Dai Zechuan, Meng Lingyun, Wang Sai, Li Jiao, Mao Xiangzhao
State Key Laboratory of Marine Food Processing and Safety Control, College of Food Science and Engineering, Ocean University of China, Qingdao 266404, PR China; Qingdao Key Laboratory of Food Biotechnology, Qingdao 266404, PR China; Key Laboratory of Biological Processing of Aquatic Products, China National Light Industry, Qingdao 266404, PR China.
State Key Laboratory of Marine Food Processing and Safety Control, College of Food Science and Engineering, Ocean University of China, Qingdao 266404, PR China; Qingdao Key Laboratory of Food Biotechnology, Qingdao 266404, PR China; Key Laboratory of Biological Processing of Aquatic Products, China National Light Industry, Qingdao 266404, PR China.
Ultrason Sonochem. 2025 Jan;112:107171. doi: 10.1016/j.ultsonch.2024.107171. Epub 2024 Nov 24.
Although there have been many studies on the efficacy of ultrasonic inactivation, the stress resistance mechanism of bacteria is still a challenge for complete ultrasonic inactivation. In this study, the dominant spoilage bacteria in crayfish, Shewanella baltica (S. baltica) and Aeromonas veronii (A. veronii), were subjected to high-intensity ultrasonic treatment. The results showed compromised cell membrane, decreased membrane fluidity, hyperpolarized membrane potential, and disrupted succinate-coenzyme Q reductase. Transmission electron microscopy revealed significant fragmentation of S. baltica, whereas A. veronii, with its thick cell wall and outer capsule membrane, demonstrated enhanced resistance to ultrasound. Real-time quantitative PCR indicated that in response to ultrasonic stress, bacteria initiated a stress response mechanism by increasing the expression of mechanosensitive channels; meanwhile, the outer capsule of A. veronii delayed the transformation of ultrasonic external forces into cell membrane stress. The study found that in response to ultrasonic stress, bacteria initiated a stress response mechanism by increasing the expression of mechanosensitive channels as "emergency valve" in short time but could not prevent the process of membrane destruction with prolonged exposure. This finding provided a basis for addressing bacterial stress tolerance in ultrasonic inactivation.
尽管已经有许多关于超声灭活效果的研究,但细菌的抗逆机制仍是实现完全超声灭活的一个挑战。在本研究中,对小龙虾中的优势腐败菌波罗的海希瓦氏菌(S. baltica)和维氏气单胞菌(A. veronii)进行了高强度超声处理。结果显示细胞膜受损、膜流动性降低、膜电位超极化以及琥珀酸 - 辅酶Q还原酶被破坏。透射电子显微镜显示波罗的海希瓦氏菌出现明显破碎,而具有厚细胞壁和外荚膜的维氏气单胞菌对超声表现出更强的抗性。实时定量PCR表明,响应超声应激,细菌通过增加机械敏感通道的表达启动应激反应机制;同时,维氏气单胞菌的外荚膜延缓了超声外力向细胞膜应激的转化。研究发现,响应超声应激时,细菌在短时间内通过增加机械敏感通道的表达启动应激反应机制作为“应急阀门”,但随着暴露时间延长并不能阻止膜破坏的过程。这一发现为解决超声灭活中细菌的应激耐受性提供了依据。