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Early and long-term responses of cucumber cells to high cadmium concentration are modulated by nitric oxide and reactive oxygen species

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Abstract

Plants are increasingly exposed to heavy metal pollution in the environment. Cadmium (Cd), a non-essential metal, is known to exert strong phytotoxic effects. The aim of the present study was to examine the role of nitric oxide (NO), reactive nitrogen (RNS) and reactive oxygen (ROS) species in the responses of cucumber (Cucumis sativus) cell culture to high Cd concentration. We observed that the early responses to Cd included enhanced levels of NO, RNS and ROS and the induction of cell death, whereas the levels of both RNS and ROS were suppressed as a long-term response to Cd. The Cd-induced increase of NO level was localized in the chloroplasts, while increased ROS and RNS levels were observed in the cytoplasm. We employed an NO scavenger, an NO synthase inhibitor and an NO donor to evaluate the involvement of RNS and ROS in the responses of C. sativus cells to Cd. The observed changes in cell viability and growth were not related to changes in NO, RNS and ROS levels. Long-term Cd exposure inhibited cell division and de-differentiation as assessed by microcallus formation. We conclude that increased NO level belongs to the early responses of plant cells to high Cd concentration and is associated with an NO synthase-like enzyme activity, whereas decreased cell viability and division in long-term Cd treatment are related to interferences with NO signalling and decreased level of both RNS and ROS.

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Acknowledgments

This research was supported by the Czech Ministry of Education, Youth and Sports (LH11013).

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Correspondence to Marek Petřivalský.

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Communicated by G. Klobus.

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Piterková, J., Luhová, L., Navrátilová, B. et al. Early and long-term responses of cucumber cells to high cadmium concentration are modulated by nitric oxide and reactive oxygen species. Acta Physiol Plant 37, 19 (2015). https://doi.org/10.1007/s11738-014-1756-9

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  • DOI: https://doi.org/10.1007/s11738-014-1756-9

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