Salt‐induced oxidative stress mediated by activated oxygen species in pea leaf mitochondria

Abstract

The effect in vivo of salt stress on the activated oxygen metabolism of mitochondria, was studied in leaves from two NaCl‐treated cultivars of Pisum sativum L. with different sensitivity to NaCl. In mitochondria from NaCl‐sensitive plants, salinity brought about a significant decrease of Mn‐SOD (EC 1. 15. 1. 1) Cu, Zn‐SOD I (EC 1. 15. 1. 1) and fumarase (EC 4. 2. 1. 2) activities. Conversely, in salt‐tolerant plants NaCl treatment produced an increase in the mitochondrial Mn‐SOD activity and, to a lesser extent, in fumarase activity. In mitochondria from both salt‐treated cultivars, the internal H 2 O 2 concentration remained unchanged. The NADH‐ and succinate‐dependent generation of O 2.−radicals by submitochondrial particles and the lipid peroxidation of mitochondrial membranes, increased as a result of salt treatment, and these changes were higher in NaCl‐sensitive than in NaCl‐tolerant plants. Accordingly, the enhanced rates of superoxide production by mitochondria from salt‐sensitive plants were concomitant with a strong decrease in the mitochondrial Mn‐SOD activity, whereas NaCl‐tolerant plants appear to have a protection mechanism against salt‐induced increased O 2.− production by means of the induction of the mitochondrial Mn‐SOD activity. These results indicate that in the subcellular toxicity of NaCl in pea plants, at the level of mitochondria, an oxidative stress mechanism mediated by superoxide radicals is involved, and also imply a function for mitochondrial Mn‐SOD in the molecular mechanisms of plant tolerance to NaCl.