Manganese-induced salt stress tolerance in rice seedlings: regulation of ion homeostasis, antioxidant defense and glyoxalase systems
Physiology and Molecular Biology of Plants, ISSN: 0971-5894, Vol: 22, Issue: 3, Page: 291-306
2016
- 120Citations
- 80Captures
- 2Mentions
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- 80
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Article Description
Hydroponically grown 12-day-old rice (Oryza sativa L. cv. BRRI dhan47) seedlings were exposed to 150 mM NaCl alone and combined with 0.5 mM MnSO. Salt stress resulted in disruption of ion homeostasis by Na influx and K efflux. Higher accumulation of Na and water imbalance under salinity caused osmotic stress, chlorosis, and growth inhibition. Salt-induced ionic toxicity and osmotic stress consequently resulted in oxidative stress by disrupting the antioxidant defense and glyoxalase systems through overproduction of reactive oxygen species (ROS) and methylglyoxal (MG), respectively. The salt-induced damage increased with the increasing duration of stress. However, exogenous application of manganese (Mn) helped the plants to partially recover from the inhibited growth and chlorosis by improving ionic and osmotic homeostasis through decreasing Na influx and increasing water status, respectively. Exogenous application of Mn increased ROS detoxification by increasing the content of the phenolic compounds, flavonoids, and ascorbate (AsA), and increasing the activities of monodehydroascorbate reductase (MDHAR), dehydroascorbate reductase (DHAR), superoxide dismutase (SOD), and catalase (CAT) in the salt-treated seedlings. Supplemental Mn also reinforced MG detoxification by increasing the activities of glyoxalase I (Gly I) and glyoxalase II (Gly II) in the salt-affected seedlings. Thus, exogenous application of Mn conferred salt-stress tolerance through the coordinated action of ion homeostasis and the antioxidant defense and glyoxalase systems in the salt-affected seedlings.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84982286084&origin=inward; http://dx.doi.org/10.1007/s12298-016-0371-1; http://www.ncbi.nlm.nih.gov/pubmed/27729716; http://link.springer.com/10.1007/s12298-016-0371-1; https://dx.doi.org/10.1007/s12298-016-0371-1; https://link.springer.com/article/10.1007/s12298-016-0371-1; http://link.springer.com/article/10.1007%2Fs12298-016-0371-1; https://link.springer.com/content/pdf/10.1007%2Fs12298-016-0371-1.pdf; http://link.springer.com/article/10.1007/s12298-016-0371-1/fulltext.html; http://link.springer.com/content/pdf/10.1007/s12298-016-0371-1.pdf
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