首页|乳酸钠共代谢对铜绿假单胞菌NY3降解四溴双酚A的促进机理

乳酸钠共代谢对铜绿假单胞菌NY3降解四溴双酚A的促进机理

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通过乳酸钠共代谢提高铜绿假单胞菌NY3对TBBPA的降解速率,并对其促进机理进行研究。结果表明,以无共代谢碳源体系为对照,乳酸钠共代谢对TBBPA降解率在48h的促进最为显著,约提高了 74%。乳酸钠共代谢体系的TBBPA降解活性物分布于胞内和胞外。与无共代谢碳源相比,乳酸钠共代谢不仅能提高铜绿假单胞菌NY3的生物量,还可提高其胞外液中过氧化氢、超氧负离子自由基和羟基自由基等活性氧水平。其中,胞外液中活性氧水平提高主要与NY3菌分泌到胞外的吩嗪类和喹诺酮类小分子分泌物相关。因此,乳酸钠共代谢通过胞内和胞外两方面对铜绿假单胞菌NY3降解TBBPA进行促进。
The promoting mechanism of sodium lactate co-metabolism on the degradation of tetrabromobisphenol A by Pseudomonas aeruginosa NY3
Degradation of TBBPA by Pseudomonas aeruginosa NY3 was improved through the co-metabolism of sodium lactate,and its promoting mechanism was studied.The results showed that,when the non co-metabolic carbon source system was as the control,degradation efficiency of TBBPA in the system with sodium lactate as co-metabolic carbon source was improved significantly at 48h,with an increase of approximately 74%.Further study revealed that,the TBBPA degrading active substances in the sodium lactate co-metabolism system are distributed both intracellular and extracellular.Compared to that without co-metabolic carbon source,the biomass of Pseudomonas aeruginosa NY3,as well as the level of reactive oxygen species,such as hydrogen peroxide,superoxide anion radical and hydroxyl radical in its extracellular fluid,were increased by the co-metabolism of sodium lactate.The increase in reactive oxygen species levels in extracellular fluid mainly related to the secretion of small molecule secretions such as phenazines and quinolones by Pseudomonas aeruginosa NY3.In summary,sodium lactate co-metabolism promotes the degradation of TBBPA by Pseudomonas aeruginosa NY3 through both intracellular and extracellular pathways.

tetrabromobisphenol Abiodegradationsodium lactateco-metabolismreactive oxygen species

张琪、聂红云、郭镝妮、陈丽娇、聂麦茜、王磊、王蕾

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西安建筑科技大学环境与市政工程学院,陕西西安 710055

膜分离重点研究室,陕西西安 710055

陕西省环境监测中心站,陕西西安 710054

四溴双酚A 生物降解 乳酸钠 共代谢 活性氧

国家重点研发计划合作单位项目西安市碑林区应用技术研发项目陕西省自然科学基础研究计划

2022YFC2904305-02GX22212021JM-425

2024

中国环境科学
中国环境科学学会

中国环境科学

CSTPCDCHSSCD北大核心
影响因子:2.174
ISSN:1000-6923
年,卷(期):2024.44(2)
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