Beauvericin Research Articles

Occurrence of Toxic Hexadepsipeptides in Preharvest Maize Ear Rot Infected by Fusarium poae in Poland

AbstractTwenty‐seven preharvest maize ears affected by Fusarium poae rot (disease score 36–100%) were selected in 1998 and 1999 in Poland and examined for the occurrence of toxic hexadepsipeptides: beauvericin (BEA), enniatin A, enniatin B and enniatin B1. The identification of F. poae was confirmed by sequence analysis of variable internal transcribed spacer regions and compared with NCBI gene bank DNA sequences. Chemical analyses were performed by HPLC‐MS. In 27 ears infected by F. poae were detected: BEA (trace to 46 μg/g) in 18 samples, enniatin A (trace to 37 μg/g) in nine samples, enniatin B (trace to 47 μg/g) in 15 samples and enniatin B1 (trace to 25 μg/g) in 12 samples. When 20 strains of F. poae isolated from these samples were cultured on rice, all produced BEA (1.9–75 μg/g), three enniatin A (1.8–2 μg/g), 12 enniatin B (1.1–5.1 μg/g) and eight enniatin B1 (1.2–5.2 μg/g). Occurrence and quantification of enniatin A, enniatin B and enniatin B1 and their co‐occurrence with BEA in maize kernels is reported for the first time.

Involvement of Bcl-2 family, cytochrome c and caspase 3 in induction of apoptosis by beauvericin in human non-small cell lung cancer cells

Beauvericin (BEA), a cyclic hexadepsipeptide from Codyceps cicadae, possesses anti-convulsion, anti-arrhythmia, sedation, and anti-tumor activities. It has been reported that BEA induces apoptosis in several cancer cell lines. However, the molecular mechanism underlying the BEA-induced apoptotic process is not yet clearly understood. In the present study, the intracellular signaling pathways of BEA-induced apoptosis in human non-small cell lung cancer (NSCLC) A549 cells were investigated using morphological analysis and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) technique. In this study, BEA-induced apoptosis in human NSCLC A549 cells demonstrated a BEA concentration- and treatment time-dependent manner. This BEA-induced apoptosis in human NSCLC A549 cells was also accompanied by the up-regulation of Bax, Bak, and p-Bad and down-regulation of p-Bcl-2, but no effect on the levels of Bcl-X L or Bad proteins. Moreover, the BEA treatment resulted in a significant reduction of mitochondrial membrane potential, increase in the release of mitochondrial cytochrome c (cyt c), and activation of caspase 3. Furthermore, treatment with caspase 3 inhibitor (z-DEVD-fmk) was capable to prevent the BEA-induced caspase 3 activity and cell death. These results clearly demonstrate that the induction of apoptosis by BEA involves multiple cellular/molecular pathways and strongly suggest that pro- and anti-apoptotic Bcl-2 family proteins, mitochondrial membrane potential, mitochondrial cyt c, and caspase 3, they all participate in BEA-induced apoptotic process in human NSCLC A549 cells.

Beauvericin induces cytotoxic effects in human acute lymphoblastic leukemia cells through cytochrome c release, caspase 3 activation: the causative role of calcium

Beauvericin (BEA), a cyclic hexadepsipeptide, induces cell death in human leukemia cells (CCRF-CEM) and the process of BEA-induced cell death has been speculated to undergo an apoptotic pathway. In the present study, several well-characterized factors, known to play important roles in apoptotic pathway, were investigated in BEA-induced CCRF-CEM cell death. CCRF-CEM cells were treated with BEA at concentrations from 1 to 10 μM for up to 24 h. The incidence of nuclear fragmentation and apoptotic body formation in the cells, cytosolic caspase-3 activity, mitochondrial membrane potential, and release of cytochrome c (Cyt c) from mitochondria in BEA-treated cells were determined and compared with that in untreated cells. Moreover, to investigate the role of intracellular Ca ++ in this cell death process, CCRF-CEM cells were primed with 3 μM of BAPTA/AM, a Ca ++ chelator, to exclude intracellular Ca ++ prior to the BEA treatment. The data revealed that BEA-induced cell death in CCRF-CEM cells exhibited a dose- and time-dependent manner. The incidence of nuclear fragmentation and apoptotic body formation was significantly increased in CCRF-CEM cells treated with BEA at concentrations of 1 μM or greater. Increase of cytosolic caspase-3 activity was also observed in BEA-treated cells with a dose-dependent manner. In addition, increased release of Cyt c from mitochondria was also observed in the cells treated with 10 μM BEA in a time-dependent pattern. The BAPTA/AM pretreatment partially blocked BEA-induced cell death in CCRF-CEM cells, indicating that intracellular Ca ++ plays an important role, maybe as a mediator in cell death signaling, in this cell death pathway. The results support the notion that BEA-induced cell death in CCRF-CEM cells likely undergo through an apoptotic pathway on the basis of increase of release of Cyt c from mitochondria, increase of caspase-3 activity, and some observed typical apoptotic cellular changes in morphology.

Diversity in metabolite production by Fusarium langsethiae, Fusarium poae, and Fusarium sporotrichioides

The production of mycotoxins and other metabolites by 109 strains of Fusarium langsethiae, Fusarium poae, Fusarium sporotrichioides, and F. kyushuense was investigated independently in four laboratories by liquid or gas chromatography analyses of cultural extracts with UV diode array, electron capture, or mass spectrometric detection systems. From the compiled results, it was found that F. langsethiae consistently produced the trichothecenes diacetoxyscirpenol (DAS), T-2 toxin (T-2), HT-2 toxin (HT-2), and neosolaniol (NEO) and, to a lesser extent, some additional trichothecene derivatives. F. langsethiae also produced culmorins, chrysogine (CHRYS), aurofusarin (AUF), and enniatin (EN). F. sporotrichioides showed a metabolite profile similar to that of F. langsethiae, while F. poae had a different profile as 41 of 49 strains produced nivalenol (NIV) and other 8-keto trichothecenes, in addition to DAS and derivatives of this metabolite. Only a trace amount of NIV was detected from one strain of F. kyushuense. In summary, all the three core taxa of this joint study were found to produce trichothecenes. Fusarin C (F-C) was not detected from F. langsethiae, but it was produced by F. poae and F. sporotrichioides. Aurofusarin was only detected from a few strains of F. langsethiae, while nearly all strains of F. poae and F. sporotrichioides produced this compound. In contrast, chrysogine was not detected from F. poae, but was produced by the other two taxa. Production of enniatins was scattered among the three main taxa of this study, whereas beauvericin (BEA) was produced by many strains of F. poae and F. sporotrichioides. Only one odd strain of F. langsethiae (IBT 9959) produced beauvericin. However, the status of this strain is uncertain. By a polyphasic approach using species-specific metabolite profiles, the fruity odour of F. poae, and morphological observations, it was concluded that F. langsethiae, F. poae, and F. sporotrichioides should be regarded as three significant taxa at a species level.

Supercritical fluid extraction of Beauvericin from maize

Beauvericin (BEA), a supercritical fluid extraction with supercritical carbon dioxide from maize was investigated. Extraction efficiencies under several different extraction conditions were examined. Pressure, temperature, extraction time, organic modifier and water matrix content (10%) were investigated. The best extraction conditions were at a temperature of 60 °C, 3200 psi, for 30 min static extraction time and methanol as modifier solvent. Extraction recovery of 36% without modifier by adding water to the matrix in the extraction vessel (reproducibility relative standard deviations (R.S.D.)=3–5%) were recorded. Extraction recovery of 76.9% with methanol as co-solvent (reproducibility R.S.D.=3–5%) was obtained. Data shows that SFE gives a lower BEA recovery compared to conventional extraction protocol with organic solvents while SFE with modifier and conventional extraction yields are comparable. BEA extract contents were determined by high pressure liquid chromatography (HPLC) with a diode array detector (DAD) at 205 nm and BEA peak confirmed by LC-MS. Acetonitrile–water as mobile phase and column C-18 were both tested. Instrumental and analytical parameters were optimized in the range linear interval from 1 to 500 mg kg −1 and reached a detection limit of 2 ng.

Einfluss von Fusarientoxinen auf die Mast- und Schlachtleistung von Broilern und Puten

In two broiler and two turkey trials the influence of Fusarium toxins in maize on growth and slaughter performance, on residues of toxins in carcass and litters and blood parameters were investigated. In one broiler and turkey trial with naturally contaminated maize the main contaminants were deoxynivalenol (DON), moniliformin (MON and beauvericin (BEA). In one further broiler and turkey trial with inoculated maize (Fusarium subglutinans) the main contaminants were MON and BEA. The level of contamination of mycotoxins in the diets was free, low, medium and high. For every broiler trial 180 and for the turkey trials 60 and 100 one day old chicken were used. The result of these investigations shows that broiler and turkeys are not very sensitive to Fusarium toxins. Growth and slaughter performance and also blood parameters were not negative influenced by higher mycotoxin dosages in the diets.

Apoptosis of murine cultured biliary epithelial cells induced by glycochenodeoxycholic acid involves Fas receptor and its ligand

Fas-mediated apoptosis of biliary epithelial cells (BECs) is suggested as a main effector process in immune-mediated biliary diseases. Glycochenodeoxycholic acid (GCDCA), a conjugated hydrophobic bile acid, is known to cause apoptosis of hepatocytes via the direct activation of Fas receptor (FasR). In this study, we investigated the apoptotic effect of GCDCA on cultured murine intrahepatic BECs. It was found that GCDCA induced apoptosis of BECs derived from BALB/c mice in a dose- and incubation time-dependent manner. The morphology and TUNEL positivity for the apoptotic process induced by GCDCA were similar to those induced by beauvericin (BV) which is known to cause apoptosis by a direct activation of caspase-3, a member of the caspase family, at its downstream. The GCDCA-induced apoptosis of BECs was accompanied by an up-regulation of FasR, Fas ligand (FasL), and also caspase-3 expression. GCDCA did not induce the apoptosis of BECs derived from C3H · MRL-Fas lpr mice possessing a non-functioning FasR, supporting that the GCDCA-induced apoptosis of BECs in BALB/c involves the Fas system. Furthermore, GCDCA induced an increase in interleukin-18 (IL-18) mRNA in BECs and secretion of activated IL-18 from BECs of BALB/c, which might have led to an up-regulation of FasL mRNA and protein expression in BECs followed by FasR/FasL interaction. These results suggest that GCDCA induces apoptosis of BECs through FasR/FasL interaction via an autocrine/paracrine effect, IL-18 is responsible for the expression of FasL in BEC, and the up-regulation of caspase-3 expression is involved in this model. This model could be useful for molecular and genetic studies of Fas-mediated apoptosis of BECs.

Beauvericin-induced channels in ventricular myocytes and liposomes

The antibiotic Beauvericin (BEA) was previously shown to express ionophoric properties under simple experimental systems. Its channel-forming activity was examined in inside–out patches of ventricular myocytes and synthetic membranes with the patch clamp and fluorescence imaging techniques. Current transitions to several open state levels were evident after wash-in. The BEA channel is cation-selective. Conductance and kinetics are presented for K+ and Na+ substates and main states. The pore was blocked by La3+. In myocytes, the [K+]i was reduced, while [Na+]i and [Ca2+]i increased, leading to cytolysis. These results indicate that BEA forms cation-selective channels in lipid membranes, which can affect the ionic homeostasis.

Accumulation of fumonisins, beauvericin and fusaproliferin in maize hybrids inoculated under field conditions with Fusarium proliferatum

The ear rot severity of 15 maize hybrids and the accumulation of fumonisin B 1 (FB 1 ), fumonisin B 2 (FB 2 ), beauvericin (BEA) and fusaproliferin (FP) after artificial inoculation in the field with a toxigenic strain of Fusarium proliferatum has been investigated in Poland during the seasons 1996, 1997 and 1999. The year of inoculation proved a significant influence on ear infection degree and mycotoxin accumulation. Inoculated ears contained 11–71% Fusarium -damaged kernels. Mycotoxins were detected in all hybrids at levels of 18–231.9 μg g −1 for FB 1 , 0.4–26.5 μg g −1 for FB 2 , 0.2–19.6 μg g −1 for BEA and 0.3–6.4 μg g −1 for FP. Mycotoxin concentrations were higher in Fusarium -damaged kernels (up to 361.5, 41.1, 44.3 and 10.0 μg g −1 for FB 1 , FB 2 , BEA and FP, respectively) than in healthy-looking kernels (up to 26.0, 2.3, 1.9, 0.3 μg g −1 for FB 1 , FB 2 , BEA and FP, respectively). All hybrids showed high susceptibility to the fungal infection and high toxin content in kernels during the three years of investigation.

Mycotoxin production by Fusarium avenaceum strains isolated from Norwegian grain and the cytotoxicity of rice culture extracts to porcine kidney epithelial cells.

The secondary metabolites of 24 isolates of Fusarium avenaceum from Norwegian cereals and grown on rice have been characterized. Moniliformin (MON), enniatins (ENNs), and beauvericin (BEA) were analyzed by high-performance liquid chromatography. Porcine kidney epithelial cells (PK15, American Type Culture Collection) were used to study the cytotoxicity of MON in the extracts. The following metabolites were produced by all isolates, ranked by concentration in rice cultures: ENN-B, MON, ENN-B1, and ENN-A. BEA was produced by eight isolates. The productions of BEA and ENN-A were significantly correlated, as was the case with ENN-B and ENN-B1. MON production was correlated neither to any of the other toxins nor to toxicity.

Mycotoxin contamination of maize hybrids after infection withFusarium proliferatum

The ear rot severity of nine maize hybrids and the accumulation of fumonisin B1(FB1), fumonisin B2(FB2), beauvericin (BEA) and fusaproliferin (FP) after artificial inoculation in the field with a toxigenic strain of Fusarium proliferatum have been investigated. Different degrees of ear rot were observed in different hybrids. Inoculated ears contained 11–38% of Fusarium-damaged kernels (FDK). Mycotoxin analyses showed a pronounced contamination of FDK with concentrations ranging from 116 to 343 mg kg−1 for FB1, from 8 to 29 mg kg−1 for FB2, from 1 to 14 mg kg−1 for BEA and from 2 to 10 mg kg−1 for FP. Lower levels of contamination were found in healthy-looking kernels (up to 26, 2, 0.2 and 0.3 mg kg−1 for FB1, FB2, BEA and FP respectively). A good correlation was observed between mycotoxin contamination and the Fusarium ear rot index, calculated on the basis of average ear infection with a scale ranging from 0 to 500 to represent healthy cobs and totally rotted cobs respectively. © 1999 Society of Chemical Industry

Production of the mycotoxins fusaproliferin and beauvericin by South African isolates in the Fusarium section Liseola.

The production of fusaproliferin (FUS), a recently described mycotoxin, and beauvericin (BEA), a mycotoxin recently reported to co-occur with FUS in Fusarium-infected corn, by South African isolates in the Fusarium section Liseola, was investigated. Five isolates each of F. verticillioides, F. proliferatum, F. subglutinans, and F. globosum were cultured on corn kernels. Four each of the five South African isolates of F. proliferatum and F. subglutinans produced FUS (10-1725 and 330-2630 mg/kg, respectively). BEA was produced by four of the F. proliferatum strains (310-1130 mg/kg) and three of the F. subglutinans strains (140-700 mg/kg). The isolates of F. verticillioides failed to produce significant levels of either of these secondary metabolites. F. globosum was a weak producer of both in that one isolate of five produced 25 mg/kg FUS and five out of five produced BEA at levels ranging between 10 and 110 mg/kg. To further characterize these strains, their production of fumonisins B(1), B(2), and B(3), as well as moniliformin, was investigated. Of the four species investigated, fumonisins were produced by all except F. subglutinans, which in turn was the only species whose isolates in this study produced moniliformin (four of five isolates, ranging from 155 to 2095 mg/kg). Analysis of visibly Fusarium-infected home-grown corn collected in the Transkei region of the Eastern Cape Province of South Africa showed that nine of the ten samples contained low levels of FUS (up to 62 microg/kg), whereas all ten samples showed BEA contamination ranging from 8 to 1734 microg/kg with a mean of 258 microg/kg.

Determination of the Fusarium mycotoxins, fusaproliferin and beauvericin by high-performance liquid chromatography–electrospray ionization mass spectrometry

A method is described using LC–MS for the detection of the mycotoxins fusaproliferin (FUS) and beauvericin (BEA) in cultures of Fusarium subglutinans and in naturally contaminated maize. Protonated molecular ion signals for FUS and BEA were observed at m/ z 445 and m/ z 784, respectively. Collision induced dissociation of the readily dehydrated protonated molecular ion of the sesterterpene FUS ( m/ z 427) led to the loss of another water molecule ( m/ z 409) and acetic acid ( m/ z 385), while the cyclic lactone trimer BEA fragmented to yield the protonated dimer ( m/ z 523) and monomer ( m/ z 262), respectively. Detection of FUS was best performed in the MS–MS mode while BEA displayed a stronger signal in the MS mode. The on-column instrumental detection limits for pure FUS and BEA were found to be 2 ng and 20 pg ( S/ N=2) while those in naturally contaminated maize were 1 μg/kg and 0.5 μg/kg, respectively. Five South African strains of F. subglutinans were analyzed following methanol extraction of which four produced FUS at levels between 330 mg/kg and 2630 mg/kg while only three produced BEA at levels between 140 mg/kg and 700 mg/kg. Application of this method to naturally contaminated maize samples from the Transkei region of South Africa showed FUS at levels of 8.8–39.6 μg/kg and BEA at 7.6–238.8 μg/kg.

The effects of cereal substrate and temperature on production of beauvericin, moniliformin and fusaproliferin by Fusarium subglutinans ITEM-1434

One strain of Fusarium subglutinans (ITEM-1434) isolated from maize ear rot in Poland was tested for the ability to synthesize moniliformin (MON), beauvericin (BEA) and fusaproliferin (FP) on six cereal substrates (wheat, rye, barley, oat, maize and rice kernels) for 3 weeks at 25oC and on rice at three different temperatures (20, 25 and 30oC). Most MON (497 mug/g) was produced on rice; most BEA (704 mug/g) on wheat or rice, and most FP (422 mug/g) on rye. When cultured on rice, F. subglutinans produced the highest levels of BEA and FP at 20-25oC, while MON production was best at 30oC.

GUDC Inhibits CytochromecRelease from Human Cholangiocyte Mitochondria

Although ursodeoxycholic acid (UDC) is considered effective treatment for primary biliary cirrhosis (PBC), its mechanism of action is unclear. We tested the hypothesis that UDC is taken up by cholangiocytes and inhibits caspase 3-dependent apoptosis. We used the human cholangiocyte cell line (H69) and assessed it for expression and function of an apical sodium-dependent bile acid transporter (ASBT) by RT-PCR and uptake of tritiated taurocholic acid. We experimentally induced apoptosis in H69 cells using beauvericin (BV) and determined caspase 3 activation using a fluorogenic substrate and mitochondrial cytochromecrelease (CC) into the cytosol by immunoblot analysis. We found that a functional ASBT is expressed by H69 cells as demonstrated by RT-PCR and bile acid uptake studies. Exposure of H69 cells to BV induced apoptosis in 39.4 ± 1.3% of cells at 2 h (0.23 ± 0.2% in controls). In contrast, when H69 cells were preincubated with GUDC (50 mM) for 24 h and then exposed to BV, apoptosis was inhibited by 23% (P< 0.03). In cholangiocytes pretreated with GUDC for 24 h and those treated with BV for 2 h, caspase 3-like activity was reduced by 79% and mitochondrial CC release was inhibited. In summary, the human cholangiocyte cell line H69 possesses a functional bile acid transporter, and GUDC decreases BV-induced apoptosis and inhibits activity of caspase 3 protease by blocking CC release from mitochondria. These preliminary results are consistent with our hypothesis that the beneficial effect of UDC on PBC may involve decreased apoptosis after GUDC uptake by cholangiocytes.

A rapid method for the determination of the Fusarium mycotoxin beauvericin in maize

The development of a rapid method for the determination of the Fusarium mycotoxin beauvericin (BEA) in corn and cereals is described. This method allows to prepare at least 5 times more samples simultaneously with similar analytical performance characteristics as previously published analytical methods.

Mycotoxin production by Fusarium proliferatum isolates from rice with Fusarium sheath rot disease.

Twenty samples of unpolished (rough) rice collected in Arkansas and Texas during the 1995 harvesting season from fields exhibiting Fusarium sheath rot disease or panicle blight were previously shown to include 8 samples positive for fumonisin B1 (FB1) in the range 2.2-5.2 ppm, and moniliformin (MON), but no beauvericin (BEA), deoxynivalenol, its derivatives or zearalenone were detected. Fifteen cultures of F. proliferatum were established from the 20 rough rice samples. Single spore isolates of each culture were grown on rice and tested for the production of fumonisins (FB1, FB2, FB3, etc.), MON and BEA. All 15 isolates produced FB1, FB2, MON and BEA in culture on rice. No deoxynivalenol, its derivatives or zearalenone were detected. Seven cultures produced FB1 at > 50 ppm (range 80-230 ppm), with the rest producing FB1 in the range 14-43 ppm. FB2 was produced in the range 5-47 ppm, and those cultures which produced the most FB1 also produced the most FB2. Of the 15 cultures producing MON, 11 produced it at > 100 ppm in the range 188-6018 ppm, with the rest producing in the range 7-64 ppm. BEA was produced in the range 109-1350 ppm. Other derivatives of fumonisins, including FA1, FA2 and partially hydrolyzed FB1, as well as several unknown metabolites including a compound with MW 414, were identified in culture extracts by continuous flow fast atom bombardment with ion spray mass spectrometry (CF/FAB/MS). Further study is needed to identify the factors that control production of FB1, MON and BEA by F. proliferatum in culture and in field samples.

FUSARIUM DISEASES OF CEREALS: SPECIES COMPLEX AND RELATED MYCOTOXIN PROFILES, IN EUROPE

Several Fusarium species occurring worldwide on cereals as causal agents of ‘head blight’ (scab) of small grain cereals and ‘ear rot’ of maize, are capable of accumulating, in infected kernels, several mycotoxins some of which of notable impact to human and animal health. The main groups of Fusarium toxins commonly recognized in grains are: trichothecenes, including T-2 toxin (T2), diacetoxyscirpenol (DAS), deoxynivalenol (DON), fusarenone X (FUS), and nivalenol (NIV); zearalenones, essentially zearalenone (ZEN); and fumonisins, in particular fumonisin B1 (FB1). In addition, moniliformin (MON), beauvericin (BEA), and fusaproliferin (FUP) were also found in Fusarium infected cereal ears, important as problems due to them are coming to light. The most frequently encountered mycotoxins in ear blight of wheat and other small grain cereals in Europe, proved to be DON and ZEN, produced by F. graminearum and F. culmorum, occurring from southern (warm) to northern (cold) European areas, respectively. In association with DON, NIV and FUS were found formed, in all climes by F. graminearum, F. crookwellense, F. culmorum and, in Nordic areas, also by F. poae. Moreover, in central to northeastern European countries, MON produced by F. avenaceum, and T-2 and DAS produced by F. sporotrichioides and F. poae, were found respectively. In maize red ear rot affected by F. graminearum ZEN, DON, NIV and FUS were found. In addition, the presence of F. avenaceum and F. subglutinans usually led to the accumulation of MON. Moreover, NIV and FUS were found associated with F. crookwellense, and DAS and T-2 with F. poae and F. sporotrichioides. In maize pink and random kernel rot caused by F. moniliforme, there is increasing evidence of the occurrence of FB1, especially in southern European areas where the same fusariosis was reinforced by the wide occurrence of F. proliferatum capable of producing FB1, MON, BEA and FUP.

Occurrence of Fusaproliferin, Fumonisin B1, and Beauvericin in Maize from Italy

The occurrence of fusaproliferin (FP) was investigated in 22 samples of preharvest maize ears Fusarium rot, collected in 1994 in Italy. The most frequently recovered Fusarium species were Fusarium moniliforme and Fusarium proliferatum. Chemical analysis by high-perfomance liquid chromatography and gas chromatography/mass spectrometry identified FP (up to 500 mg/kg) in nine samples mostly infected by F. proliferatum. FP was often found to be associated with fumonisin B1 (FB1) (up to 300 mg/kg) and beauvericin (BEA) (up to 520 mg/kg). The occurrence of FP as a natural maize contaminant and its co-occurrence with FB1 and BEA is reported here for the first time. Keywords: Fusaproliferin; fumonisin B1; beauvericin; maize; Fusarium; toxins; contamination

Liquid Chromatography/Thermospray/Mass Spectrometry Analysis of Beauvericin

Beauvericin (BEA) is a bioactive hexadepsipeptide coproduced by the same Fusarium species that produce fumonisin mycotoxins. BEA is insecticidal and antimicrobial, and, being lipophilic, has the potential to bioaccumulate. Its mammalian toxicity has only recently been characterized, and sensitive analytical methodology to analyze for BEA is lacking. On-line thermospray mass spectrometry (LC/TSP/MS) was used to analyze BEA. A reversed-phase column and a mobile phase that consisted of CH3CN/0.4 M HCO2NH4 were used to resolve BEA. Positive ion spectra yielded signals at m/z 785 (M + H)+, m/z 802 (M + NH4)+, and m/z 823 (M + K)+. Standard curves plotted in the range 10−100 ng for the ions m/z 785, 802, and 823 had coefficients of determination (r2) of 0.996, 0.992, and 0.999. The lowest detectable limit was 1 ng at a S/N of 5:1. The developed LC/TSP/MS method was used successfully to analyze Fusarium proliferatum-fermented cracked corn containing BEA and spiked meat samples. Keywords: Beauvericin; fumonisins;...