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Published on March 11, 2009; 10.1104/pp.108.131524

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Received October 21, 2008
Accepted March 8, 2009

Cellular Response of pea plants to cadmium toxicity: cross-talk between reactive oxygen species, nitric oxide and calcium

Maria Rodriguez-Serrano , Maria C. Romero-Puertas , Diana M. Pazmino , Pilar S. Testillano , Maria C. Risueno , Luis A. del Rio , and Luisa M. Sandalio *

Departamento de Bioquimica, Biologia Celular y Molecular de Plantas; Estacion Experimental del Zaidin, CSIC, Profesor Albareda 1, E-18008, Granada, Spain; Plant Development and Nuclear Architecture; Centro de Investigaciones Biologicas, CSIC, Ramiro de Maeztu 9, 28040 Madrid, Spain

* Corresponding author; email: luisamaria.sandalio{at}eez.csic.es.

Cadmium (Cd) toxicity has been widely studied in different plant species, however the mechanism involved in its toxicity as well as the cell response against the metal have not been well established yet. In this work, using pea plants we have studied the effect of Cd on antioxidants, reactive oxygen species (ROS) and nitric oxide (NO) metabolism of leaves by using different cellular, molecular and biochemical approaches.

The growth of pea plants with 50 µM CdCl2 affected differentialy the expression of superoxide dismutase isozymes at both transcriptional and post-transcriptional level, giving rise to an SOD activity reduction. The CuZn-SOD down-regulation was apparently due to the calcium (Ca) deficiency induced by the heavy-metal. In these circunstances, the overproduction of ROS (H2O2 and O2·-) could be observed in vivo by confocal laser microscopy, mainly associated with vascular tissue, epidermis, and mesophyll cells and production of superoxide radicals was prevented by exogenous Ca. On the other hand, the nitric oxide synthase (NOS)-dependent NO production was strongly depressed by Cd and the treatment with Ca prevented this effect. Under these conditions, the pathogenesis-related proteins (PRPs) PrP4A, chitinase, and the HSP 71.2, were up-regulated; probably to protect cells against damages induced by Cd. The regulation of these proteins could be mediated by jasmonic acid and ethylene, whose contents increased by Cd treatment. A model is proposed for the cellular response to long-term Cd exposure consisting in a cross-talk between Ca, ROS and NO.






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