过氧化氢可抑制藻类生长, 同时会导致微囊藻毒素(Microcystins, MCs)的释放, 实验设置4个处理组探讨了外源微囊藻毒素MC-LR对H2O2胁迫下铜绿微囊藻生理生化变化的影响。结果表明: 在H2O2胁迫下, 微囊藻的生长和光合活性受到显著抑制, 藻细胞存活率降低, ROS含量明显增加, SOD活性上升。与单独H2O2胁迫相比, 加入MC-LR能增加微囊藻细胞的存活率。250 μmol/L H2O2处理24h和48h后, 在培养基中加入200 ng/mL MC-LR可以缓解H2O2对铜绿微囊藻光合系统PSII活性的抑制作用。当微囊藻暴露于250 μmol/L H2O2环境中时, 添加了MC-LR处理组藻细胞中的ROS含量明显减少(P〈0.05)。在相同浓度H2O2且加入了外源MC-LR后藻细胞SOD活性下降(P〈0.05)。因此, 微囊藻毒素MC-LR可缓解250 μmol/L H2O2引起的氧化损伤并增强微囊藻自身的生存能力。研究结果有利于阐明H2O2胁迫影响产毒蓝藻生长代谢的途径及MCs生物学意义。
Hydrogen peroxide acts as an algicide and can also rapidly decomposition into oxygen and water. Becausemany bloom-forming cyanobacteria species produce and release microcystin, we used MC-LR to test whether MC-LR was involved in H2O2 induced growth and metabolic changes in Microcystis aeruginosa. The results showed that M. aeruginosa growth was significantly inhibited after exposure to 250 μmol/L and 350 μmol/L H2O2. The addition of 200 ng/mL MC-LR could increase the cell viability of M. aeruginosa under 250 μmol/L H2O2 stress. The inhibition of PSII activity after exposure to 250 μmol/L H2O2 was also reduced in the presence of MC-LR. Moreover, the addition of MC-LR decreased ROS accumulation (P〈0.05) in cells threated with 250 mmol/L H2O2 and reduced SOD activity (P〈0.05). Hence, MC-LR could increase the fitness of M. aeruginosa under 250 μmol/L H2O2 stress. Our findings contributed to the understanding of growth and metabolism of toxic Microcystis under H2O2 stress.