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RESEARCH PRODUCT

In vitro mechanisms of Beauvericin toxicity: A review.

Beatriz MallebreraGuillermina FontA. ProsperiniMaría José Ruiz

subject

0301 basic medicineAntioxidantmedicine.medical_treatmentApoptosisToxicologymedicine.disease_cause03 medical and health scienceschemistry.chemical_compound0404 agricultural biotechnologyFusariumDepsipeptidesmedicineAnimalsHumansCytotoxicityMycotoxin04 agricultural and veterinary sciencesGeneral MedicineMycotoxins040401 food scienceBeauvericinOxidative Stress030104 developmental biologychemistryBiochemistryToxicityDNA fragmentationMicronucleusOxidative stressFood ScienceDNA Damage

description

Beauvericin (BEA) is a mycotoxin produced by many species of fungus Fusarium and by Beauveria bassiana; BEA is a natural contaminant of cereals and cereals based products and possesses a wide variety of biological properties. The mechanism of action seems to be related to its ionophoric activity, that increases ion permeability in biological membranes. As a consequence, BEA causes cytotoxicity in several cell lines and is capable to produce oxidative stress at molecular level. Moreover, BEA is genotoxic (produces DNA fragmentation, chromosomal aberrations and micronucleus) and causes apoptosis with the involvement of mitochondrial pathway. However, several antioxidant mechanisms protect cells against oxidative stress produced by BEA. Despite its strong cytotoxicity, no risk assessment have been still carried out by authorities due to a lack of toxicity data, so research on BEA toxicological impact is still going on. This review reports information available regarding BEA mechanistic toxicology with the aim of updating information regarding last researches on this mycotoxin.

10.1016/j.fct.2017.11.019https://pubmed.ncbi.nlm.nih.gov/29154952