4.7 Article

Net cadmium flux and accumulation reveal tissue-specific oxidative stress and detoxification in Populus x canescens

Journal

PHYSIOLOGIA PLANTARUM
Volume 143, Issue 1, Pages 50-63

Publisher

WILEY
DOI: 10.1111/j.1399-3054.2011.01487.x

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Funding

  1. National Natural Science Foundation of China [31070539]
  2. Ministry of Education of China [NCET-08-0468]
  3. Fok Ying Tung Education Foundation [121026]
  4. Specialized Research Fund for the Doctoral Program of Higher Education of China [20090204110027]
  5. Chinese Academy of Sciences [KZCX2-YW-443]
  6. Deutsche Forschungsgemeinschaft

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To characterize the dynamics of Cd2+ flux in the rhizosphere and to study cadmium (Cd) plant-internal partitioning in roots, wood, bark and leaves in relation to energy metabolism, reactive oxygen species (ROS) formation and antioxidants, Populus x canescens plantlets were exposed to either 0 or 50 mu M CdSO4 for up to 20 days in the nutrient solution. A strong net Cd2+ influx in root apex was observed after Cd exposure for 24 h, even if net Cd2+ influx decreased gradually in roots. A large amount of Cd was accumulated in roots. Cd ions were uploaded via the xylem to leaves and further transported to the phloem where significant accumulation was detected. Cd accumulation led to decreased photosynthetic carbon assimilation but not to the depletion in soluble carbohydrates. Increased levels of ROS were present in all tissues, except the bark of Cd-exposed poplars. To combat Cd-induced superoxide and hydrogen peroxide, P. x canescens appeared to rely mainly on the formation of soluble phenolics as these compounds showed the highest accumulation in the bark and the lowest in wood. Other potential radical scavengers such as proline, sugar alcohols and antioxidant enzymes showed tissue-and exposure time-specific responses to Cd. These results indicate a complex pattern of internal Cd allocation in P. x canescens resulting in higher ROS stress in wood than in bark and intermediate responses in roots and leaves, probably because of differential capacities of these tissues for the production of protective phenolic compounds.

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