期刊
ENVIRONMENTAL SCIENCE & TECHNOLOGY
卷 43, 期 3, 页码 896-901出版社
AMER CHEMICAL SOC
DOI: 10.1021/es802246x
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资金
- Japan Society for Promotion Science
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.
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