plants. EGTA, LaCl3 and TFP treatment, on the other hand significantly reduce the activities of all anti-oxidative enzymes and total thiol level. The work clearly supports the view that Ca2+-signalling pathway plays significant role in limiting heat and chilling induced oxidative stress by upregulating antioxidative defense during recovery phase of post- germination event in Amaranthus lividus.
ABSTRACT
Imposition of salinity stress during early germination imposes a secondary oxidative stress in 120-hr-old Amaranthus lividus seedlings (measured in terms of accumulation of reactive oxygen species, antioxidative defense system and oxidative membrane lipid and protein damages). Seeds of Amaranthus when treated with triadimefon along with NaCI salinity significantly enhanced the activities of catalase, peroxidase and superoxide dismutase, compared to untreated salinity stressed 5-day-old seedlings. Triadimefon treatment also reduced the accumulation of both the ROS (H2O2 and O2*-) in 5-day-old Amaranthus seedlings. When oxidative membrane damages were estimated for triadimefon treated and salinity stressed juvenile seedlings and compared with untreated salinity stressed seedlings, it shows a clear reversal in oxidative membrane damages induced by triadimefon under salinity stress. Triadimefon treatment significantly reduces the membrane lipid peroxidation and the loss of membrane protein thiol level in salinity stressed Amaranthus seedlings. That triadimefon treatment under salinity stress restores the membrane integrity and improves the post-germinative seedling growth could be supported by the data of membrane injury index (MII), relative leakage ratio (RLR), membrane permeability status (MPS), relative growth index (RGI) and mean tolerance index (MTI). SDS-PAGE of total extractible proteins revealed that some new proteins were synthesized in triadimefon treated and salinity stressed seedlings as compared to untreated and salinity stressed one. However the most remarkable feature is the up-regulation of some of the stress proteins in triadimefon treated and salinity stressed seedlings. So, it appears that significant extent of salinity tolerance exhibited by triadimefon pretreated Amaranthus seedlings could be related to the mitigation of oxidative damage to the newly assembled membrane system of juvenile tissues as well as synthesis and up-regulation of stress proteins that enhanced salinity tolerance.