碩士 / 國立成功大學 / 環境工程學系碩博士班 / 101 / The proliferation of cyanobacteria in drinking water sources is problematic for water authorities as they can interfere with water treatment processes. Chlorination as a commonly used oxidation process in water treatment has shown the potential to lyse cyanobacterial cells, resulting in release of toxic metabolites and odorants. Unfortunately, the netabolites are sometimes difficult to be removed in conventional water treatment processes.
Microcystis, a toxic genus of cyanobacteria often present in colonial forms under natural conditions is studied for the effect of chlorination on the cell integrity and metabolites release and degradation. In the oxidation experiments, the colonial Microcystis were sieved into three size groups and were oxidized in algae growth medium (ASM) and in the filtrated water from Cheng Kung Lake, NCKU.
A fluorescence technique, combining SYTOX Green nucleic acid stain with flow cytometer, was successfully developed for the determination of cell integrity for colonial Microcystis. A solid-phade microextraction (SPME) concentration followed by a gas chromatograph (GC) and mass spectrometric detector (MSD) was employed to measure an odorous metabolite, β-cyclocitral, while an enzyme-linked immunosorbent assay (ELISA) was used to detect a toxic metabolite, microcystins. A series of chlorination of Microcystis-laden water was conducted at different chlorine dosages for different colony sizes. During the experiments, residual chlorine concentration, cell integrity, and metabolites concentration were monitored at different time.
The results show that the bigger the colony is the slower the cell rupture kinetics was observed, meaning that the colonial Microcystis was more resistant to chlorine than single cells. A Delayed Chick Watson Model describe the experimental data very well for the kinetic of cell rupture. The lag time and rate constant of cell rupture increased and decreased with increasing colony size, respectively. It suggests that diffusion of chlorine into the intra-colonial cells and interaction between chlorine and extracellular polymeric substances (mucilage) may be the reason to retard the reaction. In the addition, experimental results obtained for those conducted in the two waters also confirmed that lag times and rate constants were also influenced by water matrix. For the toxic metabolite, chlorination may rupture the cells and cause the release of microcystins. The degradation of microcystins only ocuured when enough chlorine was dosed. The rate may be described by a second-order model, with a rate constant of 269-483 M-1s-1. For odorant, chlorine may inactivate β-carotene oxygenase and inhibit the production of β-cyclocitral. At short reaction time, low CT value of chlorine may stimulate the prodcution of β-cyclocitral by the cells. In addition, chlorine may also react with β-carotene directly to form β-cyclocitral, causing an increase of β-cyclocitral concentration later in the experimental time.
| Identifer | oai:union.ndltd.org:TW/101NCKU5515039 |
| Date | January 2013 |
| Creators | LaRao, 饒拉 |
| Contributors | Tsair-Fuh Lin, 林財富 |
| Source Sets | National Digital Library of Theses and Dissertations in Taiwan |
| Language | zh-TW |
| Detected Language | English |
| Type | 學位論文 ; thesis |
| Format | 118 |
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