Cellular effects of epsilon toxin on the cell viability and oxidative stress of normal and lung cancer cells. (August 2022)

• Record Type: Journal Article
• Authors: Motafeghi, Farzaneh; Mortazavi, Parham; Mahdavi, Mobin; Shokrzadeh, Mohammad
• Is Part Of: Microbial pathogenesis. Volume 169(2022)
• Publication Date: 2022-08
• Subjects: Clostridium perfringens -- Epsilon toxin -- Lung cancer -- Cytotoxicity; Pathogenic microorganisms -- Periodicals; Pathology, Molecular -- Periodicals; Communicable Diseases -- microbiology -- Periodicals; Communicable Diseases -- parasitology -- Periodicals; Micro-organismes pathogènes -- Périodiques; Pathologie moléculaire -- Périodiques; Electronic journals; 616.9041
• DOI: 10.1016/j.micpath.2022.105649
• Languages: English
• ISSNs: 0882-4010

Abstract

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. Highlights: Etx is released from cells as inactive prototoxin (proEtx). proEtx activated by the removal of the N- and C-terminal peptides via digestive enzymes. Epsilon toxin disrupts the function of normal cell mitochondria and causes lipid membrane damage due to ROS production. Epsilon toxin decreases the growth rate of lung cancer cells by inducing mitochondrial damage and increasing Ros production. Results showed that epsilon toxin causes toxicity by binding to lipid membranes.