Cold acclimation increases plant tolerance to a more-severe chilling and in this process an accumulation of H(2)O(2) in plants is often observed. To examine the role of H(2)O(2) in cold acclimation in plants, the accumulation of H(2)O(2), antioxidant metabolism, the glutathione redox state, gas exchange and chlorophyll fluorescence were analyzed after cold acclimation at 12/10 °C and during the subsequent chilling at 7/4 °C in tomato (Solanum lycopersicum) plants. Cold acclimation modestly elevated the levels of H(2)O(2), the gene expression of respiratory burst oxidase homolog 1 (Rboh1) and NADPH oxidase activity, leading to the up-regulation of the expression and activity of antioxidant enzymes. In non-acclimated plants chilling caused a continuous rise in the H(2)O(2) content, an increase in the malondialdehyde (MDA) content and in the oxidized redox state of glutathione, followed by reductions in the CO(2) assimilation rate and the maximum quantum yield of photosystem II (F(v)/F(m)). However, in cold-acclimated plants chilling-induced photoinhibition, membrane peroxidation and reductions in the CO(2) assimilation rate were significantly alleviated. Furthermore, a treatment with an NADPH oxidase inhibitor or H(2)O(2) scavenger before the plants subjected to the cold acclimation abolished the cold acclimation-induced beneficial effects on photosynthesis and antioxidant metabolism, leading to a loss of the cold acclimation-induced tolerance against chilling. These results strongly suggest that the H(2)O(2) generated by NADPH oxidase in the apoplast of plant cells plays a crucial role in cold acclimation-induced chilling tolerance.
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