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At least 19 recordsLinked to original sources
PubMed1998

In vivo effects of fumonisin B1-producing and fumonisin B1-nonproducing Fusarium moniliforme isolates are similar: fumonisins B2 and B3 cause hepato- and nephrotoxicity in rats.

Fumonisins are mycotoxins produced by Fusarium moniliforme, F. proliferatum, and related Fusarium species found on corn. They occur naturally in corn-based feeds and foods and are suspected human esophageal carcinogens. Fumonisin B1 (FB1), the most common homologue, causes the animal diseases associated with F. moniliforme. Hepato- and nephrotoxicities, disrupted sphingolipid metabolism, and liver cancer have been found in rats fed FB1. To determine the in vivo effects of diets containing fumonisins B2 (FB2) or B3 or (FB3), male rats were fed culture materials (CM) of FB1 non-producing F. moniliforme isolates to provide low (4.6-6.7 ppm), mid (32-49 ppm) or high (219-295 ppm) dietary levels of either FB2 (FB2CM) or FB3 (FB3CM). Other groups were fed culture material of an FB1 producing isolate (FB1CM) providing 6.9, 53 or 303 ppm total fumonisins (FB1: FB2: FB3 = 1.0: 0.38: 0.15) and a tenth group was fed a control diet having no detectable fumonisins. One-half (n = 5/group) the animals were killed after three weeks, at which time the toxicological and histopathological effects of the three culture materials were similar, mimicked the effects of FB1, and included decreased body weight gains, serum chemical indicators of hepatotoxicity, decreased kidney weights, and apoptosis of hepatocytes and kidney tubular epithelium. FB1CM, FB2CM, and FB3CM affected sphingolipids, causing increased sphinganine to sphingosine ratios (Sa/So) in both liver and kidneys. The remaining animals (n = 5/group0 were fed a control diet for three additional weeks. All body weight and tissue specific effects, including increased Sa/So, induced by the FB2Cm, FB3CM and low level FB1CM diets were absent following the recovery period. Except for mild biliary lesions found in the high dose of FB1CM group and a few apoptotic hepatocytes present in one mid- and two high-dose FB1CM rats, no evidence of toxicity remained in these groups, following the recovery period.

Animals↗
PubMed1999

Excretion of (14)C-fumonisin B(1), (14)C-hydrolyzed fumonisin B(1), and (14)C-fumonisin B(1)-fructose in rats.

14C-Fumonisin B(1) (FB(1)) was produced by Fusarium proliferatum M-5991 in modified Myro liquid medium and purified to >95% purity with a specific activity of 1.7 mCi/mmol. Nine male and nine female F344/N rats were each dosed by gavage with 0.69 micromol of (14)C-FB(1), (14)C-hydrolyzed FB(1), or (14)C-FB(1)-fructose/kg body weight. Urinary excretion of (14)C-FB(1) and (14)C-FB(1)-fructose was 0.5% and 4.4% of the total dose, respectively, and was similar between male and female rats. Urinary excretion of (14)C-hydrolyzed HFB(1) was significantly greater (P > 0.05) in female rats as compared with male rats (17.3% vs 12.8% of the total dose, respectively). There were no significant (P > 0.05) differences in biliary excretion of the three fumonisin compounds with a mean of 1. 4% of the dose excreted at 4 h after dosing. Lesser amounts continued to be excreted up to 9.25 h after dosing. Although biliary excretion of the (14)C-FB(1), (14)C-hydrolyzed FB(1), and (14)C-FB(1)-fructose was similar, increased urinary excretion of the (14)C-hydrolyzed FB(1) as compared to (14)C-FB(1) and (14)C-FB(1)-fructose indicated a greater absorption of the hydrolyzed form.

Animals↗
PubMed2002

Pharmacological antagonism of fumonisin B1 cytotoxicity in porcine renal epithelial cells (LLC-PK1): a model for reducing fumonisin-induced nephrotoxicity in vivo.

Fumonisin B1 is a mycotoxin commonly found on corn. It is hepatotoxic and nephrotoxic in domestic and experimental animals, and causes equine leukoencephalomalacia and porcine pulmonary oedema. It is a potent inhibitor of ceramide synthase. Inhibition leads to accumulation of free sphingoid bases in cells and tissues. In pig kidney epithelial cells (LLC-PK1), fumonisin B1 induces increased tumour necrosis factor alpha (TNFalpha) expression independent of the accumulation of sphingoid bases. The objective of this study was to investigate pharmacological approaches for intervening in fumonisin B1 toxicity using the LLC-PK1 cell model. The toxicity of fumonisin B1 was assayed using cell viability and lactate dehydrogenase (lactate dehydrogenase) release. Pretreatment of cells with myriocin, preventing sphinganine accumulates, prevented the fumonisin B1-induced decrease in cell viability and increased lactate dehydrogenase release. Modulation of adenosine receptor activity did not reduce the fumonisin B1 cytotoxicity. As with myriocin, silymarin pretreatment prevented the fumonisin B1-induced effects on cell viability and lactate dehydrogenase release. When added 6 or 24 hr after treatment of cells with fumonisin B1, both myriocin and silymarin reversed the decreased cell viability and suppressed the increased lactate dehydrogenase release. Myriocin, but not silymarin, blocked the accumulation of sphinganine in fumonisin B1-treated cells. Silymarin, unlike myriocin, induced expression of TNFalpha to an extent similar to fumonisin B1, but pretreatment with silymarin decreased the fumonisin B1-induced TNFalpha expression in LLC-PK1 cells. Results suggest that the mechanisms by which myriocin and silymarin protect renal cells are different, and silymarin potentially prevents fumonisin B1-induced toxicity by modulating TNFalpha expression or signals downstream of the inhibition of ceramide synthase.

Acyltransferases↗
PubMed2003

Bound fumonisin B1: analysis of fumonisin-B1 glyco and amino acid conjugates by liquid chromatography-electrospray ionization-tandem mass spectrometry.

To study the formation of fumonisin artifacts and the binding of fumonisins to matrix components (e.g., saccharides and proteins) in thermal-treated food, model experiments were performed. Fumonisin B(1) and hydrolyzed fumonisin B(1) were incubated with alpha-d-glucose and sucrose (mono- and disaccharide models), with methyl alpha-d-glucopyranoside (starch model), and with the amino acid derivatives N-alpha-acetyl-l-lysine methyl ester and BOC-l-cysteine methyl ester (protein models). The reaction products formed were analyzed by liquid chromatography-electrospray ionization-tandem mass spectrometry. The incubation of d-glucose with fumonisin B(1) or hydrolyzed fumonisin B(1) resulted in the formation of Amadori rearrangement products. Whereas conjugates were found following the reaction of sucrose, methyl alpha-d-glucopyranoside, and the amino acid derivatives with fumonisin B(1), the heating with hydrolyzed fumonisin B(1) yielded no artifacts. For structural determination, the stable reaction product formed by heating of methyl alpha-d-glucopyranoside (as starch model) with fumonisin B(1) was purified and identified by nuclear magnetic resonance spectroscopy as the diester of the fumonisin tricarballylic acid side chains with methyl alpha-d-glucopyranoside. These model experiments demonstrate that fumonisins are able to bind to polysaccharides and proteins via their two tricarballylic acid side chains.

Amino Acids↗
PubMed1999

Screening of fungal species for fumonisin production and fumonisin-like disruption of sphingolipid biosynthesis.

Fumonisins are mycotoxins produced by several species of Fusaria. They are found on corn and in corn-based products, can cause fatal illnesses in some animals and are suspected human esophageal carcinogens. Fumonisins are believed to cause toxicity by blocking ceramide synthase, a key enzyme in sphingolipid biochemistry which converts sphinganine (or sphingosine) and fatty acyl CoA to ceramide. Relatively few fungal species have been evaluated for their ability to produce fumonisins. Fewer have been studied to determine if they produce ceramide synthase inhibitors, whether fumonisin-like structures or not, therefore potentially having toxicity similar to fumonisins. We analyzed corn cultures of 49 isolates representing 32 diverse species of fungi for their ability to produce fumonisins. We also evaluated the culture extracts for ceramide synthase activity. Only cultures prepared with species reported previously to produce fumonisins--Fusarium moniliforme and F. proliferatum--tested positive for fumonisins. Extracts of these cultures inhibited ceramide synthase, as expected. None of the other fungal isolates we examined produced fumonisins or other compounds capable of inhibiting ceramide synthase. Although the fungi we selected for these studies represent only a few of the thousands of species that exist, they share the commonality that they are frequently associated with cereal grasses, including corn, either as pathogens or as asymptomatic endophytes. Thus, these results should be encouraging to those attempting to find ways to genetically manipulate fumonisin-producing fungi, to make corn more resistant, or to develop biocontrol measures because it appears that only a relatively few fungal contaminants of corn can produce fumonisins.

Animals↗
PubMed2006

Detection of new fumonisin mycotoxins and fumonisin-like compounds by reversed-phase high-performance liquid chromatography/electrospray ionization ion trap mass spectrometry.

Fumonisins were produced in a rice culture infected with Fusarium verticillioides. To decrease the possibility of the formation of artifacts, the fumonisins were analyzed by reversed-phase high-performance liquid chromatography with electrospray ionization ion trap tandem mass spectrometry (RP-HPLC/ESI-IT-MS2) immediately after the extraction of the culture material without any sample clean-up. In addition to already known fumonisins, numerous new fumonisin mycotoxins and fumonisin-like compounds were detected. On the basis of the IT-MS2 data, detailed fragmentation pathways including new mechanisms were proposed for the different series of fumonisins. The retention times, the masses of the protonated molecules and of the product ions including the backbones and the characteristic neutral mass losses from the protonated molecules of the new compounds suggested their structures (applying the well-known designation): iso-FA1a,b, iso-FB1a-d, iso-FB2,3a-e, PHFB2a-c, PHFB4a-d, FB5/iso-FB5a-d, FBK1 2TCA, FBK4 2TCA, FC2, iso-FC2,3, PHFC4, FD and FBX series. The relative quantities of fumonisins and fumonisin-like compounds found in the sample extract were expressed as percentages of FB1 (0.02-100%). The backbone of the compound denoted FD contained fewer carbon atoms than the well-known fumonisins with the C19 or C20 backbone and may well be a precursor of the longer compounds. For the compounds denoted FBX (12 compounds), one or two OH groups attached to the fumonisin backbone were esterified by carboxylic acids other than tricarballylic acid, such as cis-aconitic acid, oxalylsuccinic acid and oxalylfumaric acid.

Chromatography, High Pressure Liquid↗
PubMed2002

N-(1-deoxy-D-fructos-1-yl) fumonisin B(1), the initial reaction product of fumonisin B(1) and D-glucose.

Incubation of fumonisin B(1) and D-glucose in aqueous solutions resulted in the formation of N-(1-deoxy-D-fructos-1-yl) fumonisin B(1) in addition to the previously reported N-(carboxymethyl) fumonisin B(1). N-(1-Deoxy-D-fructos-1-yl) fumonisin B(1) is the first stable product formed after the Amadori rearrangement of the Schiff base formed by the reaction of the primary amine of fumonisin B(1) and the aldehyde group of D-glucose. N-(1-Deoxy-D-fructos-1-yl) fumonisin B(1) was synthesized by reacting fumonisin B(1) with an excess of D-glucose in methanol and heating for 6 h at 64 degrees C. It was purified using C(18) and strong cation exchange solid-phase extraction cartridges and characterized by nuclear magnetic resonance and liquid chromatography-mass spectrometry. Subsequently, N,N-dimethylformamide was found to be a better reaction solvent, requiring reaction for only 2-3 h at 64 degrees C and eliminating the formation of methyl esters. Alkaline hydrolysis of N-(1-deoxy-D-fructos-1-yl) fumonisin B(1) gave a mixture of hydrolyzed fumonisin B(1) and hydrolyzed N-(carboxymethyl) fumonisin B(1).

Carboxylic Acids↗
PubMed2000

Identification of fumonisin B1 as an inhibitor of argininosuccinate synthetase using fumonisin affinity chromatography and in vitro kinetic studies.

Fumonisin B1, a fungal mycotoxin that grows on corn and other agricultural products, alters sphingolipid metabolism by inhibiting ceramide synthase. The precise mechanism of fumonisin B1 toxicity has not been completely elucidated; however, a central feature in the cytotoxicity is alteration of sphingolipid metabolism through interruption of de novo ceramide synthesis. An affinity column consisting of fumonisin B1 covalently bound to an HPLC column matrix was used to isolate a rat liver protein that consistently bound to the column. The protein was identified as argininosuccinate synthetase by protein sequencing. The enzyme-catalyzed formation of argininosuccinic acid from citrulline and aspartate by recombinant human and rat liver argininosuccinate synthetase was inhibited by fumonisin B1. Fumonisin B1 showed mixed inhibition against citrulline, aspartate, and ATP to the enzyme. Fumonisin B1 had a Ki' of approximately 6 mM with the recombinant human argininosuccinate synthase and a Ki' of 35 mM with a crude preparation of enzyme prepared from rat liver. Neither tricarballylic acid nor hydrolyzed fumonisin B1 inhibited recombinant human argininosuccinate synthetase. This is the first demonstration of fumonisin B1 inhibition of argininosuccinate synthethase, a urea cycle enzyme, which adds to the list of enzymes that are inhibited in vitro by fumonisin B1 (ceramide synthase, protein serine/threonine phosphatase). The extent of the inhibition of argininosuccinate synthetase in cells, and the possible role of this enzyme inhibition in the cellular toxicity of FB1, remains to be established.

Animals↗
PubMed2003

Induction of apoptosis in cultured human proximal tubule cells by fumonisins and fumonisin metabolites.

Fumonisin B1 (FB1) causes apoptosis in a variety of cell types and tissues but the apoptotic potential of other fumonisins and fumonisin metabolites has not been determined and the underlying mechanisms are not completely understood. In our studies we exposed human proximal tubule-derived cells (IHKE cells) to FB1, fumonisin B2 (FB2), fumonisin B3 (FB3), hydrolyzed fumonisin B1 (HFB1) and N-palmitoyl-hydrolyzed fumonisin B1 (N-Pal-HFB1) and investigated caspase-3 activation, chromatin condensation and DNA fragmentation. Exposure to 10 micromol/L FB1 for 24 h led to a significant increase in caspase-3 activity, chromatin condensation and to DNA fragmentation. All other tested compounds did not show any significant activation of caspase-3 activity nor chromatin condensation and DNA-fragmentation. Furthermore, we examined if a sphinganine accumulation is correlated with an induction of apoptosis in IHKE cells. Therefore we used a liquid chromatography/electrospray ionization-mass spectrometry(LC/ESI-MS)-method using phytosphingosine as an internal standard to determine sphinganine and sphingosine concentrations in IHKE cells. Whereas a significant increase of sphinganine (up to 7000% compared to control cells) was observed with all fumonisin-derivates, sphingosine levels nearly remained unchanged indicating that all substrates inhibited ceramide synthase effectively. These results demonstrate that all compounds let to increased sphinganine levels in IHKE cells but only FB1 was able to induce apoptosis. We conclude that the inhibition of the ceramide synthase is not per se a predictor whether or not fumonisins induce apoptosis.

Apoptosis↗
PubMed1998

Fumonisin B1 contamination of maize and experimental acute fumonisin toxicosis in pigs.

The fumonisin B1 content of 69 visibly mouldy and 23 mould-free maize samples grown in Hungary in 1993-1995 was determined by high-performance liquid chromatography (HPLC). Fumonisin B1 was found to occur in 70-73% of the mouldy samples. The mycotoxin level increased from year to year: the highest fumonisin B1 concentration was 75.1 mg/kg. The samples that were mould-free on visual inspection showed a much lower prevalence of fumonisin B1 contamination (30%) and contained fumonisin B1 in markedly lower concentrations (average, 1.52 mg/kg; maximum concentration, 5.1 mg/kg). Using the Fusarium moniliforme strain designated 14/A, isolated from the sample that had the highest mycotoxin concentrations, fumonisin B1 toxin was produced on maize by an internationally accepted procedure. Subsequently, two weaned piglets were fed a diet containing 330 mg fumonisin B1 per kg of feed. The experimental animals developed hydrothorax and pulmonary oedema, and died in 5-6 days. The clinical symptoms and pathological lesions were consistent with those of porcine pulmonary oedema (PPE) diagnosed in the USA in 1989-1990, as well as with those of a disease entity that had already been described in Hungary in the 1950s as the so-called fattening or unique pulmonary oedema of pigs but considered to be of unknown aetiology. The results of the feeding trial confirm that this pig disease, which has occurred in Hungary for a long time, is caused by the mycotoxin fumonisin B1.

Animal Feed↗
PubMed1996

Fumonisins Veratox. A new rapid quantitative ELISA for determination of fumonisin in food and feed.

Polyclonal antibodies against fumonisin B1 were produced by immunizing sheep with fumonisin B1-keyhole limpet hemocyanin as an immunogen. A quantitative competitive enzyme-linked immunosorbent assay was developed whereby free fumonisins or sample extract containing fumonisins and enzyme-labelled fumonisin competed for binding to the solid phase-bound antibodies. The color intensity of wells, formed by substrate reaction with the enzyme, was inversely related to FB1 concentration. Detection limits for the assay were 0.1 ng/mL fumonisin B1 and concentrations of fumonisins B1, B2, and B3 required for 50% binding inhibition were 5.5, 23 and 18 ng/mL, respectively. For food and feed analyses, samples were extracted with 70% methanol and dilution of the extracts were used directly for ELISA. ELISA results were compared to HPLC analyses by a reference laboratory and the correlation (r value) between ELISA and HPLC was 0.967. The assay may be used to quantitate fumonisins in food and feed within 30 minutes.

Animal Feed↗
PubMed2004

Fumonisins disrupt sphingolipid metabolism, folate transport, and neural tube development in embryo culture and in vivo: a potential risk factor for human neural tube defects among populations consuming fumonisin-contaminated maize.

Fumonisins are a family of toxic and carcinogenic mycotoxins produced by Fusarium verticillioides (formerly Fusarium moniliforme), a common fungal contaminant of maize. Fumonisins inhibit ceramide synthase, causing accumulation of bioactive intermediates of sphingolipid metabolism (sphinganine and other sphingoid bases and derivatives) as well as depletion of complex sphingolipids, which interferes with the function of some membrane proteins, including the folate-binding protein (human folate receptor alpha). Fumonisin causes neural tube and craniofacial defects in mouse embryos in culture. Many of these effects are prevented by supplemental folic acid. Recent studies in LMBc mice found that fumonisin exposure in utero increases the frequency of developmental defects and administration of folate or a complex sphingolipid is preventive. High incidences of neural tube defects (NTD) occur in some regions of the world where substantial consumption of fumonisins has been documented or plausibly suggested (Guatemala, South Africa, and China); furthermore, a recent study of NTD in border counties of Texas found a significant association between NTD and consumption of tortillas during the first trimester. Hence, we propose that fumonisins are potential risk factors for NTD, craniofacial anomalies, and other birth defects arising from neural crest cells because of their apparent interference with folate utilization.

Animals↗
PubMed2006

[Development of monoclonal antibody against fumonisin B1 and ELISA-kit of quantitative analysis for fumonisin B1].

OBJECTIVE: To detect the contamination level of fumonisin B1 in grain, and to develop rapid detection kit that possess patent of China. METHODS: Hybridoma cell line excreting monoclonal antibody against fumonisin B, was produced using B cell hybridoma technique and develop a rapid, sensitive, quantitative ELISA-kit for detection fumonisin B1. RESULTS: The monoclonal antibody used in the ELISA-kit were tested for subtype as IgG1 and its affinity constant was 8.3 x 10(-8) mol/L. The monoclonal antibody obtained in the present study was highly specific to fumonisin B1 , because no cross reactions between the monoclonal antibodies against fumonisin B1 with the analogues of fumonisin B, were found. The limited concentration of the ELISA-kit was 5 ng/ml, linear range was 50-500 ng/ml, the linear equation was Y = -0.582 x +1.793( = 0.99, P < 0.05). The recovery rate of maize on the level of 50n g/ml, 200 ng/ml and 500 ng/ml was among 71.89%-112.95%. The kit can be stored at normal tempertature in ten months at least. The coefficient of variant winthin-laboratory and between-laboratory was less than 20%.

Animals↗
PubMed2002

Fumonisins and fumonisin analogs as inhibitors of ceramide synthase and inducers of apoptosis.

Sphingoid bases are growth inhibitory and pro-apoptotic for many types of cells when added to cells exogenously, and can be elevated to toxic amounts endogenously when cells are exposed to inhibitors of ceramide synthase. An important category of naturally occurring inhibitors are the fumonisins, which inhibit ceramide synthase through structural similarities with both the sphingoid base and fatty acyl-CoA co-substrates. Fumonisins cause a wide spectrum of disease (liver and renal toxicity and carcinogenesis, neurotoxicity, induction of pulmonary edema, and others), and most-possibly all-of the pathophysiologic effects of fumonisins are attributable to disruption of the sphingolipid metabolism. The products of alkaline hydrolysis of fumonisins (which occurs during the preparation of masa flour for tortillas) are aminopentols that also inhibit ceramide synthase, but more weakly. Nonetheless, the aminopentols (and other 1-deoxy analogs of sphinganine) are acylated to derivatives that inhibit ceramide synthase, perhaps as product analogs, elevate sphinganine, and kill the cells. Somewhat paradoxically, fumonisins sometimes stimulate growth and inhibit apoptosis, possibly due to elevation of sphinganine 1-phosphate, which is known to have these cellular effects. These findings underscore the complexity of sphingolipid metabolism and the difficulty of identifying the pertinent mediators unless a full profile of the potentially bioactive species is evaluated.

Animals↗
PubMed2001

Preliminary evaluation of fumonisins by the Nordic countries and occurrence of fumonisins (FB1 and FB2) in corn-based foods on the Danish market.

Experts from the Nordic countries (Denmark, Norway, Sweden, Finland and Iceland) have carried out an evaluation of fumonisins. The working group members concluded that, at that time point, it was not possible to carry out a complete risk assessment. However, it was recommended that the human daily' intake of fumonisins should be less than 1 microg/kg bw/day. Subsequently, the presence of the Fusarium mycotoxins fumonisin B1 and B2 (FB1 and FB2) in corn-based food on the Danish retail market has been determined. A total of 70 samples were analysed and 37% contained FB1 and 21% contained FB2. No fumonisins were found in sweet corn (canned or frozen), corn-on-the-cob, corn starch or gruel powder for babies. FB1 was found in about half of the corn flakes, corn snack and popcorn (not popped) samples, whereas FB2 was seen to a lesser extent. Both FB1 and FB2 were found in 75% or more of the corn flour, tacos and polenta samples. In general, the content of FB1 was in the range of 1-1000 micro/kg and the content of FB2 was in the range of 4-250 microg/kg. Corn-based foods are consumed in rather low amounts and irregularly among the Danish population and therefore it is not meaningful to calculate an average daily funonisin intake. An estimate for an 'eater' shows that the intake of fumonisins will not exceed 0.4 microg/kg bw/day.

Animals↗
PubMed2004

Analysis of heat-processed corn foods for fumonisins and bound fumonisins.

Thirty retail samples of heat-processed corn foods, i.e. corn flakes, corn-based breakfast cereals, tortilla chips and corn chips, were analysed for fumonisins--fumonisin B1 (FB1), fumonisin B2 (FB2) and hydrolysed FB1 (HFB1)--as well as for protein- and total-bound FB1. Bound (hidden) fumonisins cannot be detected by conventional analysis. Improved methods for the determination of bound FB1 were developed. The protein-bound FB1 was extracted with 1% sodium dodecylsulfate (SDS) solution. The SDS, which interfered with high-performance liquid chromatography (HPLC) analysis, was then separated from protein-bound FB1 by complexing with methylene blue followed by solvent extraction and hydrolysis with 2 N KOH. To measure total-bound FB1, the sample itself was hydrolysed with KOH. In both cases, clean-up was accomplished on an OASIS polymeric solid-phase extraction column and the bound fumonisins were determined by HPLC measurement of HFB1. Fourteen of 15 samples of corn flakes and other corn-based breakfast cereals analysed contained detectable levels of FB1 with a mean in positive samples of 67ng g(-1) (13-237 ng g(-1)). Two samples also had detectable levels of FB2 (21-23ng g(-1)). Bound FB1 was found in all samples; the mean protein-bound FB1 measured was 58 ng g(-1) (22-176 ng g(-1)) and the mean total-bound FB1 measured was 106 ng g(-1) (28-418 ng g(-1)), reported as FB1 equivalents after correction for recoveries of HFB1. There was an average of about 1.3 times more FB1 in the bound form compared with extractable FB1, and this was about twice as much as protein-bound FB1. Seven of the 15 samples of alkali-processed corn-based foods, such as tortilla chips and corn chips, contained FB1 and three contained HFB1 with means in measurable positive samples of 78 (48-134) and 29 (13-47) ng g(-1), respectively. Five of these alkali-processed corn foods contained bound FB1; the mean measurable protein-bound FB1 was 42 ng g(-1) (39-46 ng g(-1)) and the mean measurable total-bound FB1 was 100 ng g(-1) (54-209 ng g(-1)). HFB1 derived from bound FB1 in selected samples was confirmed by HPLC with mass spectrometry (MS).

Carcinogens, Environmental↗
PubMed1996

Fumonisin toxicity and metabolism studies at the USDA. Fumonisin toxicity and metabolism.

Fumonisins are responsible for many of the toxic effects of the common corn fungus, Fusarium moniliforme. They are acute renal and liver toxins in rats, and have tumor promoting activity. Fumonisin B1 is poorly absorbed, rapidly excreted, and persists in small amounts in the liver and kidney. Fumonisins are specific inhibitors of ceramide synthase, and the toxic effects they produce may be related to their ability to disrupt sphingolipid metabolism, resulting in a myriad of problems in cell regulation and communication. In this paper, research that has been conducted on F. monilforme and the fumonisins at the USDA's Russell Research Center is reviewed.

Animals↗
PubMed1996

Effects of fumonisin B1 and (hydrolyzed) fumonisin backbone AP1 on membranes: a spin-label study.

Electron spin resonance (ESR) spectroscopy and spin label techniques have been used to study the effects of fumonisin B1 (FB1) and hydrolyzed fumonisin backbone (AP1) on the structural and dynamic properties of phosphatidylcholine membranes at the molecular level. Multilamellar liposomes consisting of dimyristoylphosphatidylcholine (DMPC) and egg yolk phosphatidylcholine (EYPC) were used. Six different nitroxide spin labels were used to determine what effects FB1 may impart on the ordering and mobility of lipids in membranes. The experimental results disclose the following: (1) In the fluid phase membrane, FB1 significantly increases the fluidities of n-doxylstearic acid (SA) spin labels (SL) attached to carbons 5 and 7, which disorders the alkyl chains and perturbs the surface region of the bilayer; by comparison, minimal effects were detected near the center of the bilayer. (2) In the gel phase, FB1 and AP1 imparts marked rigidifying effects on membrane fluidity, which enlarges the change in ordering on the phase transition even further. (3) FB1 also restricts the mobility of the (rigid) cholestane spin label. (4) A reduction in mobility of the tempo-stearate spin label suggests that the tricarballylic acid (TCA) moieties of FB1 might mimic the structure of polar headgroups in phospholipids. The present results may provide additional mechanisms to elucidate the toxicological activities of the fumonisins.

Dimyristoylphosphatidylcholine↗