Exogenous Silicon Protects Brassica napus Plants from Salinity-Induced Oxidative Stress Through the Modulation of AsA-GSH Pathway, Thiol-Dependent Antioxidant Enzymes and Glyoxalase Systems
Although silicon (Si) has showed its potential role in mitigating abiotic stress-induced damages in many plant species its role in coordinated induction of antioxidant defense is yet to be elucidated. Therefore, we studied rapeseed ( Brassica napus ) seedlings applied with exogenous Si for changes o...
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Published in | Gesunde Pflanzen Vol. 70; no. 4; pp. 185 - 194 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Berlin/Heidelberg
Springer Berlin Heidelberg
01.12.2018
Springer Nature B.V |
Subjects | |
Online Access | Get full text |
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Summary: | Although silicon (Si) has showed its potential role in mitigating abiotic stress-induced damages in many plant species its role in coordinated induction of antioxidant defense is yet to be elucidated. Therefore, we studied rapeseed (
Brassica napus
) seedlings applied with exogenous Si for changes occurring in antioxidant defense and glyoxalase systems. Seedlings (12-day-old) grown semi-hydroponically were exposed to Si (silicon dioxide, SiO
2
; 1 mM) solely and in combination with NaCl (100 and 200 mM) for 48 h. Salinity created oxidative damage by increasing H
2
O
2
and malondialdehyde (MDA) contents resulting in disruption of antioxidant defense system and in arousing methylglyoxal (MG) toxicity by the down-regulation of glyoxalase enzyme activities. Exogenous Si treatment showed reduction of both H
2
O
2
and MDA contents and up-regulation of antioxidant components including the activities of related enzymes (APX, MDHAR, DHAR, GR, GST, GPX and CAT) and the contents of AsA and GSH. Enhanced activities of glyoxalase I (Gly I) and glyoxalase II (Gly II) detoxified the toxic MG. Thus, this study clearly indicates that Si improved plant tolerance to salinity stress through enhancement of both antioxidant defense and glyoxalase systems that led to reduced oxidative damage and MG toxicity. |
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ISSN: | 0367-4223 1439-0345 |
DOI: | 10.1007/s10343-018-0430-3 |