在基于硫的脱化过程中,Cr(VI) 的抑制机制:生物毒性,生物电子特征和微生物进化
Qian Wang1, Chenggong Zhang1, Jinxin Song1
1School of Environmental Science and Engineering, Tianjin University, Tianjin 300350, China.
Journal of hazardous materials
|May 1, 2024
概括
六价 (Cr) 通过破坏微生物酶和破坏电子转移来抑制基于硫的脱. 生物膜提供部分保护,但高度的Cr (VI) 会导致氧化应激和细胞损伤,损害废水处理.
科学领域:
- 环境科学 环境科学
- 环境生物技术 环境生物技术
- 微生物生态学 微生物生态学
背景情况:
- 基于硫的脱 (SBD) 对于从低碳废水中去除至关重要.
- 有毒物质,如六价[Cr(VI) ],可以显著抑制SBD的效率.
- 了解Cr (VI) 毒性机制对于优化废水处理至关重要.
研究的目的:
- 阐明基于硫酸盐的脱化过程中Cr (VI) 的抑制机制.
- 研究Cr(VI) 对微生物生物毒性和生物电子特性的影响.
- 评估生物膜和微生物群落在Cr (VI) 耐药性中的作用.
主要方法:
- 在不同度的CrVI下量化了关键脱酶 (酸盐减少酶[NIR]和酸盐减少酶[NAR]) 的活性.
- 分析了细胞外聚合物物质 (EPS) 和细胞内吸收.
- 测量了活性氧物种 (ROS) 积累和细胞内电子转移组件 (黄氨酸二核酸,细胞染色体c).
- 以其脱和抗性能力为主要微生物属 (Thermomonas) 的特征.
主要成果:
- Cr(VI) 比NAR更显著地抑制了NIR活动,导致酸盐的积累.
- 生物膜通过通过增加的EPS拦截Cr(VI) 部分保护了微生物,但高Cr(VI) 水平导致细胞内入侵,ROS积累和氧化应激.
- 通过抑制硫酸乙烯氧化和减少酶的电子获取,破坏了电子转移,减少了flavin adenine dinucleotide和cytochrome c.
- 主导的Thermomonas属表现出对Cr (VI) 的耐药性,并在抗氧化应激和生物膜形成中发挥了作用.
结论:
- (VI) 通过直接的生物毒性,氧化应激和破坏微生物电子转移通路,损害了基于硫的脱.
- 生物膜的形成提供了一定的保护,但在较高的Cr (VI) 度下会被压倒.
- 了解这些机制对于开发能够处理Cr (VI) 污染的强大的废水处理系统至关重要.
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