6533b823fe1ef96bd127f7a1

RESEARCH PRODUCT

Mechanisms of beauvericin toxicity and antioxidant cellular defense

Ana Juan-garcíaMaría-josé RuizGuillermina FontBeatriz Mallebrera

subject

0301 basic medicineProgrammed cell deathCell SurvivalDNA damageApoptosisCHO CellsToxicologyAntioxidantsSuperoxide dismutase03 medical and health sciencesCricetulus0404 agricultural biotechnologyDepsipeptidesAnimalsViability assayCell ProliferationMembrane Potential MitochondrialbiologySuperoxide DismutaseCell growthChinese hamster ovary cell04 agricultural and veterinary sciencesGeneral MedicineCatalase040401 food scienceCell biology030104 developmental biologyBiochemistryApoptosisbiology.proteinIntracellularDNA Damage

description

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 24h 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.

yearjournalcountryeditionlanguage
2015-11-27Toxicology Letters
https://doi.org/10.1016/j.toxlet.2016.01.013