The effect in vivo of salt stress on the activated oxygen metabolism o
f mitochondria, was studied in leaves from two NaCl-treated cultivars
of Pisum sativum L. with different sensitivity to NaCl. In mitochondri
a from NaCl-sensitive plants, salinity brought about a significant dec
rease 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 treat
ment 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 H2O2 concentration remained unchanged
. The NADH- and succinate-dependent generation of O2.- radicals by sub
mitochondrial particles and the lipid peroxidation of mitochondrial me
mbranes, increased as a result of salt treatment, and these changes we
re 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 mitoc
hondrial MnSOD activity, whereas NaCl-tolerant plants appear to have a
protection mechanism against salt-induced increased O2.- production b
y means of the induction of the mitochondrial Mn-SOD activity. These r
esults 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 mit
ochondrial Mn-SOD in the molecular mechanisms of plant tolerance to Na
Cl.