RBOH-dependent H2O2 burst induced by silicon dioxide nanoparticles establishes systemic acquired acclimation in quinoa under lead toxicity

The role of silicon dioxide nanoparticles (nSiO 2 ) and hydrogen peroxide (H 2 O 2 ) in heavy metal tolerance of plants has been well defined; however, their interaction together remains largely unknown. Therefore, two experiments were conducted to determine whether RBOH-dependent signaling is involved in nSiO 2 -induced systemic lead (Pb) acclimation in Chenopodium quinoa . In the first experiment, quinoa leaves were sprayed with nSiO 2 (0, 2, 4 mM) under various Pb concentrations (0, 200 and 400 mu M). After 12 h, an H 2 O 2 burst, and higher transcription levels of RBOHD and PCS1 genes (encoding NADPH oxidase and phytochelatin synthase) were recorded in leaves of nSiO 2 -treated plants. After 15 days, Pb toxicity reduced growth parameters, and Chl a , Chl b contents and increased electrolyte leakage, and foliar spray with nSiO 2 reversed this tendency. In the second experiment, foliar application of 4 mM nSiO 2 minimized intracellular H 2 O 2 and O 2 (center dot) hyde content and leaf Pb concentration under 400 mu M Pb. While, this treatment increased the content of reduced ascorbate, and thiol compounds and enhanced the activities of superoxide dismutase and ascorbate peroxidase not only in leaves but also in untreated roots. However, H 2 O 2 scavenging with DMTU and the inhibition of RBOH-dependent signaling by DPI aggravated Pb phytotoxicity and impaired the beneficial effects of nSiO 2 on aforementioned attributes; thereby reduced tolerance index in both leaves and roots. Together, our pharmacological and molecular evidence for the first time unraveled that RBOH-dependent H 2 O 2 burst plays vital role in triggering nSiO 2 -induced systemic acquired acclimation in Pb-stressed plants. and reduced malondialde