Salt tolerance of Centaurea ragusina L. is associated with efficient osmotic adjustment and increased antioxidative capacity

The present study investigated the effects of salinity on the perennial species Centaurea ragusina L. interesting as a potential cash crop plant. Plants grown in culture conditions were subjected to increasing salt (0-600. mM NaCl) or mannitol (300. mM) treatments for two weeks. Effects of isoosmotic concentrations of NaCl (150. mM) and mannitol were compared and discussed in order to discriminate possible differences in C. ragusina response to ionic (NaCl) and osmotic (mannitol) components of salinity. C. ragusina plants used Na and to a lesser extent Cl ions as a primary osmotica though with higher salinity, proline accumulation increased as well. Concurrently, with increasing salinity significant reductions in plant K, Mg and Ca concentrations occurred. In addition, lower salt concentrations induced leaf succulence and increased leaf relative water content (RWC). A threshold salinity above which C. ragusina L. showed signs of damage and growth inhibition was reached at 300. mM. Activities of superoxide dismutase, catalase and ascorbate peroxidase in salinized plants seem to play an essential protective role in the scavenging processes. Regardless of the high induction of antioxidative system and massive proline accumulation, mannitol caused decrease of RWC and oxidative damage to proteins and lipids. Considering the abundance of some photosynthetic proteins (Rubisco, D1, LHCI, LHII and FNR) and PSII efficiency, it can be concluded that both salt and mannitol impaired photosynthesis in C. ragusina though salt to a much lesser extent. The results suggest that the major reason for the particular threshold of salinity tolerance in C. ragusina can be attributed to limited dilution capacity of succulent tissue. The tolerance strategies of C. ragusina to moderate salinity seem to include osmotic adjustment achieved through salt ions uptake as a dominant strategy but also highly inducible antioxidative defense.