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基于细菌细胞间通讯的磺胺类药物对发光菌发光的适应机制。

Hormetic mechanism of sulfonamides on Aliivibrio fischeri luminescence based on a bacterial cell-cell communication.

机构信息

State Key Laboratory of Pollution Control and Resource Reuse, College of Environmental Science and Engineering, Tongji University, Shanghai 200092, China.

State Key Laboratory of Pollution Control and Resource Reuse, College of Environmental Science and Engineering, Tongji University, Shanghai 200092, China; School of Environment, Jinan University, Guangzhou 510632, China.

出版信息

Chemosphere. 2019 Jan;215:793-799. doi: 10.1016/j.chemosphere.2018.10.045. Epub 2018 Oct 9.

DOI:10.1016/j.chemosphere.2018.10.045
PMID:30352376
Abstract

Hormesis is a biphasic dose-response model with low-dose stimulation and high-dose inhibition. The mechanism for hormesis remains inconclusive, although it is becoming a central concept in toxicology. In this paper, the hormetic mechanism of sulfachloropyridazine (SCP) on Aliivibrio fischeri (A. fischeri) luminescence was explored by investigating into the interference of SCP with the bacterial quorum sensing (QS) communications. It was revealed that the SCP-induced hormesis on luminescence was due to its action on LitR - a key protein that connects lux and ain QS communications in A. fischeri. It was suggested SCP acted on LitR proteins to change its active forms, which subsequently induced hormetic effects on luxR (QS signal receptor) and thereby the luminescence. It is the first time that the hormetic mechanism based on bacterial QS was proposed, which provides a novel insight into the essence of the hormesis on A. fischeri luminescence.

摘要

胁迫是一种双相剂量反应模型,具有低剂量刺激和高剂量抑制作用。尽管胁迫作用机制尚不清楚,但它已成为毒理学的一个核心概念。本文通过研究磺胺氯哒嗪(SCP)对费氏弧菌(A. fischeri)发光的群体感应(QS)通讯的干扰,探讨了 SCP 对发光的胁迫作用机制。结果表明,SCP 对发光的诱导胁迫作用是由于其对 LitR 的作用,LitR 是连接 lux 和 ain QS 通讯的关键蛋白。结果表明,SCP 作用于 LitR 蛋白改变其活性形式,进而对 luxR(QS 信号受体)产生胁迫效应,从而导致发光。这是首次提出基于细菌 QS 的胁迫作用机制,为费氏弧菌发光的胁迫作用本质提供了新的认识。

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