2012 Fiscal Year Final Research Report
Development of a rapid startup technology applicable to autotrophic nitrogen removal
| Project/Area Number |
22710072
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Environmental technology/Environmental materials
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| Research Institution | Tokyo University of Agriculture and Technology |
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Principal Investigator |
TERADA Akihiko 東京農工大学, 大学院・工学研究院, 准教授 (30434327)
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| Project Period (FY) |
2010 – 2012
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| Keywords | 環境技術 / 微生物 / バイオフィルム / アナモックス / 微生物付着 |
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| Research Abstract |
Ammonia-oxidizing bacteria (AOB) and anaerobic ammonium-oxidizing (anammox) bacteria have slow growth rates due to their autotrophic nature, which is always an engineering challenge. In order to shorten the startup time of a process for completely autotrophic nitrogen removal, surface of a bacterial carrier was chemically modified to attract bacterial adhesion and biofilm formation. Since it has been reported that these bacterial biofilm formations are potentially mediated by quorum sensing (QS) mechanism as cell-cell communication, another objective of the study was to elucidate biofilm formation mechanisms of AOB and anammox bacteria. Radiation-induced graft polymerization (RIGP) was applied to chemically graft glycidyl methacrylate (GMA) on a non-woven sheet made of polyethylene. The epoxy-group of GMA was converted into diethylamine (DEA sheet) to form a positively-charged surface attractive to bacterial adhesion. The DEA sheet immobilized AOB rapidly, the rate of which was 104-fold as high as a pristine non-woven sheet. After 9 day of AOB incubation, ammonia oxidation rate of DEA sheet was higher than that of the pristine sheet by a factor of 4.4. The DEA sheet enhanced immobilization of anammox bacterial sludge, resulting in 2.4 times higher anammox rate than that on a pristine non-woven sheet.
An enzyme-immobilized sheet was fabricated to interrupt cell-cell communication among bacterial cells, which is a trigger to form biofilm. Acylase I, capable of degradingQS-mediated signaling compounds, i.e. N-acyl-L-homoserine lactones (AHLs), was immobilized onto a DEA sheet. AOB biofilm on this sheet was less robust and rather more sparse than that on a pristine non-woven sheet. This suggests that AOB biofilm without cell-cell communication was suppressed on the sheet because of breaking down AHLs in the biofilm. On the other hand, this trend was not observed regarding anammox biofilm. Another mechanism was involved to form the biofilm.
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