4.5 Article

Rutin, a flavonoid with antioxidant activity, improves plant salinity tolerance by regulating K+ retention and Na+ exclusion from leaf mesophyll in quinoa and broad beans

Journal

FUNCTIONAL PLANT BIOLOGY
Volume 43, Issue 1, Pages 75-86

Publisher

CSIRO PUBLISHING
DOI: 10.1071/FP15312

Keywords

ascorbate peroxidase; catalase; Chenopodium quinoa; enzymatic and non-enzymatic antioxidants; oxidative stress; phenols; proline; reactive oxygen species; ROS; superoxide dismutase

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Funding

  1. Australian Research Council
  2. Grain research and Development Corporation
  3. Serbian Ministry of Education, Science and Technological Development [173040]
  4. Egyptian Ministry of higher Education

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The causal relationship between salinity and oxidative stress tolerance is well established, but specific downstream targets and the role of specific antioxidant compounds in controlling cellular ionic homeostasis remains elusive. In this work, we have compared antioxidant profiles of leaves of two quinoa genotypes contrasting in their salt tolerance, with the aim of understanding the role of enzymatic and non-enzymatic antioxidants in salinity stress tolerance. Only changes in superoxide dismutase activity were correlated with plant adaptive responses to salinity. Proline accumulation played no major role in either osmotic adjustment or in the tissue tolerance mechanism. Among other nonenzymatic antioxidants, rutin levels were increased by over 25 fold in quinoa leaves. Exogenous application of rutin to glycophyte bean leaves improved tissue tolerance and reduced detrimental effects of salinity on leaf photochemistry. Electrophysiological experiments revealed that these beneficial effects were attributed to improved potassium retention and increased rate of Na+ pumping from the cell. The lack of correlation between rutin-induced changes in K+ and H+ fluxes suggest that rutin accumulation in the cytosol scavenges hydroxyl radical formed in response to salinity treatment thus preventing K+ leak via one of ROS-activated K+ efflux pathways, rather than controlling K+ flux via voltage-gated K+-permeable channels.

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