Phản ứng của enzym chất chống oxy hóa và chất chống oxy hóa không enzym trong cyanobacterium M.aeruginosa để acetoacetate 2-methyl ethyl allelochemical (EMA) bị cô lập từ reed (Phragmites communis)Tóm tắtMacrophytic allelochemicals are considered an environment-friendly and promising alternative to control algal bloom. However, studies examining the potential mechanisms of inhibitory allelochemicals on algae are few. The allelochemical ethyl 2-methyl acetoacetate (EMA), isolated from reed (Phragmites communis), was a strong allelopathic inhibitor on the growth of M.aeruginosa. EMA-induced antioxidant responses were investigated in the cyanobacterium M.aeruginosa to understand the mechanism of EMA inhibition on algal growth. The activities of enzymatic antioxidants superoxide dismutase (SOD) and catalase (CAT), and the contents of non-enzymatic antioxidants reduced glutathione (GSH) and ascorbic acid (AsA) of M.aeruginosa cells were analyzed after treatments with different concentrations of EMA. Exposure of M.aeruginosa to EMA caused changes in enzyme activities and contents of non-enzymatic antioxidants in different manners. The decrease in SOD activity occurred first after 4h of EMA exposure, and more markedly after 40h. CAT activity did not change after 4h of EMA exposure, but increased obviously after 40h. The contents of AsA and GSH were increased greatly by EMA after 4h. After 60h, low EMA concenrtations still increased the CAT activity and the contents of AsA and GSH, but high EMA concentrations started to impose a marked suppression on them. EMA increased dehydroascorbate (DHAsA) and oxidized glutathione (GSSG) contents during all exposure times. After 60, the regeneration rates of AsA and GSH (represented by the AsA/DHAsA ratio and GSH/GSSH ratio, respectively) were reduced by high EMA concentrations. These results suggest that the activation of CAT and the availability of AsA and GSH at early exposure are important to counteract the oxidative stress included by EMA, and the inactivation of SOD may be crucial to the growth inhibition of M.aeruginosa by EMA. All rights reserved.
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