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UV-A 光增强没食子酸和没食子酸丙酯对大肠杆菌 O157:H7 的抗菌活性的作用机制。

On mechanism behind UV-A light enhanced antibacterial activity of gallic acid and propyl gallate against Escherichia coli O157:H7.

机构信息

Department of Nutrition and Food Science, University of Maryland, College Park, MD, 20742, USA.

Department of Food Science and Technology, University of California, Davis, CA, 95616, USA.

出版信息

Sci Rep. 2017 Aug 16;7(1):8325. doi: 10.1038/s41598-017-08449-1.

Abstract

Possible mechanisms behind the enhanced antimicrobial activity of gallic acid (GA) and its ester propyl gallate (PG) in the presence of UV-A light against Escherichia coli O157:H7 were investigated. GA by itself is a mild antimicrobial and has a pro-oxidant ability. We found that the presence of UV-A light increases the uptake of GA by the bacteria. Once GA is internalized, the interaction between GA and UV-A induces intracellular ROS formation, leading to oxidative damage. Concurrently, GA + UV-A also inhibits the activity of superoxide dismutase (SOD), magnifying the imbalance of redox status of E. coli O157:H7. In addition to ROS induced damage, UV-A light and GA also cause injury to the cell membrane of E. coli O157:H7. UV-A exposed PG caused oxidative damage to the cell and significantly higher damage to the cell membrane than GA + UV-A treatment, explaining its higher effectiveness than GA + UV-A treatment. The findings presented here may be useful in developing new antimicrobial sanitation technologies for food and pharmaceutical industries.

摘要

研究了在 UV-A 光存在下,没食子酸(GA)及其酯丙基没食子酸(PG)对大肠杆菌 O157:H7 的增强抗菌活性背后的可能机制。GA 本身是一种温和的抗菌剂,具有促氧化剂能力。我们发现,UV-A 光的存在增加了细菌对 GA 的摄取。一旦 GA 被内化,GA 与 UV-A 的相互作用会诱导细胞内 ROS 的形成,导致氧化损伤。同时,GA+UV-A 还抑制超氧化物歧化酶(SOD)的活性,放大了大肠杆菌 O157:H7 的氧化还原状态失衡。除了 ROS 诱导的损伤外,UV-A 光和 GA 还会对大肠杆菌 O157:H7 的细胞膜造成损伤。暴露在 UV-A 下的 PG 会对细胞造成氧化损伤,对细胞膜的损伤明显高于 GA+UV-A 处理,这解释了其比 GA+UV-A 处理更有效的原因。本研究结果可能有助于开发食品和制药工业的新型抗菌卫生技术。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2be2/5559599/0f65415202e2/41598_2017_8449_Fig1_HTML.jpg

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