In vitro mechanisms of Beauvericin toxicity: A review.

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.

Antioxidant capacity of trans-resveratrol dietary supplements alone or combined with the mycotoxin beauvericin.

Trans-resveratrol (trans-RSV) is a polyphenol with multiples biological properties, such as anti-inflammatory, antioxidant, anti-aging, anti-diabetic, and antiplatelet. It occurs naturally in grapes and derivate, peanuts and berries. Beauvericin (BEA) is a mycotoxin present in cereals that produces cytotoxicity, intracellular reactive oxygen species and lipid peroxidation. The general objective of this research was to evaluate whether trans-RSV could be used as a good polyphenol against damages produced by BEA. Because trans-RSV can be ingested through dietary supplements, to reach this goal, the following specific objectives were proposed: to determine a) the trans-RSV content in different polyphenol dietary supplements by capillary electrophoresis, b) the antioxidant capacity of the trans-RSV in polyphenol supplements, and c) the influence of BEA in the antioxidant capacity of trans-RSV when they are in combination by photochemioluminiscence assay. The results obtained in this study showed that all polyphenol dietary supplements present higher RSV content that the content of the label. The polyphenol supplements present antioxidant capacity. And the combination of trans-RSV and BEA did not affect the antioxidant capacity of trans-RSV. Thus, RSV could contribute to decrease oxidant effects produced by BEA.

Cytotoxic effects induced by patulin, sterigmatocystin and beauvericin on CHO-K1 cells.

Mycotoxins are produced by different genera of fungi; mainly Aspergillus, Penicillium and Fusarium. The natural co-occurrence of beauvericin (BEA), patulin (PAT) and sterigmatocystin (STE) has been proved in feed and food commodities. This study investigates the cytotoxicity of individual and combined mycotoxins BEA, PAT and STE. The cytotoxicity on immortalized ovarian cells (CHO-K1) was evaluated using the MTT assay. After 24, 48 and 72 h, the IC50 values were 2.9 µM for PAT and ranged from 10.7 to 2.2 µM and from 25.0 to 12.5 µM for BEA and STE, respectively. Cytotoxic interactions were assayed by the isobologram method, which provides a combination index (CI) value as a quantitative measure of the three mycotoxin interaction's degree. Binary and tertiary combinations showed a dose dependent effect. At low fraction affected, mycotoxin combinations were synergetic; whereas, at higher fraction affected, the combinations showed additive effect. Our results indicate that the co-occurrence of low concentrations of mycotoxin in food may increase their toxic effects.

Mechanisms of beauvericin toxicity and antioxidant cellular defense.

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.