This work was focused on the role of silicon (Si) in amelioration of manganese (Mn) toxicity caused by elevated production of hydroxyl radicals (·OH) in the leaf apoplast of cucumber (Cucumis sativus L.). The plants were grown in nutrient solutions with adequate (0.5 μM) or excessive (100 μM) Mn concentrations with or without Si being supplied. The symptoms of Mn toxicity were absent in the leaves of Si-treated plants subjected to excess Mn, although the leaf Mn concentration remained extremely high. The apoplastic concentration of free Mn²⁺ and H₂O₂ of high Mn-treated plants was significantly decreased by Si treatment. Si supply suppressed the Mn-induced increased abundance of peroxidase (POD) isoforms in the leaf apoplastic fluid, and led to a rapid suppression of guaiacol-POD activity under excess Mn. The spin-trapping reagent 5-(diethoxyphosphoryl)-5-methyl-1-pyrroline-N-oxide was used to detect ·OH by electron paramagnetic resonance spectroscopy. Although supplying Si markedly decreased the accumulation of ·OH in the leaf apoplast with excess Mn, adding monosilicic acid to the Mn²⁺/H₂O₂ reaction mixture did not directly affect the Fenton reaction in vitro. The results indicate that Si contributes indirectly to a decrease in ·OH in the leaf apoplast by decreasing the free apoplastic Mn²⁺, thus regulating the Fenton reaction. A direct inhibitory effect of Si on guaiacol-POD activity (demonstrated in vitro) may also contribute to decreasing the POD-mediated generation of ·OH.

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 non-enzymatic 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.