Title : NO induced chromium tolerance in maize (Zea mays L.) seedlings through regulating oxido-nitrosative events and metabolic homeostasis
Effects of exogenous NO application on chromium (Cr) induced oxido-nitrosative stress were investigated on 9-day-old maize seedlings. Enhancement of SOD and NADPH oxidase activities indicated that Cr (200 µM) induced oxidative stress. In both radicles and epicotyls, NADPH oxidase up-regulation leads to oxidative damage which is attested by application of diphenylene iodonium (DPI; NADPH oxidase inhibitor). Application of 500 µM of sodium nitroprusside (SNP, NO donor) suppressed Cr elicited stress symptoms on embryonic axis growth and suppressed NADPH oxidase activity. SNP attenuated the accumulation of hydrogen peroxide, methylglyoxal and proline in Cr-stressed seedlings. Chromium increased thiol and S-nitrosothiol levels but this was restored to control levels by SNP, in spite of a competing NO reaction leading to increase of S-nitrosoglutathione content. Simultaneously, Cr+SNP increased S-nitrosoglutathione contents probably to prevent excess NO deleteriously affecting cellular function. Endogenous NO over-production induced by Cr was declined by addition of arginine analogue N(ω)-nitro-arginine methyl ester (L-NAME) in the germinating medium. L-NAME did not alleviate the negative effects of Cr on maize seedlings due to cellular NO deficiency. In addition, Cr+L-NAME significantly decreased the contents of arginine, spermidine and spermine in epicotyls as compared to Cr treatment alone. Similarly, exposure to Cr+SNP decreased spermidine and spermine levels in both radicles and epicotyls. This study helped to suggest a mechanism of NO-induced Cr tolerance through regulating oxido-nitrosative activities.