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Bacterial toxins, such as Epsilon toxin (Etx) from  Clostridium perfringens , represent a promising, albeit underexplored, avenue for anticancer agent development. This study was therefore designed to systematically investigate the cytotoxic mechanisms of Etx on the human colon cancer cell lines HT-29 and Caco-2. The primary focus was on the toxin’s capacity to induce oxidative stress and pro-inflammatory responses, two key pathways in cancer pathology. Key parameters evaluated included cytotoxicity, ROS generation, lipid peroxidation, LDH release, and inflammatory cytokines (TNF-α and IL-6). The results demonstrated that treatment with Etx significantly inhibited the proliferation of both cell lines in a concentration-dependent manner, reducing cell viability by approximately 60% at the highest concentration. This cytotoxic effect was linked to a substantial increase in intracellular ROS and lipid peroxidation, confirming the induction of severe oxidative damage. Concurrently, Etx compromised cell membrane integrity, as evidenced by a marked increase in LDH release. Furthermore, the toxin fostered a potent pro-inflammatory environment by upregulating key cytokines. These findings collectively demonstrate that Etx exerts its potent cytotoxicity on colon cancer cells by concurrently triggering oxidative stress and a robust inflammatory cascade. This dual-mechanism of action highlights the potential of Etx as a novel therapeutic candidate, warranting further investigation into targeted delivery systems to translate its efficacy into clinical applications.

toxicology research

Cytotoxic effects of epsilon toxin from  Clostridium perfringens  on colon cancer cell lines (HT-29) and (Caco2) in terms of oxidative stress and inflammatory cytokines