We investigated the mechanistic consequences of selenium (Se)-toxicity, and its possible mitigation using salicylic acid (SA) in rice. In comparison with control, sodium selenate-exposed 'Se1' (0.5 mM) and 'Se2' (1.0 mM) plants showed accumulation of Se by 190.63 and 288.00 % in roots, 2359.42 and 2054.35 % in leaf sheaths, and 7869.91 and 9063.72 % in leaves, respectively, resulting in severe toxicity symptoms, such as growth inhibition, chlorosis, burning of leaves, and oxidative stress. In contrast, SA addition to Se-stressed plants significantly alleviated the Se-toxicity symptoms, and radically improved shoot height (28.88 %), dry biomass (34.00 %), total chlorophyll (37.51 %), soluble sugar (17.31 %) and leaf water contents (22.31 %) in 'SA + Se2' plants over 'Se2' plants. Notably, SA maintained Se-homeostasis, and decreased 'Se2'-induced oxidative stress by enhancing ascorbate level (67.75 %) and the activities of antioxidant enzymes like superoxide dismutase (20.99 %), catalase (40.97 %), glutathione peroxidase (12.26 %), and glutathione reductase (32.58 %) relative to that in 'Se2' plants. Additionally, SA protected rice plants from the deleterious effects of methylglyoxal by stimulating the activities of glyoxalase enzymes. Furthermore, SA upregulated several genes associated with reactive oxygen species (e.g. OsCuZnSOD1, OsCATB, OsGPX1 and OsAPX2) and methylglyoxal (e.g. OsGLYI-1) detoxifications. These findings unravel a decisive role of SA in alleviating Se-phytotoxicity in rice.
Keywords: Antioxidant defense; Gene expression; Glyoxalase system; Metalloid toxicity; Phytohormone.
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