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Ecotoxicology and Environmental Safety 2019-Aug

SA and AM symbiosis modulate antioxidant defense mechanisms and asada pathway in chickpea genotypes under salt stress.

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Amrit Bharti
Neera Garg

Ključne riječi

Sažetak

Salt stress disturbs redox homeostasis by perturbing equilibrium between generation and removal of reactive oxygen species (ROS), which alters the normal metabolism of plants through membrane damage, lipid peroxidation and denaturation of proteins. Salicylic acid (SA) seed priming and arbuscular mycorrhizal (AM) fungi impart salt tolerance in legumes by maintaining redox balance. The present investigation focused on the relative and combined applications of SA and Rhizoglomus intraradices in scavenging ROS in Cicer arietinum L. (chickpea) genotypes (salt tolerant-PBG 5, relatively sensitive-BG 256) subjected to salt stress. Despite the enhanced antioxidant mechanisms under salt stress, ROS (superoxide, O2- and hydrogen peroxide, H2O2) accumulation increased significantly and induced lipid peroxidation and lipoxygenase (LOX) activities, which disrupted membrane stability, more in BG 256 than PBG 5. Salt stress also caused redox imbalance by lowering ascorbate/dehydroascorbate (ASA/DHA) and reduced glutathione/oxidized glutathione (GSH/GSSG) ratios, indicating that redox-homeostasis was crucial for salt-tolerance. Exogenous SA was more promising in reducing ROS-generation and lipid-peroxidation, which provided higher membrane stability as compared to AM inoculation. Although, the enzymatic antioxidants were more active in SA treated plants, yet, AM inoculation outperformed in increasing reformative enzyme activities of Foyer-Halliwell-Asada cycle, which resulted in higher plant biomass in a genotype-dependent manner. SA increased AM root colonization and provided functional complementarity to R. intraradices and thereby strengthening antioxidant defense mechanisms through their cumulative contribution. The study suggested the use of +SA+AM as an eco-friendly tool in imparting salt tolerance in chickpea genotypes subjected to long-term salinity.

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