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用氯、高锰酸盐、臭氧、过氧化氢和羟基自由基氧化蓝藻神经毒素β-N-甲基氨基-L-丙氨酸(BMAA)。

Oxidation of cyanobacterial neurotoxin beta-N-methylamino-L-alanine (BMAA) with chlorine, permanganate, ozone, hydrogen peroxide and hydroxyl radical.

机构信息

Department of Environmental Engineering and Global Water Quality Research Center, National Cheng Kung University, Tainan City, 70101, Taiwan.

Department of Environmental Engineering and Global Water Quality Research Center, National Cheng Kung University, Tainan City, 70101, Taiwan.

出版信息

Water Res. 2018 Oct 1;142:187-195. doi: 10.1016/j.watres.2018.05.056. Epub 2018 May 31.

DOI:10.1016/j.watres.2018.05.056
PMID:29879656
Abstract

Beta-N-methylamino-L-alanine (BMAA), a new cyanobacterial neurotoxin produced by more than 20 genera of cyanobacteria, has been associated with amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC) or Alzheimer's disease. Although BMAA has been shown to be removed in drinking water treatment plants (DWTPs), studies regarding the reactions between BMAA and the commonly used oxidants in DWTPs are limited to chlorine under specific conditions. In this study, the reaction kinetics between BMAA and five oxidants commonly used in DWTPs, including chlorine, potassium permanganate, ozone, hydrogen peroxide and hydroxyl radical were investigated. The oxidation of BMAA by chlorine, ozone or OH radical followed the second order reaction rate law, and the reaction rate was in the order of OH radicals > ozone >> chlorine. The rate constants increased by 20 times from 2 × 10 Ms at pH 5.8 to 4.93 × 10 Ms at pH 7, and kept in a relatively stable level at pH 7-9.5; rate constants of OH radicals were 1.11 × 10 Ms at pH 6.5 and 5.51 × 10- 1.35 × 10 Ms at pH > 6.5. For both permanganate and HO only, the removal of BMAA was negligible. The pH dependency of chlorine and the OH radical may be attributed to the neutral form of BMAA with free lone pair electrons readily to be attacked by oxidants. However, for ozonation of BMAA, the rate constants were 1.88 × 10-3.72 × 10 Ms, with a linear dependency on pH, implying that the hydroxide concentration governs the reaction. In addition, the rate of BMAA degradation was found to be slower in natural water if compared with that in deionized water.

摘要

β-N-甲基氨基-L-丙氨酸(BMAA)是一种新的蓝藻神经毒素,由 20 多种蓝藻属产生,与肌萎缩侧索硬化症/帕金森病-痴呆症复合征(ALS/PDC)或阿尔茨海默病有关。虽然 BMAA 已被证明可在饮用水处理厂(DWTP)中去除,但关于 BMAA 与 DWTP 中常用氧化剂之间的反应的研究仅限于在特定条件下的氯。在这项研究中,研究了 BMAA 与 DWTP 中常用的五种氧化剂(包括氯、高锰酸钾、臭氧、过氧化氢和羟基自由基)之间的反应动力学。氯、臭氧或 OH 自由基氧化 BMAA 遵循二级反应速率定律,反应速率顺序为 OH 自由基>臭氧>氯。在 pH 值为 5.8 时,速率常数为 2×10 M s,在 pH 值为 7 时增加到 4.93×10 M s,在 pH 值为 7-9.5 时保持相对稳定水平;在 pH 值为 6.5 时,OH 自由基的速率常数为 1.11×10 M s,在 pH 值大于 6.5 时为 5.51×10-1.35×10 M s。对于高锰酸盐和 HO 自由基,BMAA 的去除可以忽略不计。氯和 OH 自由基的 pH 依赖性可能归因于带自由孤对电子的 BMAA 的中性形式,容易受到氧化剂的攻击。然而,对于臭氧氧化 BMAA,速率常数为 1.88×10-3.72×10 M s,与 pH 值呈线性关系,这意味着氢氧化物浓度控制着反应。此外,如果与去离子水相比,在天然水中 BMAA 的降解速度较慢。

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