Modified hydra bioassay to evaluate the toxicity of multiple mycotoxins and predict the detoxification efficacy of a clay-based sorbent.

Food shortages and a lack of food supply regulation in developing countries often leads to chronic exposure of vulnerable populations to hazardous mixtures of mycotoxins, including aflatoxin B(1) (AFB(1)) and fumonisin B(1) (FB(1)). A refined calcium montmorillonite clay [i.e. uniform particle size NovaSil (UPSN)] has been reported to tightly bind these toxins, thereby decreasing bioavailability in humans and animals. Hence, our objectives in the present study were to examine the ability of UPSN to bind mixtures of AFB(1) and FB(1) at gastrointestinally relevant pH in vitro, and to utilize a rapid in vivo bioassay to evaluate AFB(1) and FB(1) toxicity and UPSN efficacy. Isothermal sorption data indicated tight AFB(1) binding to UPSN surfaces at both pH 2.0 and 6.5, but substantially more FB(1) bound at pH 2.0 than 6.5. Site-specific competition occurred between the toxins when exposed to UPSN in combination. Importantly, treatment with UPSN resulted in significant protection to mycotoxin-exposed hydra maintained at pH 6.9-7.0. Hydra were exposed to FB(1), AFB(1) and FB(1) /AFB(1) combinations with and without UPSN. A toxic response over 92 h was rated based on morphology and mortality. Hydra assay results indicated a minimum effective concentration (MEC) of 20 µg ml(-1) for AFB(1), whereas the MEC for FB(1) was not reached. The MEC for co-exposure was 400 µg ml(-1) FB(1) + 10 µg ml(-1) AFB(1). This study demonstrates that UPSN sorbs both mycotoxins tightly at physiologically relevant pH levels, resulting in decreased bioavailability, and that a modified hydra bioassay can be used as an initial screen in vivo to predict efficacy of toxin-binding agents.

Toxic interaction between fumonisin B1 and moniliformin for cardiac lesions in Japanese quail.

This study examined the effects of fumonisin B1 (FB1) and moniliformin (M) on the heart of Japanese quail (Coturnix coturnix japonica). Three hundred and ninety day-old Japanese quail were randomly divided into four groups: 1) FB1 alone (FX), 2) M alone (MX), 3) FB1 and M (FM), and 4) chick mash alone (CX). We used three pen replicates of 35 quail per pen in groups FX, MX, and FM and three pen replicates of 25 quail per pen in group CX. Gross and microscopic changes in the heart were studied in nine birds (three birds per replicate) from each group at weekly intervals up to 28 days postfeeding (DPF). Ultrastructural changes were studied in the heart of three birds (one bird per replicate) from each group at 21 DPF. Thinning of the heart was the only significant gross lesion in group FX. In contrast, mild-to-severe cardiomegaly was a significant finding in groups MX and FM throughout the study. Microscopically, thinning of cardiomyocytes was evident at 7 DPF in group FX. In addition to the hypertrophy of cardiomyocytes evident as early as 7 DPF, myocardial karyomegaly, nuclear hyperchromasia, and myofibril disarray exhibiting a wavy pattern were more pronounced at 28 DPF in group MX. Similar but more severe lesions were observed in the FM combination group that included myocardial hemorrhages, vacuolar changes, hypertrophy of cardiomyocytes, focal myocarditis, and loss of myofibrils cross-striations. Via transmission electron microscopy, the maximum effect of FB1 toxicity was observed on mitochondria. In addition to an increase in the number of mitochondria, the mitochondria seemed invariably swollen and pleomorphic, although the outer membrane was intact, and the membrane cristae were usually distinct. Myofibrils seemed thinner, without much disruption in their architecture. Large numbers of vacuolar bodies of irregular size, both in the sarcoplasm and in between the myofibrils, were conspicuous in group FX. In contrast to group FX, the increase in number of mitochondria resulted in widespread separation of muscle fibers in group MX. In addition, the mitochondria were swollen and varied from round to oval to slightly elongated and occasionally forked, and vacuolation was rarely noticed in group MX. In the FM combination group, a significant increase in the number of mitochondria caused muscle fibers to look much thinner and assume a wavy pattern. We conclude that the effect of M on the heart is exaggerated in the presence of FB1. Although the overall interactive effect of FB1 and M was less than additive, the interactive effects between the two toxins for cardiac lesions were greater than additive to synergistic up to the second week, raising serious concerns on early age exposure to a combination of these two mycotoxins.

Toxicokinetics of fumonisin B2 in ducks and turkeys.

Two extraction steps combined with HPLC with fluorescence detection were developed to determine the toxicokinetics of fumonisin B(2) (FB(2)) in ducks and turkeys. The limit of quantification of the method was 25 ng of FB(2)/mL. The mean extraction was 63%. After intravenous administration (single dose: 1 mg of FB(2)/kg of BW), plasma concentration time curves were best described by a 2-compartment open model. In ducks, elimination half-life, mean residence time, and clearance of FB(2) were 32 min, 12.9 min, and 9.3 mL/min per kilogram, respectively. In turkeys, these toxicokinetics parameters were 12.4 min, 5 min, and 8.7 mL/min per kilogram, respectively. Only a small amount of FB(2) was detected in plasma after oral dosing of 10 mg of FB(2)/kg of BW.

Fumonisins and zearalenone fed at low levels can persist several days in the liver of turkeys and broiler chickens after exposure to the contaminated diet was stopped.

Previous studies using zearalenone (ZEN) and fumonisins (FB) revealed alpha-zearalanol (α-ZOL) and FB1 in the liver of turkeys and chickens with no sign of toxicity. The aim of the present study was to determine whether contamination persists after distribution of a mycotoxin-free diet for several days. Turkeys and broilers were fed for 14 days with a diet containing respectively, 7.5 and 0.6 mg/kg of FB and ZEN, then fed for 0, 2 or 4 days with a mycotoxin-free diet. FB1 and total α-ZOL were the most abundant metabolites found, and their concentration decreased with time. The decrease was linear for FB1 (P < 0.001) and exponential for α-ZOL. Mean concentrations of FB1 on days 0, 2, and 4 were respectively, 4.9, 4, and 2.9 ng/g in turkeys, and respectively, 5, 2.3, and 1.3 ng/g in chickens. The decrease in concentration of FB1 with time was modeled by linear regression (P < 0.001). Mean concentrations of α-ZOL on days 0, 2 and 4, were respectively, 4.8, 0.8, and 0.5 ng/g in turkeys, whereas α-ZOL was only quantified in chickens on day 0 at 0.3 ng/g. A strong correlation was found between α-ZOL and ß-zearalenol (P < 0.001).

[Fumonisin intake and human health]. / Consumo de fumonisinas y daños a la salud humana.

Fumonisins are mycotoxins that contaminate maize, disrupt the folate and sphingolipid metabolism, are associated with neural tube defects, and are considered by the International Agency for Research on Cancer (IARC) as possible human carcinogens. Since maize-based foods are significant components of the Mexican diet and there is a high prevalence of genetic susceptibility for folate deficiency among Mexicans, this essay presents international and national evidence of fumonisin exposure and the relevance that such exposure represents for Mexico.

Toxicokinetics of Hydrolyzed Fumonisin B1 after Single Oral or Intravenous Bolus to Broiler Chickens Fed a Control or a Fumonisins-Contaminated Diet.

The toxicokinetics (TK) of hydrolyzed fumonisin B1 (HFB1) were evaluated in 16 broiler chickens after being fed either a control or a fumonisins-contaminated diet (10.8 mg fumonisin B1, 3.3 mg B2 and 1.5 mg B3/kg feed) for two weeks, followed by a single oral (PO) or intravenous (IV) dose of 1.25 mg/kg bodyweight (BW) of HFB1. Fumonisin B1 (FB1), its partially hydrolyzed metabolites pHFB1a and pHFB1b, and fully hydrolyzed metabolite HFB1, were determined in chicken plasma using a validated ultra-performance liquid chromatography-tandem mass spectrometry method. None of the broiler chicken showed clinical symptoms of fumonisins (FBs) or HFB1 toxicity during the trial, nor was an aberration in body weight observed between the animals fed the FBs-contaminated diet and those fed the control diet. HFB1 was shown to follow a two-compartmental pharmacokinetic model with first order elimination in broiler chickens after IV administration. Toxicokinetic parameters of HFB1 demonstrated a total body clearance of 16.39 L/kg·h and an intercompartmental flow of 8.34 L/kg·h. Low levels of FB1 and traces of pHFB1b were found in plasma of chickens fed the FBs-contaminated diet. Due to plasma concentrations being under the limit of quantification (LOQ) after oral administration of HFB1, no toxicokinetic modelling could be performed in broiler chickens after oral administration of HFB1. Moreover, no phase II metabolites, nor N-acyl-metabolites of HFB1 could be detected in this study.

Fumonisin B1, B2 and B3 in Muscle and Liver of Broiler Chickens and Turkey Poults Fed with Diets Containing Fusariotoxins at the EU Maximum Tolerable Level.

Although provisional maximum tolerable daily intake and recommended guidelines have been established for fumonisins (FB) in food, few data are available concerning levels of FB in edible animal tissues. Such data are of particular interest in avian species that can tolerate relatively high levels of fumonisins in their feed. Also, even if multiple contamination of animal feed by toxins produced by Fusarium is very frequent, little is known about the consequences of multiple contamination for FB levels in tissues. The aim of this study was to analyze the concentrations of FB in the muscle and liver of chickens and turkeys fed with FB alone and with FB combined with deoxynivalenol (DON), and with zearalenone (ZEN). Experimental diets were formulated by incorporating ground cultured toxigenic Fusarium strains in corn-soybean based feeds. Control diets were free of mycotoxins, FB diets contained 20 mg FB1+FB2/kg, and FBDONZEN diets contained 20, 5, and 0.5 mg/kg of FB1+FB2, DON, and ZEN, respectively. Animals were reared in individual cages with free access to water and feed. The feed was distributed to male Ross chickens from the 1st to the 35th day of age and to male Grade Maker turkeys from the 55th to the 70th day of age. On the last day of the study, the birds were starved for eight hours, killed, and autopsied for tissues sampling. No sign of toxicity was observed. A UHPLC-MS/MS method with isotopic dilution and immunoaffinity clean-up of samples has been developed for analysis of FB in muscle (n = 8 per diet) and liver (n = 8 per diet). Only traces of FB that were below the LOQ of 0.25 µg/kg were found in most of the samples of animals fed with the control diets. Mean concentrations of FB1, FB2, and FB3 in muscle were 17.5, 3.39, and 1.26 µg/kg, respectively, in chickens, and 5.77, 1.52, and 0.54 µg/kg in turkeys, respectively. In the liver, the respective FB1, FB2, and FB3 concentrations were 44.7, 2.61, and 0.79 µg/kg in chickens, and 41.47, 4.23, and 1.41 µg/kg, in turkeys. Cumulated level of FB1+FB2+FB3 in the highly contaminated samples were above 60 and 100 µg/kg in muscle and liver, respectively. The concentrations of FB in the tissues of animals fed the FBDONZEN diet did not greatly differ from the concentrations measured in animals fed the diet containing only FB.

Developmental Toxicity of Mycotoxin Fumonisin B1 in Animal Embryogenesis: An Overview.

A teratogenic agent or teratogen can disturb the development of an embryo or a fetus. Fumonisin B1 (FB1), produced by Fusarium verticillioides and F. proliferatum, is among the most commonly seen mycotoxins and contaminants from stale maize and other farm products. It may cause physical or functional defects in embryos or fetuses, if the pregnant animal is exposed to mycotoxin FB1. Due to its high similarity in chemical structure with lipid sphinganine (Sa) and sphingosine (So), the primary component of sphingolipids, FB1 plays a role in competitively inhibiting Sa and So, which are key enzymes in de novo ceramide synthase in the sphingolipid biosynthetic pathway. Therefore, it causes growth retardation and developmental abnormalities to the embryos of hamsters, rats, mice, and chickens. Moreover, maternal FB1 toxicity can be passed onto the embryo or fetus, leading to mortality. FB1 also disrupts folate metabolism via the high-affinity folate transporter that can then result in folate insufficiency. The deficiencies are closely linked to incidences of neural tube defects (NTDs) in mice or humans. The purpose of this review is to understand the toxicity and mechanisms of mycotoxin FB1 on the development of embryos or fetuses.

Determination of Fumonisin B1 in animal tissues with immunoaffinity purification.

Immunoaffinity extraction combined with high-performance liquid chromatography (HPLC) with fluorescence detection was developed to determine Fumonisin B1 (FB1) in duck tissues. The method was linear over a concentration range of 0.013-0.250 microg of FB1/g of liver, kidney and muscle. The limit of quantification was 0.013 microg FB1/g in tissue. The mean percentage of extraction was 75% for liver and kidney and 53% for muscle. This method can be used in duck for the detection of FB1 contamination after exposure, the liver being the most contaminated tissue.

Toxicokinetics of fumonisin B1 in turkey poults and tissue persistence after exposure to a diet containing the maximum European tolerance for fumonisins in avian feeds.

The kinetic of fumonisin B1 (FB1) after a single IV and oral dose, and FB1 persistence in tissue were investigated in turkey poults by HPLC after purification of samples on columns. After IV administration (single-dose: 10mg FB1/kg bw), serum concentration-time curves were best described by a three-compartment open model. Elimination half-life and mean residence time of FB1 were 85 and 52min, respectively. After oral administration (single-dose: 100mg FB1/kg bw) bioavailability was 3.2%; elimination half-life and mean residence time were 214 and 408min, respectively. Clearance of FB1 was 7.6 and 7.5ml/min/kg for IV and oral administration, respectively. Twenty-four hours after the administration of FB1 by the intravenous route, liver and kidney contained the highest levels of FB1 in tissues, level in muscle was low or below the limit of detection (LD, 13microg/kg). The persistence of FB1 in tissue was also studied after administration for 9 weeks of a feed that contained 5, 10 and 20mg FB1+FB2/kg diet. Eight hours after the last intake of 20mg FB1+FB2/kg feed (maximum recommended concentration of fumonisins established by the EU for avian feed), hepatic and renal FB1 concentrations were 119 and 22microg/kg, level in muscles was below the LD.

Oral and Intravenous Fumonisin Exposure in Pigs-A Single-Dose Treatment Experiment Evaluating Toxicokinetics and Detoxification.

We examined the toxicokinetics of fumonisin B1 (FB1) and its main metabolites after single dose application intravenously (iv) of 139 nmol FB1 or hydrolyzed FB1 (HFB1)/kg bodyweight (BW) in barrows (BW: 34.4 kg ± 2.7 kg), as well as the toxicokinetics of FB1, FB2, FB3 and FB1 bioavailability from oral exposure (3425 nmol FB1/kg BW, on top of ration). Additionally, detoxification efficacy of FumD (240 U/kg feed; 3321 nmol FB1/kg BW), a fumonisin esterase, was examined for oral fumonisin application. Urine and feces were collected quantitatively and serum samples were taken over a period of 120 h. Serum toxicokinetics of FB1iv showed a short distribution half-life of 6 min followed by a longer elimination half-life of 36 min. After HFB1iv administration, serum clearance was three times higher compared to FB1iv group (5.6 and 1.8 L/kg/h respectively) which together with a 5-times higher volume of distribution indicates that HFB1 is more rapidly cleared from systemic circulation but distributed more extensively into the extravasal space than FB1. The bioavailability of FB1 in orally exposed pigs was 5.2% (incl. metabolites). Moreover, we found a significant reduction of FB1 bioavailability by 90% caused by the action of fumonisin esterase in the gastrointestinal tract, clearly demonstrating the efficacy of FumD.

The intestine as a possible target for fumonisin toxicity.

Fumonisins constitute a family of toxic and carcinogenic mycotoxins produced by Fusarium verticillioides (formerly F. moniliforme), a common fungal contaminant of corn. Contamination with fumonisin B(1) (FB(1)) is of concern as this mycotoxin causes various animal diseases. The gastrointestinal tract represents the first barrier against ingested chemicals, food contaminants, and natural toxins. Following ingestion of fumonisin-contaminated food or feed, intestinal epithelial cells could be exposed to a high concentration of toxin. In this review, we have summarized the data dealing with the impact of FB(1) on the intestine. Although FB(1 )is poorly absorbed and metabolized in the intestine, it induces intestinal disturbances (abdominal pain or diarrhea) and causes extra-intestinal organ pathologies (pulmonary edema, leukoencephalomalacia, or neural tube defects). The main toxicological effect of FB(1) reported in vivo and in vitro is the accumulation of sphingoid bases associated with the depletion of complex sphingolipids. This disturbance of the sphingolipid biosynthesis pathway could explain the other observed toxicological effects such as an alteration in intestinal epithelial cell viability and proliferation, a modification of cytokine production, and a modulation of intestinal physical barrier function.

Determination of fumonisin B1 levels in body fluids and hair from piglets fed fumonisin B1-contaminated diets.

The levels of fumonisin B1 (FB1) residues in plasma, urine, feces and hair from 24 piglets fed FB1-contaminated diets containing 3.1, 6.1 or 9.0 µg FB1.g-1 for 28 days were determined using liquid chromatography coupled to mass spectrometry (LC-MS/MS). The levels of FB1 in plasma, urine, feces and pooled hair (n = 3) samples varied from 0.15 to 1.08 µg.L-1, 16.09-75.01 µg.L-1, 1.87-13.89 µg.g-1 and 2.08-8.09 ng.g-1, respectively. Significant correlations (r = 0.808-0.885; P < 0.001; N = 18) were found between FB1 intake and plasma FB1 on days 7, 14, 21 and 28. However, urinary FB1 correlated with FB1 intake only on days 7 and 14 (r = 0.561-572; P = 0.02; N = 18). A significant correlation (r = 0.509; P = 0.02; N = 24) was also found for the first time between FB1 in hair samples and FB1 intake. Plasma and urinary FB1 are good biomarkers of early exposure of pigs to low dietary FB1 levels, although plasma is recommended to assess prolonged exposure (>14 days). The possibility to evaluate hair as a biomarker of fumonisin exposure was established, although further studies are needed to provide physiologically based toxicokinetics of residual FB1 in the pig hair.

Differential sensitivity of rat kidney and liver to fumonisin toxicity: organ-specific differences in toxin accumulation and sphingoid base metabolism.

Fumonisins (FBs) are mycotoxins in maize and are inhibitors of ceramide synthase (CS), the most likely proximate cause of FB toxicity. In liver and kidney, the primary target organs in FB-fed rats, inhibition of CS results in a marked increase in the ceramide precursor sphinganine (Sa). This study was conducted to investigate the differential time- and dose-dependent changes in Sa, sphingosine (So), sphinganine 1-phosphate (Sa-1-P), and sphingosine 1-phosphate (So-1-P) in kidney, liver, serum, and heart of male Sprague-Dawley rats (3-4 weeks old) fed diets containing 1.1, 13.5, and 88.6 mug/g of total FB for 10 days. The tissues were microscopically examined for the presence and severity of lesions consistent with FB exposure. There was a time- and dose-dependent increase in Sa in both liver and kidney, which was closely correlated with the tissue concentration of fumonisin B(1) (FB(1)) and histopathologic findings. However, the Sa alone greatly underestimated the degree of disruption of sphingolipid metabolism since accumulated Sa and So were quickly metabolized to Sa-1-P and So-1-P as evidenced by large increases in these metabolites in kidney but not in liver. The concentration of FB(1) in liver and kidney that first elicited an increase in Sa was similar in both tissues, however, over time, the kidney accumulated significantly more FB(1) (10x) and total Sa (Sa plus Sa-1-P) compared to liver. Thus, the relative sensitivity of male Sprague-Dawley rat kidney and liver is most likely a consequence of differences in the mechanisms responsible for both FB(1) uptake/clearance and Sa metabolism.

Serum sphinganine and the sphinganine to sphingosine ratio as a biomarker of dietary fumonisins during chronic exposure in ducks.

Sphinganine concentration (Sa) and sphinganine to sphingosine ratio (Sa/So) are sensitive biomarkers of fumonisin B1 (FB1) exposure in animals and have been proposed to reveal FB1 exposure in humans. They correlate with liver and kidney toxicity and often precede signs of toxicity. However, the use of Sa and Sa/So is confusing during chronic exposure. Indeed, some authors report altered sphingolipids metabolism, whereas others fail to demonstrate significant effect. The aim of this study was to investigate the kinetics of Sa and Sa/So in the serum of ducks over a 77-day exposure to 0, 2, 8, 32 and 128 mg FB1/kg feeds. Serum biochemistry was also investigated to reveal hepatotoxicity. The results obtained indicate that the kinetics of sphingolipids and serum biochemistry are closely linked with the duration of the exposure. After a strong and rapid increase Sa and Sa/So decrease then stabilize. The lowest investigated dose able to determine a detectable effect is 2 mg/kg feeds, the Sa/So ratio being the most sensitive biomarker of FB1 exposure.

Effects of fumonisins on liver and kidney sphinganine and the sphinganine to sphingosine ratio during chronic exposure in ducks.

Sa and the Sa/So ratio are very sensitive biomarkers of exposure to fumonisins in several species. We previously demonstrated that increases in Sa and in the Sa/So ratio in serum were less pronounced when ducks ingested fumonisins for more than 7 weeks than when animals were exposed for only 1-2 weeks [S.T. Tran, D. Tardieu, A. Auvergne, J.D. Bailly, R. Babilé, S. Durand, G. Benard, P. Guerre, Serum sphinganine and the sphinganine to sphingosine ratio as biomarker of dietary fumonisins during chronic exposure in ducks, Chem. Biol. Interact., in press]. The aim of this study was to investigate the kinetics of Sa and of the Sa/So in both liver and kidney of ducks that have been previously tested for Sa and the Sa/So ratio in serum. Analysis were performed on treatment days 0, 7, 14, 28 and 77 in five groups of ducks fed fumonisins obtained from an extract of Fusarium verticillioides culture material by daily gavage to obtain an exposure equal to 0, 2, 8, 32 and 128 mg FB1/kg feed. Sa and the Sa/So ratio in tissues were then correlated with Sa and the Sa/So ratio previously obtained in serum. The amounts on sphinganine 1-phosphate (Sa1P) and sphingosine1-phosphate (So1P) in the liver were also investigated. On day 7 of treatment, 2mg/kg FB1 in the feed were sufficient to increase Sa and the Sa/So ratio in liver (by 165 and 148%, respectively) and kidney (by 193 and 104%, respectively). At a rate of 128 mg/kg FB1 in the feed, a very high increase in Sa concentration was observed in both liver and kidney without mortality and/or signs of necrosis (respective increase of 2034 and 3768%). Although the precise mechanism of the resistance of ducks to fumonisin-induced hepatotoxicity is still uncertain, it might be linked to the rate at which the sphingoid bases sphinganine and sphingosine are converted to their 1-phosphate or other metabolite and eliminated from target tissues.

Absorption of fumonisin B1 and aminopentol on an in vitro model of intestinal epithelium; the role of P-glycoprotein.

The aim of the present paper is to evaluate the absorption of fumonisin B1 and its principal metabolite, aminopentol on a human intestinal model, Caco-2 cells, cultured on semi-permeable inserts, that reproduces the two different intestinal compartments: luminal (apical) and serosal (basolateral) side. Following separate exposure in apical and in basolateral compartments, aminopentol passage through the cell layer (in particular from basolateral to apical direction) was shown, while it was not observed for the parent compound. The different aminopentol distribution between the two compartments of the culture system, and its variation in presence of verapamil or probenecid (P-gp and MRP inhibitors respectively), strongly suggests the involvement of P-glycoprotein in the influx/efflux mechanisms of aminopentol in the intestinal cells, reducing its oral bioavailability.

Efficacy of sodium bentonite as a detoxifier of broiler feed contaminated with aflatoxin and fumonisin.

Sodium bentonite (SB) was evaluated for its ability to reduce the deleterious effects of fumonisin B1 (FB1) and aflatoxin B1 (AFB1) in broiler diets. It was incorporated into the diets (0.3%) containing 2.5 mg/kg AFB1, 200 mg/kg FB1, or a combination of 2.5 mg/kg AFB1 and 200 mg/kg FB1. Aflatoxin B1 significantly diminished body weight gain, whereas FB1 or the combination of FB1 and SB had no effect. Addition of SB in the diets significantly diminished the inhibitory effects of dietary AFB1. Feeding AFB1 alone caused significant increases in the relative weights of most observed organs. Feeding FB1 alone did not alter relative weights of any organs. In the combined diet (AFB1 plus FB1) relative weights of the liver, kidney, gizzard, and spleen were increased. Addition of SB to the diet containing AFB1 diminished the relative weights of liver, kidney, and spleen. Addition of SB to diets containing AFB1 and FB1 only decreased liver weights. In relation to the control, lower serum levels of total protein, albumin, and globulins were observed for all AFB, containing diets without SB addition, whereas all other treatments were not altered. Livers of birds fed diets containing AFB1 and a combination of AFB1 and FB1 were enlarged, yellowish, friable, and had rounded borders. The histopathology of them, stained with hematoxylin and eosin, showed multifocal and varied cytoplasmatic vacuolization with perilobular location. Incorporation of SB reduced the incidence and severity of the hepatic histopathology changes associated with aflatoxicosis.

Nanocellulose coated with various free fatty acids can adsorb fumonisin B1, and decrease its toxicity.

The aim of this study was to evaluate the adsorption and biological properties of nanocellulose coated with free fatty acids (NCCFFAs). At first, nanocellulose was synthesized by acid hydrolysis, and then separately coated with different free fatty acids (FFAs), including lauric acid, alpha linoleic acid, oleic acid, and palmitic acid. Next, the serial concentrations of NCCFFAs (1, 10, 100, and 1000 µg/mL) was separately added to fumonisin B1 (FB1) at 1000 µg/mL, and separately incubated at 37 °C for 1, 2, and 3h. Then, the percentage of adsorption was calculated. In the next experiment, the viability of mouse liver cells was measured when they exposed to serial concentrations of NCCFFAs, FFAs, and FB1. This study showed that the increase of incubation time and concentration of NCCFFAs led to increase of FB1 adsorption. Although FFAs and NCCFFAs had no remarkable toxicity, the high toxicity was observed for FB1. Importantly, the toxicity of FB1 was highly decreased, when incubated together with FFAs or NCCFFAs. These novel adsorbents, NCCFFAs, can be used together with different foodstuffs to remove FB1.

Chronic exposure to deoxynivalenol has no influence on the oral bioavailability of fumonisin B1 in broiler chickens.

Both deoxynivalenol (DON) and fumonisin B1 (FB1) are common contaminants of feed. Fumonisins (FBs) in general have a very limited oral bioavailability in healthy animals. Previous studies have demonstrated that chronic exposure to DON impairs the intestinal barrier function and integrity, by affecting the intestinal surface area and function of the tight junctions. This might influence the oral bioavailability of FB1, and possibly lead to altered toxicity of this mycotoxin. A toxicokinetic study was performed with two groups of 6 broiler chickens, which were all administered an oral bolus of 2.5 mg FBs/kg BW after three-week exposure to either uncontaminated feed (group 1) or feed contaminated with 3.12 mg DON/kg feed (group 2). No significant differences in toxicokinetic parameters of FB1 could be demonstrated between the groups. Also, no increased or decreased body exposure to FB1 was observed, since the relative oral bioavailability of FB1 after chronic DON exposure was 92.2%.