Mechanisms of beauvericin toxicity and antioxidant cellular defense

• BEA produces cytotoxic effects in CHO-K1 cells.
• BEA alters mitochondrial membrane potential in CHO-K1 cells.
• BEA produces DNA strand breakage in CHO-K1 cells.
• At 24 h, BEA exposure arrests G0/G1 phase of cell cycle and produces apoptosis.
• Enzymatic defense (SOD and CAT) increases in CHO-K1 cells exposed to BEA.

Beauvericin (BEA) is a secondary metabolite produced by many species of fungus Fusarium. This study determines the injury (cell viability, cell proliferation, mitochondrial membrane potential, cell death and DNA damage) and the intracellular defense mechanisms (catalase and superoxide dismutase) in Chinese Hamster ovary (CHO-K1) cells after BEA exposure. The results obtained in this study demonstrated that BEA induces cytotoxicity in a dose- and time-dependent manner in CHO-K1 cells. Moreover, disruption in mitochondrial enzymatic activity and cell proliferation has been observed after BEA exposure, which can lead or be consequence of cell death. BEA inhibits cell proliferation by arresting cells in G0/G1 and increasing apoptosis. Moreover, at higher exposure times, BEA induces differentiation of CHO-K1 cells through G2/M arrest, preventing that cells entry into mitosis. DNA strand breaks were observed at 1 μM after 24 h of exposure. On the other hand, the SOD and CAT activities were increased after BEA exposure and as a defense system they could contribute to eliminate damage produced by BEA and oxidants products generated in CHO-K1 cells.