微囊藻毒素对束丝藻细胞生长和抗氧化系统的影响

为从活性氧(ROS)角度探讨微囊藻毒素(MC)导致藻类细胞死亡的机理及揭示藻细胞对MC诱发的氧化胁迫的响应机制,采用50和500μg·L-1的微囊藻毒素LR(MC-LR)处理束丝藻(Aphanizomenon sp. DC01)细胞,测定了细胞生长、细胞内活性氧(ROS)含量及抗氧化系统的变化.结果表明,50μg·L-1的MC-LR处理对藻细胞的生长无显著影响,而500μg·L-1的MC-LR处理可诱导藻细胞死亡.50μg·L-1的MC-LR处理的藻细胞ROS含量在处理第2d显著高于对照;但藻细胞能通过还原型谷胱甘肽(GSH)含量,超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GPX)活性改变修复氧化损伤,使ROS水平在处理第3d恢复到对照水平.500μg·L-1的MC-LR处理可显著降低藻细胞GSH含量和SOD与GPX活性,刺激藻细胞生成过量的ROS;ROS在毒素处理4d后突然暴发,过量的ROS引起膜质过氧化,并最终导致藻细胞死亡。

Effects of Microcystin-LR on the Growth and Antioxidant Systems in Aphanizomenon sp. DC01 Cells

To investigate the toxic effects of microcystin(MC)on microalgae cells and elucidate the mechanism of cell death and responses of antioxidant systems in microalgae to oxidative stress induced by MC from the perspective of reactive oxygen species(ROS), the changes of cell growth, ROS production and antioxidant systems in the cells were determined using 50μg·L-1 and 500μg·L-1 MC-LR to treat Aphanizomenon sp. DC01 cells. Results showed that 50μg·L-1 MC-LR had no significant effects on the growth of Aphanizomenon sp. DC01 while 500μg·L-1 MC-LR induced cell death of Aphanizomenon sp. DC01. The ROS content in 50μg·L-1 MC-LR treated cells was significantly higher than that in the control group after 2 days toxin exposure, but Aphanizomenon cells could rehabilitate the oxidative injury through changes of glutathione(GSH)content and superoxide dismutase(SOD), glutathione peroxidas(GPX)activities. ROS content recovered to the control level after 3 days. 500μg·L-1 MC-LR treat significantly decreased GSH content and SOD, GPX activities, and induced the excessive production of ROS in Aphanizomenon cells. ROS production burst after 4d toxin exposure, causing lipid peroxidation of Aphanizomenon cells, which led to cell death at last.