Changes of polyamine levels in roots of Sagittaria sagittifolia L. under copper stress.
Ključne riječi
Sažetak
BACKGROUND
The goal of the present study was to investigate the effects of Cu contamination on the above-mentioned biochemical and physiological parameters in order to explore possible prevention strategies against heavy metal stress.
METHODS
Effects of copper (Cu) on the roots of Sagittaria sagittifolia L. were studied after 10 days of treatment at five concentration levels. The accumulation of Cu, the generation rate of O(2) (·-), the contents of thiobarbituric acid reactive substances (TBARS) and polyamines, as well as the activities of arginine decarboxylase (ADC) and polyamine oxidase (PAO) in the roots were measured and analyzed.
CONCLUSIONS
It was observed that endogenous Cu content increased in roots of S. sagittifolia L. in a concentration-dependent manner, along with an increased production of O(2) (·-). TBARS content increased progressively up to 5 μmol l(-1) Cu. A constant increase in ADC activity was also observed. The results indicated that lower Cu concentrations (2.5 and 5 μmol l(-1), respectively) had greater enhancing effect on the contents of free Put and perchloric acid-soluble conjugated (PS-conjugated) putrescine (Put), while Cu treatments at different concentration levels had similar enhancing effect on the content of perchloric acid-insoluble bound Put. In total, Put content in each Cu-treated group was higher than that in the control group. PAO activity was inhibited up to 10 μmol l(-1) Cu but enhanced at higher Cu concentrations (20 and 40 μmol l(-1)). This explained the initial rise and subsequent decline of the contents of all forms of spermine (Spm), free and PS-conjugated spermidine (Spd). However, with the increase of Cu concentration, total Spm content increased gradually while total Spd content decreased. Our results suggest that Cu is phytotoxic to the roots of S. sagittifolia L. at high concentrations, and that the increased Spm level is not sufficient to resist Cu-induced oxidative damages.
