镉对集胞藻光合活性的影响

Effects of Cadmium on Photosynthetic Activity of Synechocystis PCC 6803

镉是环境中的主要重金属污染物,研究镉胁迫下蓝藻光合活性的变化,有助于深入认识镉的细胞毒性以及蓝藻细胞对镉胁迫的响应特性,可为评价镉的生态环境风险提供科学依据。为探索镉对淡水蓝藻的毒性效应,选择集胞藻PCC 6803作为受试生物,以0、0.05、0.25、0.50和1.00 mg·L^(-1)Cd^(2+)处理24 h后,测定其光合色素含量、光合活性以及活性氧(ROS)、超氧化物歧化酶(SOD)的变化。结果表明,0.05 mg·L^(-1)Cd^(2+)处理下细胞的光合活性与对照组无显著差异;高于0.25 mg·L^(-1)的Cd^(2+)处理,细胞叶绿素a含量下降,PSⅡ反应中心受损,活性氧积累并激活抗氧化酶活性。Cd^(2+)浓度高于0.50 mg·L^(-1),最大光化学效率(Fv/Fm)显著下降,PSⅡ线性电子传递链受阻;QA-动力学曲线的快相和中相时长明显增加,QA-到QB电子传递受到抑制,PSⅡ受体侧受损,QB空位点对PQ的结合速率减慢。结果表明,集胞藻能耐受低于0.05 mg·L^(-1)Cd^(2+)胁迫并表现出毒性兴奋效应;高浓度Cd^(2+)通过干扰PSⅡ导致生长抑制作用,影响线性电子传递链中QA-和QB,主要毒性作用位点(受体蛋白)尚不清楚。

Cadmium is the main heavy metal pollutant in the current environment.Studying the changes of cyanobacterial photosynthetic activity under cadmium stress is helpful to deeply understand the cytotoxicity of cadmium and the response characteristics of cyanobacterial cells to cadmium stress.In order to provide basis for evaluating the ecological and environmental risks of cadmium,toxic effects of cadmium to freshwater cyanobacteria was studied,selecting Synechocystis PCC 6803 as the test organism.After treatment with 0,0.05,0.25,0.50 and 1.00 mg·L^(-1)Cd^(2+)for 24 h,the content of photosynthetic pigments,photosynthetic activity,reactive oxygen species(ROS)content and superoxide dismutase(SOD)activities were determined.The results showed that there was no significant difference in photosynthetic activity between the low-dose 0.05 mg·L^(-1)Cd^(2+)treatment and the control group.Under treatment with 0.25 mg·L^(-1)Cd^(2+),chlorophyll a content decreased,the PSⅡreaction center was damaged,ROS content was accumulated,the antioxidant enzyme was activated and growth was inhibited.The maximum photochemical efficiency(Fv/Fm)decreased significantly at Cd^(2+)concentrations above 0.50 mg·L^(-1),and the linear electron transport chain of PSⅡwas blocked.The fast and middle phases of the QA-reoxidation kinetics curve became significantly longer,inhibiting electron transfer between QA-and QB,impairing the receptor side of PSⅡ,and slowing down the binding rate between the vacancy site of QBand PQ.The results showed that Synechocystis PCC 6803 could tolerate less than 0.05 mg·L^(-1)Cd^(2+)stress and Cd^(2+)exhibited stimulant effects;high concentrations of Cd^(2+)cause growth inhibition by interfering with PSⅡ,affecting QA-and QBin the linear electron transport chain,and the main toxic sites of action of cadmium(receptor proteins)are not known.