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ε 型毒素对正常细胞和肺癌细胞活力及氧化应激的细胞效应。

Cellular effects of epsilon toxin on the cell viability and oxidative stress of normal and lung cancer cells.

机构信息

Department of Pharmacology and Toxicology, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran.

Student Research Committee, Faculty of Pharmacy, Mazandaran University of Medical Sciences, Sari, Iran.

出版信息

Microb Pathog. 2022 Aug;169:105649. doi: 10.1016/j.micpath.2022.105649. Epub 2022 Jun 20.

DOI:10.1016/j.micpath.2022.105649
PMID:35738467
Abstract

INTRODUCTION

Clostridium perfringens is a type of gram-positive anaerobic bacilli. C.perfringens produces many toxins, of which epsilon (ε) is one of the major ones. The mechanism of epsilon's toxicity is located in the lipid of cell membrane tissues. Epsilon toxin is known as a bioterrorism agent. Inhalation of these aerosols can destroy pulmonary vascular endothelial cells and cause lung injury, which increases vascular permeability and pulmonary edema.

METHODS

In this study, we investigated the toxicity of epsilon toxin by using the MTT assay, evaluated oxidative stress effects such as ROS and LPO using the DCFH and TBA reagents, and measured the GSH of the normal and lung cancer cells by using the DTNB reagent.

RESULTS

The result showed that 1 μg/ml of epsilon toxin caused mitochondrial disorder and reduced the growth of the normal cell line. This toxin also induced ROS and damage to lipid membranes. Furthermore, the same effect occurred in the lung cancer cell, and the epsilon toxin inhibited cancer cell proliferation.

CONCLUSION

This toxin causes toxicity by binding to lipid membranes. As the present study results have confirmed, epsilon toxin inhibits mitochondrial function and induces ROS and lipid membrane damage.

摘要

简介

产气荚膜梭菌是一种革兰氏阳性厌氧杆菌。C. perfringens 产生许多毒素,其中 ε 是主要毒素之一。ε 毒素的毒性机制位于细胞膜组织的脂质中。ε 毒素被认为是一种生物恐怖主义剂。吸入这些气溶胶会破坏肺血管内皮细胞并导致肺损伤,增加血管通透性和肺水肿。

方法

在这项研究中,我们使用 MTT 测定法研究了 ε 毒素的毒性,使用 DCFH 和 TBA 试剂评估了 ROS 和 LPO 等氧化应激效应,并使用 DTNB 试剂测量了正常和肺癌细胞中的 GSH。

结果

结果表明,1μg/ml 的 ε 毒素引起线粒体紊乱并降低正常细胞系的生长。这种毒素还诱导了 ROS 和脂质膜的损伤。此外,在肺癌细胞中也发生了同样的作用,ε 毒素抑制了癌细胞的增殖。

结论

这种毒素通过与脂质膜结合而产生毒性。正如本研究结果所证实的那样,ε 毒素抑制线粒体功能并诱导 ROS 和脂质膜损伤。

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