Insight into the surface discharge cold plasma efficient inactivation of Pseudomonas fluorescens in water based on exogenous reactive oxygen and nitrogen species: Synergistic mechanism and energy benefits
文献类型: 外文期刊
第一作者: Ni, Jia-Bao
作者: Ni, Jia-Bao;Zhang, Jing-Shou;Xiao, Hong-Wei;Ni, Jia-Bao;Fang, Xiao-Ming;Ding, Chang-Jiang
作者机构:
关键词: Surface discharge cold plasma; Inactivation; Pseudomonas fluorescens; Energy efficiency; Genes
期刊名称:JOURNAL OF HAZARDOUS MATERIALS ( 影响因子:12.2; 五年影响因子:11.9 )
ISSN: 0304-3894
年卷期: 2024 年 476 卷
页码:
收录情况: SCI
摘要: As well known, surface discharge cold plasma has efficient inactivation ability and a variety of RONS are main active particles for inactivation, but their synergistic mechanism is still not clear. Therefore, surface discharge cold plasma system was applied to treat Pseudomonas fluorescens to study bacterial inactivation mechanism and energy benefit. Results showed that energy efficiency was directly proportional to applied voltage and inversely proportional to initial concentration. Cold plasma treatment for 20 min was inactivated by approximately > 4-log(10) Pseudomonas fluorescens and application of center dot OH and O-1(2) scavengers significantly improved survival rate. In addition, center dot OH and O-1(2) destroyed cell membrane structure and membrane permeability, which promoted diffusion of RONS into cells and affecting energy metabolism and antioxidant capacity, leading to bacterial inactivation. Furthermore, accumulation of intracellular NO and ONOOH was related to infiltration of exogenous RNS, while accumulation of center dot OH, H2O2, O-1(2), O-2(-) was the result of joint action of endogenous and exogenous ROS. Transcriptome analysis revealed that different RONS of cold plasma were responsible for Pseudomonas fluorescens inactivation and related to activation of intracellular antioxidant defense system and regulation of genes expression related to amino acid metabolism and energy metabolism, which promoting cellular process, catalytic activity and other biochemical pathways.
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