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  • Stress response and tolerance of Zea mays to CeO2 nanoparticles: cross talk among H2O2, heat shock protein, and lipid peroxidation.

Stress response and tolerance of Zea mays to CeO2 nanoparticles: cross talk among H2O2, heat shock protein, and lipid peroxidation.

ACS nano (2012-10-12)
Lijuan Zhao, Bo Peng, Jose A Hernandez-Viezcas, Cyren Rico, Youping Sun, Jose R Peralta-Videa, Xiaolei Tang, Genhua Niu, Lixin Jin, Armando Varela-Ramirez, Jian-ying Zhang, Jorge L Gardea-Torresdey
要旨

The rapid development of nanotechnology will inevitably release nanoparticles (NPs) into the environment with unidentified consequences. In addition, the potential toxicity of CeO(2) NPs to plants and the possible transfer into the food chain are still unknown. Corn plants (Zea mays) were germinated and grown in soil treated with CeO(2) NPs at 400 or 800 mg/kg. Stress-related parameters, such as H(2)O(2), catalase (CAT), and ascorbate peroxidase (APX) activity, heat shock protein 70 (HSP70), lipid peroxidation, cell death, and leaf gas exchange were analyzed at 10, 15, and 20 days post-germination. Confocal laser scanning microscopy was used to image H(2)O(2) distribution in corn leaves. Results showed that the CeO(2) NP treatments increased accumulation of H(2)O(2), up to day 15, in phloem, xylem, bundle sheath cells and epidermal cells of shoots. The CAT and APX activities were also increased in the corn shoot, concomitant with the H(2)O(2) levels. Both 400 and 800 mg/kg CeO(2) NPs triggered the up-regulation of the HSP70 in roots, indicating a systemic stress response. None of the CeO(2) NPs increased the level of thiobarbituric acid reacting substances, indicating that no lipid peroxidation occurred. CeO(2) NPs, at both concentrations, did not induce ion leakage in either roots or shoots, suggesting that membrane integrity was not compromised. Leaf net photosynthetic rate, transpiration, and stomatal conductance were not affected by CeO(2) NPs. Our results suggest that the CAT, APX, and HSP70 might help the plants defend against CeO(2) NP-induced oxidative injury and survive NP exposure.

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