4.7 Article

Effect of exogenous silicon (Si) on H+-ATPase activity, phospholipids and fluidity of plasma membrane in leaves of salt-stressed barley (Hordeum vulgare L.)

Journal

ENVIRONMENTAL AND EXPERIMENTAL BOTANY
Volume 57, Issue 3, Pages 212-219

Publisher

PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.envexpbot.2005.05.012

Keywords

barley (Hordeum vulgare L.); H+-ATPase activity; membrane fluidity; phospholipid; salt stress; silicon

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Silicon (Si) is generally considered a beneficial element for the growth of higher plants, especially for those grown under stressed environments. Recently, the mitigating role of Si in salt stress has received worldwide attention. However, its mechanisms involved remain poorly understood. We studied the effects of Si on plasma membrane fluidity, phospholipids and H+-ATPase activity and reduced glutathione (GSH) concentration with two contrasting barley cultivars differing in their salt tolerance. The results showed that plasma membrane H+-ATPase activity decreased in leaves of plants treated with 120 mM NaCl, and this decrease was more obvious in salt-sensitive cultivar (Kepin No. 7) than in salt-tolerant cultivar (Jian 4). Under NaCl stress, plasma membrane fluidity decreased, and the ratio of phospholipids to proteins in plasma membrane vesicles increased. GSH concentration decreased in leaves of plants exposed to 120 mM NaCl in salt-sensitive cultivar (but not in salt-tolerant cultivar). Inclusion of 1.0 mM Si to the salt treatment increased plasma membrane H+-ATPase activity in both cultivars as compared with the plants treated with 120 mM NaCl only. The addition of Si to salt treatment was also found to recover membrane fluidity to control (neither NaCl nor Si added) level, and decrease the ratio of phospholipids to protein. Furthermore, GSH concentration in leaves of salt-treated plants was increased by addition of Si. It is suggested that Si maintain the optimal membrane fluidity and increase GSH concentration, which contributes to reducing oxidative damage to enzymes induced by active oxygen species and enhances plasma membrane H+-ATPase activity under NaCl stress. (c) 2005 Elsevier B.V. All rights reserved.

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