Kinetics of Microcystis aeruginosa Growth and Intracellular Microcystins Release after UV Irradiation
Kinetics of Microcystis aeruginosa Growth and Intracellular Microcystins Release after UV Irradiation
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DOI：
10.1021/es802246x
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发表时间：
2009-02-01
影响因子：
11.4
通讯作者：
Ohgaki, Shinichiro
中科院分区：
文献类型：
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作者：
Sakai, Hiroshi;Katayama, Hiroyuki;Ohgaki, Shinichiro
研究了紫外线（UV）照射后细胞内微囊藻毒素的释放并建立了模型。实验结果表明，抑制铜绿微囊藻生长需要90 mJ cm（-2）的紫外线能量密度。细胞内微囊藻毒素的释放也被抑制在较高的紫外线能量密度;微囊藻毒素在水中的浓度并没有增加在紫外线照射的样品在控制。基于以下假设，建立了一个模型来描述M.铜绿假单胞菌细胞数和微囊藻毒素浓度。M.铜绿假单胞菌细胞，仅在细胞死亡时释放。两种类型的M紫外线照射后，铜绿假单胞菌细胞存活，非生长期细胞受紫外线损伤，生长期细胞未受紫外线损伤。为了计算模型参数，在添加0.3 mg L-1细胞壁合成抑制剂头孢菌素后，分别计数这两种细胞类型。只有生长中的细胞才会受到头孢菌素的影响。模型对观测数据的解释较好，表明模型结构合理。微囊藻毒素的释放模型包括非生长和生长细胞的释放。后者下降为M。铜绿假单胞菌的生长受到紫外线的抑制。从nongrowing细胞的释放被延迟，防止快速释放的微囊藻毒素，这可以解释由一个较大的反应顺序的nongrowing细胞的衰变。在600和1800 mJ cm（-2）时，细胞内毒素被紫外光降解，导致细胞内毒素释放减少。
The release of intracellular microcystins following ultraviolet (UV) irradiation was studied and modeled. Experimental results indicated that 90 mJ cm(-2) of UV fluence were required to inhibit Microcystis aeruginosa growth. The release of intracellular microcystins was also suppressed at higher UV fluence; microcystins concentrations in water did not increase as much in UV-irradiated samples as in controls. A model, based on the following assumptions, was developed to describe the profiles of M. aeruginosa cell number and microcystins concentration in water. Microcystins were contained in M. aeruginosa cells and released only upon cell death. Two types of M. aeruginosa cells existed after UV irradiation; nongrowing cells damaged by UV and growing cells undamaged by UV. To calculate model parameters, these two cell types were counted separately following the addition 0.3 mg L-1 of cephalosporin, a cell wall synthesis inhibitor. Only growing cells are affected by cephalosporin. The model explained the observed data well, suggesting that the model structure was reasonable. The microcystins release model included release from nongrowing and growing cells. The latter declined as M. aeruginosa growth was inhibited by UV. Release from nongrowing cells was delayed, preventing rapid release of microcystins, which could be explained by a larger reaction order of the decay of nongrowing cells. At 600 and 1800 mJ cm(-2) UV fluence intracellular microcystins were decomposed by UV, which led to reduced intracellular microcystins release after UV irradiation.