These authors contributed equally to this work.
Response of mitochondrial antioxidant system and respiratory pathways to reactive nitrogen species in pea leaves
Article first published online: 27 JUN 2012
Copyright © Physiologia Plantarum 2012
Volume 147, Issue 2, pages 194–206, February 2013
How to Cite
Martí, M. C., Florez-Sarasa, I., Camejo, D., Pallol, B., Ortiz, A., Ribas-Carbó, M., Jiménez, A. and Sevilla, F. (2013), Response of mitochondrial antioxidant system and respiratory pathways to reactive nitrogen species in pea leaves. Physiologia Plantarum, 147: 194–206. doi: 10.1111/j.1399-3054.2012.01654.x
- Issue published online: 22 JAN 2013
- Article first published online: 27 JUN 2012
- Accepted manuscript online: 18 MAY 2012 11:13AM EST
- Received 7 February 2012;, revised 20 March 2012
Nitric oxide (NO) has emerged as an important signaling molecule in plants, but little is known about the effects of reactive nitrogen species in plant mitochondria. In this study, the effects of DETA-NONOate, a pure NO slow generator, and of SIN-1 (3-morpholinosydnonimine), a peroxynitrite producer, on the activities of respiratory pathways, enzymatic and non-enzymatic antioxidants have been investigated in isolated mitochondria from pea leaves. No significant changes in lipid peroxidation, protein oxidation or in ascorbate and glutathione redox state were observed after DETA-NONOate treatments whereas cytochrome pathway (CP) respiration was reversibly inhibited and alternative pathway (AP) respiration showed little inhibition. On the other hand, NO did not affect neither activities of Mn superoxide dismutase (Mn-SOD) nor enzymes involved in the ascorbate and glutathione regeneration in mitochondria except for ascorbate peroxidase (APX), which was reversely inhibited depending on ascorbate concentration. Finally, SIN-1 treatment of mitochondria produced a decrease in CP respiration, an increase in protein oxidation and strongly inhibited APX activity (90%), with glutathione reductase and dehydroascorbate reductase (DHAR) being moderately inhibited (30 and 20%, respectively). This treatment did not affect monodehydroascorbate reductase (MDHAR) and Mn-SOD activities. Results showed that mitochondrial nitrosative stress was not necessarily accompanied by oxidative stress. We suggest that NO-resistant AP and mitochondrial APX may be important components of the H2O2-signaling pathways under nitrosative stress induced by NO in this organelle. Also, MDHAR and DHAR, via ascorbate regeneration, could constitute an essential antioxidant defense together with Mn-SOD, against NO and ONOO− stress in plant mitochondria.