fumonisin-b1 and moniliformin

Extrusion cooking is one of the fastest growing food-processing operations in recent years due to several advantages over traditional methods. Apart from its main goal of improving the quality of intermediate and final processed products, it may incidentally also improve safety because of the potential to reduce mycotoxin levels in cereals. This review is focused on extrusion cooking and aims to give a general overview of its impact in reducing mycotoxin levels in cereals. Extrusion cooking generally decreases the mycotoxins levels at rates depending on different factors such as the type of extruder, the type of screw, the die configuration, the initial mycotoxin concentration, the barrel temperature, the screw speed, the moisture content of the raw material and the use of additives. Reductions of 100, 95 and 83% for fumonisins, aflatoxins and zearalenone, respectively, have been reported during extrusion cooking of cereals, while lower reductions were observed for deoxynivalenol, ochratoxin A and moniliformin, where maximum reductions did not exceed 55, 40 and 30%, respectively.

Topics: Aflatoxins; Carcinogens; Carcinogens, Environmental; Cooking; Cyclobutanes; Edible Grain; Estrogens, Non-Steroidal; Food Contamination; Fumonisins; Hydrolysis; Mycotoxins; Ochratoxins; Trichothecenes; Zearalenone

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 inte

Topics: Animal Feed; Animals; Coturnix; Cyclobutanes; Drug Interactions; Food Contamination; Fumonisins; Heart Diseases; Poultry Diseases

Fusarium temperatum is an emerging maize pathogen that causes maize ear and stalk rot diseases and produces various mycotoxins including moniliformin, beauvericin, enniatins and fumonisin B1, which poses a potential risk to the human food or animal feed supply chains. Early detection of F. temperatum is crucial to prevent its derived mycotoxins from entering the food chain, and is also a useful tool in disease management practices. Here, we describe a loop-mediated isothermal amplification (LAMP) assay for rapid diagnosis of F. temperatum. The 28S ribosomal DNA sequences (28S rDNA) of F. temperatum were used to design a set of six primers. The reaction conditions were optimized for developing a fast assay with high specificity and sensitivity, and were able to detect the presence of less than 10 pg of target DNA per reaction within 60 min. Furthermore, the resulting amplicons were visualized by adding SYBR Green I to the reaction tubes. Suspected F. temperatum infected maize stalk samples collected from Yunnan province, China were identified using the developed LAMP assay. In conclusion, the method not only provides a rapid and specific screening for the existence of F. temperatum in a bulk of maize samples without using sophisticated equipment, but also is potentially useful for other agriculturally important toxigenic fungi.

Topics: China; Cyclobutanes; Depsipeptides; Fumonisins; Fusarium; Mycotoxins; Nucleic Acid Amplification Techniques; RNA, Ribosomal, 28S; Sensitivity and Specificity; Zea mays

The effect of water activity (aw = 0.95, 0.98 and 0.995), temperature (15, 25 and 30°C), incubation time (7, 14, 21 and 28 days), and their interactions on growth and moniliformin (MON), beauvericin (BEA), fusaproliferin (FUS) and fumonisin B1 (FB1) production by two strains of Fusarium temperatum isolated from Argentinean maize were determined in vitro on sterile layers of maize grains. The results showed that there was a wide range of conditions for growth and mycotoxins production by F. temperatum. Both strains were found to grow faster with increasing aw and at 30°C. In relation to mycotoxin production, the two strains produced more FUS than the other mycotoxins regardless of aw or temperature evaluated (maximum = 50,000 μg g(-1)). For FUS, MON and BEA, the maximum levels were observed at 0.98 aw and 30°C (50,000, 5000 and 2000 μg g(-1) respectively). The lowest levels for these three mycotoxins were detected at 15°C and 0.95 aw (1700 and 100 μg g(-1) for FUS and MON respectively), and at 0.98 aw (400 μg g(-1) for BEA). The maximum levels of FB1 were produced at 15°C and 0.98 aw (1000 μg g(-1)). At all aw and temperatures combinations evaluated there was an increase in toxin concentrations with time incubation. The maximum levels were detected at 21 days. Statistical analyses of aw, temperature, incubation time, and the two- and three-way interactions between them showed significant effects on mycotoxins production by F. temperatum. For its versatility on growth and mycotoxin production, F. temperatum represents a toxicological risk for maize in the field and also during grain storage.

Topics: Argentina; Cyclobutanes; Depsipeptides; Food Microbiology; Fumonisins; Fusarium; Temperature; Terpenes; Time Factors; Water; Zea mays

Thirty single-spore isolates of a toxigenic fungus, Fusarium oxysporum, were isolated from asparagus spears and identified by species-specific polymerase chain reaction (PCR) and translation elongation factor 1-α (TEF) sequence analysis. In the examined sets of F. oxysporum isolates, the DNA sequences of mating type genes (MAT) were identified. The distribution of MAT idiomorph may suggest that MAT1-2 is a predominant mating type in the F. oxysporum population. F. oxysporum is mainly recognised as a producer of moniliformin-the highly toxic secondary metabolite. Moniliformin content was determined by high-performance liquid chromatography (HPLC) analysis in the range 0.05-1,007.47 μg g(-1) (mean 115.93 μg g(-1)) but, also, fumonisin B(1) was detected, in the concentration range 0.01-0.91 μg g(-1) (mean 0.19 μg g(-1)). There was no association between mating types and the mycotoxins biosynthesis level. Additionally, a significant intra-species genetic diversity was revealed and molecular markers associated with toxins biosynthesis were identified.

Topics: Asparagus Plant; Biomarkers; Chromatography, High Pressure Liquid; Cyclobutanes; DNA Fingerprinting; Fumonisins; Fungal Proteins; Fusarium; Genes, Mating Type, Fungal; Genetic Variation; Peptide Elongation Factor 1; Phylogeny; Plant Diseases; Polymerase Chain Reaction; Sequence Analysis, DNA; Spores, Fungal

Internal fruit rot, caused by Fusarium lactis, is an important disease of sweet pepper (Capsicum annuum) in Canadian greenhouses. Production of the mycotoxins fumonisin B₁ (FB₁), moniliformin (MON) and beauvericin (BEA) by F. lactis (17 isolates) and the related species F. proliferatum (three isolates) and F. verticillioides (one isolate), which are also associated with internal fruit rot, was evaluated on rice medium. All 21 isolates examined were found to produce BEA, at concentrations ranging from 13.28 to 1674.60 ppm, while 13 of 17 F. lactis isolates and two of three F. proliferatum isolates produced MON (0.23 to 181.85 ppm). Only one isolate of F. lactis produced detectable levels of FB₁ in culture, whereas all three F. proliferatum isolates and the F. verticilloides isolate produced this mycotoxin (0.28 to 314 ppm). Production of FB₁, MON and BEA was also evaluated in inoculated pepper fruits showing mild or severe symptoms of infection. FB₁ could be detected in both lightly and heavily diseased fruit tissue after inoculation with F. lactis, F. proliferatum or F. verticilloides, at concentrations ranging from 0.61 to 8.04 ppm. BEA was also detected in lightly and heavily diseased fruit tissue inoculated with F. lactis, as well as in heavily diseased tissue inoculated with F. proliferatum (3.00 to 19.43 ppm), but not in tissue inoculated with F. verticilloides. MON was detected in all tissues inoculated with F. proliferatum or F. verticilloides, and in heavily diseased tissue inoculated with F. lactis (0.03 to 0.27 ppm). The three mycotoxins were also found in naturally infected sweet pepper fruits exhibiting symptoms of internal fruit rot and collected from a commercial greenhouse. The production of MON, BEA and FB₁ alone or in combination by isolates of F. lactis suggests that development of internal fruit rot of sweet pepper is an important food safety concern, and that every effort should be made to cull infected fruit before it makes it to market.

Topics: Canada; Capsicum; Cyclobutanes; Depsipeptides; Food Contamination; Fruit; Fumonisins; Fusarium; Mycotoxins; Oryza; Plant Diseases

The principal aim of this study was to estimate the formation of fumonisins (FB(1) and FB(2)), moniliformin (MON), and ergosterol (ERG) by Fusarium oxysporum and Fusarium proliferatum, while the formation of beauvericin (BEA) was estimated by the latter Fusarium species only. Moreover, the effect of temperature on the biosynthesis of mycotoxins was also evaluated. Fumonisins were formed by F. proliferatum, with the highest yield at 18 degrees C (720.0-1976.6 microg g(-1) for FB(1), 74.2-670.8 microg g(-1) for FB(2)) and only by three of four F. oxysporum strains at a very low level (0.02-4.77 microg g(-1) for FB(1), 0.02-2.15 microg g(-1) for FB(2)). The amount of MON formed by F. proliferatum was the highest (p < 0.001) at 32 degrees C (3056.87 microg g(-1)), while MON biosynthesis by F. oxysporum was lower 227.54 microg g(-1) (p < 0.001). BEA was produced by F. proliferatum with the highest level at 25 degrees C (p < 0.001). ERG-recognized as an indicator of fungal biomass development and as a consequence of mycotoxin formation-was found at the highest concentration at a biosynthesis temperature of 25 degrees C for F. proliferatum and F. oxysporum (p < 0.001).

Topics: Asparagus Plant; Cyclobutanes; Depsipeptides; Ergosterol; Food Contamination; Fumonisins; Fusarium; Mycological Typing Techniques; Plant Diseases; Plant Shoots; Polymerase Chain Reaction; Species Specificity; Temperature; Vegetables

A total of 390 one-day-old quail chicks (Coturnix coturnix japonica) were divided into 4 groups (3 replicates per treatment), viz. CX, FX, MX, and FM, containing 75, 105, 105, and 105 birds, respectively. Birds in the control group (CX) were fed quail mash alone, whereas birds in group FX were fed 200 ppm of fumonisin B(1) (FB(1)) from Fusarium verticillioides culture material; group MX was fed 100 ppm of moniliformin (M) from Fusarium fujikuroi culture material; and group FM was fed a combination of 200 ppm of FB(1) and 100 ppm of M. Diets were fed from d 1 to 35 to study clinical signs, growth response, serum biochemical changes, and cell-mediated immune response. Birds fed FB(1) (FX) showed ruffled feathers and poor growth. Birds in group MX appeared more stunted than those in group FX and exhibited signs of poor feathering and decreased feed and water intake. Clinical signs observed in group FM were more or less similar to those observed in groups FX and MX. Total mortality was 12.38, 7.62, and 20.95% for groups FX, MX, and FM, respectively. Mean BW in groups FX, MX, and FM were significantly lower than those in the control group (CX) at almost all intervals. Total serum proteins, albumin, cholesterol, aspartate transaminase, lactate dehydrogenase, and creatine kinase values were higher in all treatment groups compared with the control group. Cell-mediated immune response was more or less comparable in groups CX and MX, whereas the presence of FB(1) in the diet of groups FX and FM was found to be associated with a gradual increase in skin thickness, and the mononuclear inflammatory cell response was poor as compared with groups CX and MX throughout the study. Except for mortality (additive effect) and serum aspartate transaminase values (less than an additive effect up to 14 DPF), no additive or synergistic effects were observed for any of the other response variables measured in the current study, where all statistical differences were attributed to either one mycotoxin or the other.

Topics: Animal Feed; Animals; Blood Proteins; Coturnix; Cyclobutanes; Dermatitis, Contact; Fumonisins; Growth; Housing, Animal; Immunity, Cellular; Mycotoxins; Skin

Fusarium mycotoxins occur worldwide in cereal grains and animal feeds and cause outbreaks of Fusarium mycotoxicoses in humans and animals. In this study mammalian cell cultures were used to screen the cytotoxicity of the most common Fusarium mycotoxins; deoxynivalenol (DON), zearalenone (ZEN), fumonisin B(1) (FB(1)) and moniliformin (MON). The most sensitive cell line for each Fusarium mycotoxin was determined for further toxicological investigations as an alternative to whole animal testing. Chinese hamster ovary cells (CHO-K1) were found to be the most sensitive for DON and FB(1) with IC(50) values of 0.27 and 85.5 microg/ml, respectively, after 48-h exposure. The hepatocellular carcinoma cells (HepG2) showed the highest sensitivity to MON with IC(50) values of 39.5 for 48 h and 26.8 microg/ml for 72-h exposure. Balb/c mice keratinocyte cell line (C5-O) was found to be the most sensitive to ZEN with IC(50) of 24.1 microg/ml after 72-h exposure. DON was found the most cytotoxic to the cell cultures of all the mycotoxins tested, followed by MON, ZEN, and FB(1). The results indicated that CHO-K1, C5-O, and HepG2 cells were found to be the sensitive cell lines for preliminary screening of DON, ZEN and MON contaminated feed and food extracts, respectively.

Topics: Animal Feed; Animals; Biological Assay; Cell Line; Cell Line, Tumor; CHO Cells; Cricetinae; Cricetulus; Cyclobutanes; Dose-Response Relationship, Drug; Edible Grain; Food Contamination; Fumonisins; Fusarium; Humans; Inhibitory Concentration 50; Mice; Mice, Inbred BALB C; Mycotoxins; Time Factors; Trichothecenes; Zearalenone

Feed amended with autoclaved culture material (CM) of Fusarium proliferatum containing fumonisin B1 (FB1) (61-546 ppm), fumonisin B2 (FB2) (14-98 ppm) and moniliformin (66-367 ppm) was given to 228 male chicks in three separate feeding trials. In a fourth feeding trial, purified FB1 (125 and 274 ppm) and moniliformin (27 and 154 ppm) were given separately and in combination (137 and 77 ppm, respectively). Chicks that died during the trial periods, survivors and controls were subjected to postmortem examination. Specimens (liver, kidney, pancreas, lung, brain, intestine, testis, bursa of Fabricius, heart and skeletal muscle) were examined grossly and preserved for subsequent histopathologic and ultrastructural examination. Prominent gross lesions in affected birds fed diets amended with CM or purified FB1 and moniliformin included ascites, hydropericardium, hepatopathy, nephropathy, cardiomyopathy, pneumonitis, gizzard ulceration, and enlarged bursa of Fabricius filled with caseous material. The various concentrations of FB1 and moniliformin in the amended rations produced well-defined dose-response lesions in all groups in all four trials. Histopathologic changes included hemorrhage, leucocytic infiltration, fatty change or infiltration, individual cell necrosis and fibrosis in liver, kidneys, lungs, heart, intestines, gizzard, bursa of Fabricius and pancreas. Edema and hemorrhage were prominent in brains of treated birds. Ultrastructural changes included cytoplasmic and nuclear enlargement of cells in affected liver, lungs, kidneys, heart and pancreas. There were thickened membranes of the smooth endoplasmic reticulum, dilation of the rough endoplasmic reticulum with loss of ribosomes and vacuolated or deformed mitochondria.

Topics: Animal Feed; Animals; Chickens; Cyclobutanes; Fumonisins; Fusarium; Histocytochemistry; Male; Microscopy, Electron; Poultry Diseases

Landraces of maize (Zea mays ssp. mays) and its wild teosinte relatives (Zea mays spp. parviglumis and mexicana) were surveyed for sensitivity to fumonisin B(1), a phytotoxin produced by the maize pathogen Gibberella moniliformis. Only two of 42 Z. mays samples were highly insensitive to FB(1) (ED(50) = ca. 200 microM). The teosintes and 76% of the maize landraces were moderately or highly sensitive to FB(1) (ED(50) < or = 30 microM), which indicates that FB(1) sensitivity is likely to be an ancestral trait in Z. mays. F(1) generations derived from crosses between FB(1)-sensitive maize inbred B73 and insensitive landraces were significantly less sensitive than B73. Thus, our data indicate that FB(1)-insensitivity is a relatively rare but heritable trait in maize. We also report the sensitivity of maize to other Gibberella toxins - beauvericin, diacetoxyscirpenol, and moniliformin.

Topics: Cyclobutanes; Depsipeptides; Fumonisins; Genetic Predisposition to Disease; Genetics, Population; Gibberella; Heterocyclic Compounds, 4 or More Rings; Zea mays

In this study, Fusarium species isolated from 29 patients with mycotic keratitis were identified and tested for their ability to produce mycotoxins. Members of the F. solani species complex (Fs complex) were the predominant species isolated, followed by F. verticillioides, F. dimerum, members of the F. oxysporum species complex Fo complex), F. incarnatum, F. chlamydosporum and F. lateritium. Of these, 76% of the Fusarium isolates produced fusaric acid, moniliformin or fumonisin B1. Many of the fusaria isolated are common aetiological agents of mycotic keratitis infections. However, F. incarnatum, F. chlamydosporum and F. lateritium have previously not been found in this infection. These findings indicate that a greater variety of fusarial species are becoming associated with mycotic keratitis infections. This paper further demonstrates the mycotoxin-producing ability of these clinical isolates and assesses cellular cytotoxicity.

Topics: Animals; Cell Line; Cornea; Corneal Ulcer; Cyclobutanes; Cytotoxins; Epithelial Cells; Eye Infections, Fungal; Fumonisins; Fusaric Acid; Fusarium; Humans; Macaca mulatta; Mycotoxins

The addition of nutritionally inert adsorbents to mycotoxin-contaminated animal feed has been a popular approach to decreasing toxicity in animals and carryover of mycotoxins from contaminated feed to animal by-products. Some studies suggest that esterified glucomannan derived from the cell wall of Saccharomyces cerevisiae is effective in reducing the bioavailability of at least some of the mycotoxins occurring in contaminated feed. Because cereal grains are important components of ranch mink diets, mycotoxicoses in mink is a potential problem faced by mink ranchers. We conducted a series of studies to determine if inclusion of a commercially available esterified glucomannan in ranch mink feed was effective in alleviating clinical signs indicative of exposure to ochratoxin A, fumonisin B1, moniliformin or zearalenone in adult mink. In 4 separate trials, mink were fed diets that contained 2.5, 5 or 10 mg ochratoxin A/kg feed, 200 mg fumonisin B1/kg feed, 20 mg moniliformin/kg feed, or 30 mg zearalenone/kg feed with or without 2 g esterified glucomannan/kg feed. Male mink fed diets containing ochratoxin A had significantly decreased feed intake as well as renal lesions characteristic of exposure to that mycotoxin. Inclusion of the esterified glucomannan did not ameliorate these effects. Male mink exposed to fumonisin B1 had increased urinary sphinganine concentration, which was not significantly reduced by the mycotoxin adsorbent. Male mink that consumed monilformin-contaminated diets had characteristic ultrastructural changes in the heart that were not reduced in severity by the esterified glucomannan. Female mink exposed to zearalenone had increased uterine weight, which was not reversed by inclusion of commercial mycotoxin binder in the contaminated feed. The results of this study suggest that a commercial esterified glucomannan was generally ineffective in alleviating effects indicative of exposure to ochratoxin A, fumonisin B1, monilformin and zearalenone in mink.

Topics: Adsorption; Animal Feed; Animals; Cyclobutanes; Female; Food Contamination; Fumonisins; Male; Mannans; Mink; Mycotoxicosis; Mycotoxins; Ochratoxins; Zearalenone

Fifteen Fusarium species were analyzed by high-performance liquid chromatography for the production of six mycotoxins in corn grits cultures. Production of mycotoxins ranged from 66 to 2,500 micro g/kg for fumonisin B(1), 0.6 to 1,500 micro g/g for moniliformin, 2.2 to 720 micro g/g for beauvericin, and 12 to 130 micro g/g for fusaproliferin. Fumonisin B(2) (360 micro g/kg) was produced by two species, fumonisin B(3) was not detected in any of the 15 species examined, and Fusarium bulbicola produced none of the six mycotoxins that we analyzed.

Topics: Anti-Bacterial Agents; Chromatography, High Pressure Liquid; Cyclobutanes; Depsipeptides; Fumonisins; Fusarium; Mycotoxins; Peptides; Terpenes; Zea mays

The effects of fumonisin B1 (FB1) from Fasarium verticillioides culture material and moniliformin from Fusarum fujikuroi culture material on growing barrows were evaluated. Four groups of six barrows (three replicates of two each; mean body weight, 11.1 kg) were fed diets containing 0 mg of FB1 and 0 mg of moniliformin per kg of feed (control), 100 mg of FB1 per kg of feed, 100 mg of moniliformin per kg of feed, and 100 mg of FB1 plus 100 mg of moniliformin per kg of feed. Barrows were fed these diets for 28 days. Body weight gain, feed efficiency, serum biochemical analytes, and hematological values were adversely affected by the FB1 and the FB1-plus-moniliformin diets. The moniliformin diet decreased body weight gain. Two barrows in the moniliformin diet group died, and two barrows in the FB1-plus-moniliformin diet group died. All deaths occurred during the first 6 days of the study. Mild to moderate lesions were observed microscopically in heart and lung tissues of the groups fed moniliformin and FB1 plus moniliformin and in liver tissues of the groups fed FB1 and FB1 plus moniliformin. Except for the acute mortality associated with the two diets containing moniliformin. clinical disease induced by the combined feeding of these two mycotoxins appears to be additive or less than additive and due primarily to the toxic expression of FB1.

Topics: Animal Feed; Animals; Carboxylic Acids; Cyclobutanes; Energy Intake; Food Contamination; Food Microbiology; Fumonisins; Fusarium; Liver; Lung; Male; Myocardium; Swine; Weight Gain

Effects of feeding diets containing fumonisin B1 (FB1) and moniliformin (M), singly or in combination, on performance and immune response were evaluated in poults. Day-old poults were randomly assigned to one of four dietary treatments with four replicates of four poults each. Dietary treatments were 1) control; 2) 200 mg FB1, 0 mg M/kg diet; 3) 0 mg FB1, 100 mg M/kg diet; and 4) 200 mg FB1, 100 mg M/kg diet. In Experiment 1, poults were injected with 0.25 mL Newcastle disease virus (NDV) vaccine on Weeks 2 and 3 of the experiment, and anti-NDV antibody titers were measured 7 d after each injection. Compared with controls, poults fed FB1 had significantly lower (P < 0.05) secondary antibody response. Poults fed M and the combination of FB1 and M had significantly lower (P < 0.05) primary and secondary antibody response. Lower relative thymus weights were observed in poults fed diets containing FB1 or M. Decreased relative bursa and spleen weights were observed in poults fed M. In Experiment 2, poults were placed on dietary treatments for 3 wk. On Day 21, 2 x 10(6) peripheral lymphocytes were incubated with mitogens. Poults fed diets containing FB1 had a significantly lower (P < 0.05) proliferative response to mitogens in comparison to controls. In Experiment 3, poults were placed on the diets for 3 wk and were injected with 4.4 x 10(7) E. coli/kg body weight on Day 21. Significantly higher (P < 0.05) numbers of E. coli colonies were observed in the blood and tissue homogenates of poults fed M. In all three experiments, feed intake and body weight gains were significantly lower (P < 0.05) in turkeys fed diets containing M. Data from the present study suggest that FB1 and M are immunosuppressive in poults and that M not only suppresses immune response but also performance. However, neither synergistic nor additive effects between FB1 and M were observed for any of the parameters measured.

Topics: Animals; Antibodies, Viral; Carboxylic Acids; Cyclobutanes; Diet; Eating; Escherichia coli; Escherichia coli Infections; Female; Fumonisins; Immunity; Immunosuppressive Agents; Lymphocyte Activation; Newcastle disease virus; Turkeys; Viral Vaccines; Weight Gain

Food-grade corn and corn-based food products intended for human consumption were analyzed for the incidence and levels of fumonisin B1 (FB1), fumonisin B2 (FB2), moniliformin, and Fusarium molds. A total of 100 food-grade commercial corn samples were obtained from two corn processing companies at five different locations in the United States. Seventy-one percent of the samples contained FB1 with concentrations ranging from 43 to 1,642 microg/kg. None of the samples contained FB2. Fifty percent of the samples contained moniliformin with concentrations ranging from 26 to 774 microg/kg. All samples were infected by Fusarium molds, and the infection rates ranged from 8 to 88%. Thirty-four samples of corn-based food products were purchased from supermarkets in Arizona, California, Nebraska, and Ohio. Sixty-five percent of the samples contained FB1, ranging in concentrations from 28 to 2,679 microg/kg. FB2 was detected in 29% of the samples with concentrations ranging from 30 to 797 microg/kg. Sixty-eight percent of the samples contained moniliformin with concentrations ranging from 31 to 858 microg/kg. Sixty-two percent of the samples contained viable Fusarium mold propagules ranging from 9.5 x 10(1) to 5.5 x 10(5)/g. The simultaneous occurrence of FB1 and moniliformin was observed in 34% of corn samples and 53% of corn-based food products. This study has shown co-occurrence of fumonisins and moniliformin in food-grade corn and corn-based foods that indicates a risk of simultaneous exposure of consumers to both toxins.

Topics: Arizona; California; Carboxylic Acids; Chromatography, High Pressure Liquid; Cyclobutanes; Food Contamination; Food Handling; Food Microbiology; Fumonisins; Fusarium; Mycotoxins; Nebraska; Ohio; Zea mays

Beginning at 24 wk of age, control diets or diets containing 50 or 100 mg/kg moniliformin (M), 100 or 200 mg/kg fumonisin B1 (FB1), or a combination of 50 mg M and 100 mg FB1/kg of diet were fed to White Leghorn laying hens for 420 d. The hens were then fed the control diet for an additional 60 d. At the beginning of the experiment, each treatment consisted of four replicates of six hens. Egg production was reduced by approximately 50% by the end of the second 28-d laying period and remained at approximately this level for the 420 d in only the hens fed the diet containing 100 mg M/kg feed. Production returned to control levels or above within 60 d after hens were fed the control diet. Egg weights were reduced by the 100-mg M diet during the first three 28-d laying periods before returning to weights comparable with controls. The hens in this group also had significantly lower body weights than the other treatments. Mortality was minimal except in hens fed the 100 mg M/kg diet and the 100 mg FB1/kg diet, on which approximately 20% of the hens died. The hens were artificially inseminated with semen from males fed control diets, and fertility was not affected by the dietary treatments. Importantly, toxic synergy between M and FB1 was not observed for any of the parameters measured. Results indicate that laying hens may be able to tolerate relatively high concentrations of M and FB1 for long periods of time without adversely affecting health and performance. Interestingly, hens fed the 100-mg M/kg diet were able to recover when returned to control diets. The likelihood of encountering M or FB1 at these concentrations in finished feed is small.

Topics: Animal Feed; Animals; Body Weight; Carboxylic Acids; Chickens; Culture Media, Conditioned; Cyclobutanes; Diet; Drug Synergism; Female; Fertility; Food Contamination; Fumonisins; Fusarium; Mycotoxins; Oviposition

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.

Topics: Anti-Bacterial Agents; Carboxylic Acids; Chromatography, High Pressure Liquid; Chromatography, Thin Layer; Cyclobutanes; Depsipeptides; Fumonisins; Fusarium; Mycotoxins; Oryza; Peptides; Plant Diseases; Spectrometry, Mass, Fast Atom Bombardment; Spores

Maize samples were collected from nine Grain Marketing Board (G.M.B) centers in Zimbabwe during the 1991 harvest season. A further 47 samples collected directly from farmers and from the G.M.B., centers in Chinhoyi and Kwekwe during the 1992 harvest season. These samples were analyzed mycologically and the predominant flora was Fusarium although Penicillium, Nigrospora, Aspergillus and Chaetomium could be isolated from some samples. From the first nine samples studied, F. verticillioides and F. subglutinans were isolated in almost equal proportions on samples from the central and the south of the country whereas only F. verticillioides was isolated on the samples from the north. The subsequent study demonstrated that there was a greater fungal diversity in samples from North (Mashonaland West) than samples from the South (Midlands area) with species of Nigrospora, Chaetomium, Acremonium and Diplodia occurring in significant numbers. From a total of 2821 fungal isolates obtained from all the maize samples analyzed, 1485 (53%) were found to belong to the liseola section of Fusarium. The ability of these isolates to produce the mycotoxins zearalenone, moniliformin and fumonisin B1 was tested using a simplified TLC Agar plate method. Out of the 886 isolates tested, only one produced all the three mycotoxins simultaneously whilst most produced fumonisin B1 and/or moniliformin. Only nine isolates produced zearalenone.

Topics: Carboxylic Acids; Crops, Agricultural; Cyclobutanes; Fumonisins; Fusarium; Mycotoxins; Plant Diseases; Prevalence; Zea mays; Zearalenone; Zimbabwe

Five isolates of Fusarium moniliforme and two isolates Fusarium proliferatum of the Section Liseola were each fermented on rice for 21 d at 25 C. Each Fusarium-fermented rice, when dried and mixed into a poultry diet (10% by weight), caused a varied degree of acute mortality in baby Pekin ducklings. The acute (death in less than 48 h) mortality correlated significantly only to the amount of moniliformin in fermented rice, thus in the diet, but not to the amount of fumonisin B1 in fermented rice. This correlation of moniliformin concentration and noncorrelation of fumonisin B1 concentrations to acute toxicity were confirmed by duckling assay using diets containing these purified mycotoxins.

Topics: Animal Feed; Animals; Carboxylic Acids; Culture Media; Cyclobutanes; Ducks; Fumonisins; Fusarium; Mycoses; Mycotoxins; Poultry Diseases

Four Fusarium metabolites, 2,5-anhydro-D-mannitol, 2,5-anhydro-D-sorbitol, moniliformin, and fumonisin B1, were tested for their ability to inhibit gluconeogenesis and cell viability in a primary chicken embryo hepatocyte culture system. The hepatocyte system was established from fertilized chicken eggs that were incubated for 14 days. The hepatocytes produced and secreted glucose into the supernatant of a Krebs incubation solution amended with 3 mM of either lactate or fructose as a precursor for glucose formation. 2,5-Anhydro-D-mannitol and 2,5-anhydro-D-sorbitol inhibited gluconeogenesis in these cells from both lactate and fructose. The former anhydro sugar was more inhibitory when lactate was the precursor (50% inhibition, IC50, 6 mM) and the latter anhydro sugar more inhibitory when fructose was the precursor (IC50, 12 mM). Moniliformin was more inhibitory to glucose formation from lactate (IC50, 100 microM) than from fructose in these cells. The degrees of inhibition of gluconeogenesis by the two anhydro sugars and moniliformin were greater than their effect on cell viability. Fumonisin B1 as high as 1 mM neither inhibited gluconeogenesis, nor affected cell viability.

Topics: Animals; Carboxylic Acids; Cells, Cultured; Chick Embryo; Cyclobutanes; Fructose; Fumonisins; Fusarium; Gluconeogenesis; Liver; Mannitol

The genotoxic effects of three widespread Fusarium toxins, vomitoxin (VOM), moniliformin (MON) and fumonisin B1 (FB1) were investigated in bacterial tests and in micronucleus (MN) and chromosomal aberration (CA) assays with primary rat hepatocytes. All three toxins were devoid of activity in gene mutation assays with Salmonella typhimurium strains TA98 and TA100 and in SOS chromotests with E. coli strain PQ37 in the presence and absence of metabolic activation. FB1 and VOM gave negative results in differential DNA repair assays with E. coli K-12 strains (343/753, uvrB/recA and 343/765, uvr+/rec+); with MON, a marginal effect was seen in the absence of metabolic activation mix at relatively high concentrations (> or = 55 micrograms/ml). In metabolically competent rat hepatocytes stimulated to proliferate with EGF and subphysiological Ca2+ concentrations, a decrease of cell division was observed with all three toxins at concentrations > or = 10 micrograms/ml, VOM was strongly cytotoxic at 100 micrograms/ml. All three mycotoxins caused moderate increases of the MN frequencies at low concentrations (< or = 1 microgram/ml), but no clear dose-response effects were seen and at higher exposure levels the MN frequencies declined. In the CA experiments with hepatocytes, pronounced dose-dependent effects were observed with all three toxins. MON caused a 9-fold increase over the spontaneous background level after exposure of the cells to 1 microgram/ml for 3 h, with FB1 and VOM, the increases were 6- to 7-fold under identical experimental conditions. This is the first report on clastogenic effects of VOM and FB1 in mammalian cells, with MON induction of CAs in V-79 cells has been described earlier. Since all three mycotoxins caused CAs at very low concentration levels in liver cells in vitro, it is possible that such effects may also occur in humans and mammals upon consumption of Fusarium-infected cereals.

Topics: Animals; Carboxylic Acids; Carcinogens, Environmental; Cells, Cultured; Chromosome Aberrations; Cyclobutanes; Dose-Response Relationship, Drug; Escherichia coli; Female; Fumonisins; Fusarium; Liver; Micronucleus Tests; Mutagenicity Tests; Mutagens; Mycotoxins; Rats; Rats, Inbred F344; Salmonella typhi; Trichothecenes

Two biological species of Gibberella fujikuroi (A and F mating populations) share the Fusarium moniliforme anamorph. Twenty strains of each of these biological species were tested for the ability to produce fumonisins B1, B2, and B3 and moniliformin and for toxicity to 1-day-old ducklings. Most of the members of the A mating population (19 of 20 strains) produced more than 60 micrograms of total fumonisins per g, whereas only 3 of 20 members of the F mating population produced more than trace levels of these toxins and none produced more than 40 micrograms of total fumonisins per g. In addition, only 3 of 20 members of the A mating population produced more than 1 microgram of moniliformin per g (and none produced more than 175 micrograms/g), while all 20 strains of the F mating population produced more than 85 micrograms of this toxin per g and 1 strain produced 10,345 micrograms/g. The duckling toxicity profiles of the strains of the two mating populations were similar, however, and the level of either toxin by itself was not strongly correlated with duckling toxicity. On the basis of our data we think that it is likely that the members of both of these mating populations produce additional toxins that have yet to be chemically identified. These toxins may act singly or synergistically with other compounds to induce the observed duckling toxicity.

Topics: Animals; Cyclobutanes; Ducks; Female; Fumonisins; Fusarium; Gibberella; Male; Mycotoxins; Species Specificity

Topics: Animal Feed; Animals; Carcinogens, Environmental; Chickens; Cyclobutanes; Dose-Response Relationship, Drug; Fumonisins; Fusarium; Male; Mycotoxins; Vitamin A

Sixty nine samples of maize were collected from pre-harvest standing crops and on-farm storage facilities from 52 smallholder farms located within 4 regions of Honduras during October 1992 and November 1993. Samples were visually assessed for insect damage and fungal spoilage, and the mycoflora quantified on artificial media. The major components of the ear rot complex were: Fusarium moniliforme, F. moniliforme var. subglutinans, Penicillium species, Stenocarpella maydis, S. macrospora and Acremonium spp. Representative samples were also assayed for mycotoxin content. Fumonisin B1 was detected in all 24 samples tested at levels of between 68-6,555 (micrograms/kg), and aflatoxin was detected in 2 samples heavily contaminated with Aspergillus flavus. Moniliformin and tenuazonic acid were not detected in the samples tested. The implications of these findings for human and livestock health risk are discussed, together with possible strategies for controlling these pathogens.

Topics: Aflatoxins; Cyclobutanes; Food Microbiology; Fumonisins; Honduras; Mitosporic Fungi; Mycotoxins; Tenuazonic Acid; Zea mays

Duodenitis/proximal jejunitis syndrome (DPJ) is a small intestinal disease of horses that is associated with depression and copious gastric reflux. Since an infectious cause for DPJ remains unsubstantiated, these studies were designed to investigate the possible role of Fusarium moniliforme toxins in this disease. Fusarium moniliforme was isolated by culturing 2 samples of feed that had been fed to horses with clinical signs of DPJ. These isolates (AU 2/3) were subsequently grown concurrently on autoclaved corn and their toxicity evaluated in a feeding trial utilizing horses. Isolates of F moniliforme known to be low and high producers (RRC 415 and MRC 826, respectively) of fumonisin B1 (FB1) were cultured individually on corn and each fed separately to other groups of horses. Control horses were fed autoclaved corn that was not inoculated with fungus. Production of FB1 by isolates RRC 415, MRC 826 and AU 2/3 were 19, 4360 and 1455 ppm, respectively. Each group contained 2 horses and the test diets were prepared by diluting culture material with sweet feed and clean corn. The test diets consisted of control corn that contained < 1 ppm FB1, RRC 415 diluted to < 1 ppm FB1, MRC 826 diluted to 200 ppm FB1, and AU 2/3 culture material diluted to contain 65 ppm FB1 on days 1-10 and 130 ppm on days 11-27. Horses fed either MRC 826 or AU 2/3 had elevated serum gamma-glutamyltransferase after 7 to 21 d exposure and elevated serum L-iditol dehydrogenase activity after 7 to 19 d exposure to test diets.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animal Feed; Animals; Cyclobutanes; Duodenitis; Enteritis; Fumonisins; Fusarium; Horse Diseases; Horses; Jejunal Diseases; Male; Mycotoxins; Sphingolipids

A new toxic sesterterpene, named fusaproliferin, was purified from corn kernel cultures (120 mg/kg dry culture) of a strain of Fusarium proliferatum isolated from corn ear rot in northern Italy. The stain, designated ITEM-1494, also produced fumonisin B1 (1.500 mg/kg dry culture) and beauvericin (90 mg/kg dry culture), but not moniliformin. To monitor toxicity, the brine shrimp assay was used throughout the isolation procedure. Fusaproliferin had a molecular formula of C27H40O5, and it is the first sesterterpene isolated from a Fusarium species.

Topics: Animals; Anti-Bacterial Agents; Artemia; Carcinogens, Environmental; Culture Media; Cyclobutanes; Depsipeptides; Fumonisins; Fusarium; Magnetic Resonance Spectroscopy; Mass Spectrometry; Mycotoxins; Peptides; Terpenes; Zea mays

White Leghorn Cornell K-strain chicks (3 replicates of 16 per pen) were started at Day 7 on feed amended with Fusarium proliferatum culture material containing fumonisin B1, fumonisin B2, and moniliformin at 61, 10.5, and 42.7 ppm, respectively. Observed effects on performance of treated birds included reduced feed conversion at 2 wk, and reduced body weight of males and females up to 6 wk (P < or = .05). Splenic, thymic, and liver weights, normalized for body weight, were reduced (P < or = .05) with no change in bursa of Fabricius. No significant changes were observed histologically in the spleen, bursa, kidney, heart, liver, cecal tonsils, colon, or tibia. Significant suppression in total Ig and IgG levels occurred. Macrophages from treated chicks exhibited a 34% reduction in phagocytic activity. Natural killer cell activity was not affected. These findings, which showed that Fusarium toxins alter performance and immune end points in chickens, imply that chickens exposed to mycotoxins may be more susceptible to infectious diseases.

Topics: Animals; Antibody Formation; Body Weight; Chickens; Cyclobutanes; Female; Fumonisins; Fusarium; Immunity; Macrophages; Male; Mycotoxins; Organ Size; Sheep

Two hundred twenty-eight male broiler chicks (Columbia x New Hampshire) were given feed amended with autoclaved culture material of Fusarium proliferatum containing fumonisin B1 (FB1) at 61, 193, and 546 ppm, fumonisin B2 (FB2) at 14, 38, and 98 ppm, and moniliformin at 66, 193, and 367 ppm in 3 separate feeding trials (amounts of toxin in each trial, respectively). Birds were started on amended rations at days 1, 7, and 21 and continuing for 14 days. Of serum chemistry parameters, only glucose was significantly decreased. Significant increases were noted in serum cholesterol, sodium, alkaline phosphatase, aspartate aminotransferase, alanine aminotransferase, lactate dehydrogenase, and gamma-glutamyl transferase. Of the hematologic parameters, significant decreases were noted in red blood cell counts, hemoglobin, packed cell volume, and white blood cell counts. Immunologic changes included impaired anti-Newcastle disease antibody hemagglutination inhibition titers associated with relative decreases in total serum globulins and increases in albumin/globulin ratios. The changes were noted in all treatment groups when compared to controls.

Topics: Animal Feed; Animals; Blood Glucose; Blood Urea Nitrogen; Chickens; Cholesterol; Creatinine; Cyclobutanes; Enzymes; Erythrocyte Count; Food, Fortified; Fumonisins; Fusarium; Hemagglutination Inhibition Tests; Hemoglobins; Leukocyte Count; Male; Mycotoxins; Sodium; Teratogens; Time Factors

Two water-soluble Fusarium metabolites, fumonisin B1 (FB1) and moniliformin (MN) were compared for their cytotoxicity in a variety of chicken primary cell cultures. Cardiac and skeletal myocytes and hepatocytes derived from embryos, and splenocytes, macrophages, and chondrocytes derived from 3- to 4-week old chickens were cultured in media containing either FB1 or MN (0 to 1 mM) for 48 hr. The colorimetric tetrazolium cleavage assay was then used for measuring cell survival. FB1 was not toxic to macrophages, hepatocytes, cardiac and skeletal myocytes but toxic to splenocytes and chondrocytes. MN was not toxic to chondrocytes and macrophages, but toxic to splenocytes, cardiac and skeletal myocytes. Median effective concentration (EC50) of MN in skeletal myocytes was 42 mu M (fiducial limits: 33 to 50 mu M) and in cardiac myocytes was 95 mu M (fiducial limits: 84 to 122 mu M). Estimated EC50 of FB1 in chondrocytes and splenocytes and EC50 of MN in splenocytes were all greater than 200 mu M.

Topics: Animals; Cartilage; Cell Survival; Cells, Cultured; Chick Embryo; Chickens; Cyclobutanes; Dose-Response Relationship, Drug; Fumonisins; Liver; Macrophages; Muscles; Mycotoxins; Spleen; Toxicity Tests

A shipment of South African corn (1989) exported to Taiwan, was analyzed for various ear-rot fungi and Fusarium mycotoxins. Two sets of samples, one from the points of origin in South Africa prior to shipment, and the other from the end-point distributors in Taiwan, were studied. Surface-sterilized kernels were plated onto two different agar media and the fungal colonies identified. High Performance Liquid Chromatography was used to analyze mycotoxin levels. The predominant ear-rot fungi, in decreasing order of isolation frequency, were Fusarium subglutinans, F. moniliforme, Diploidia maydis and F. graminearum. Aspergillus flavus and A. parasiticus were not isolated from samples prior to export, but a small number of A. flavus isolates were found after shipment. The predominant mycotoxins were fumonisins B1 (0-865 ng/g) and B2 (0-250 ng/g). Low levels of moniliformin (< or = 390 ng/g) were detected in some samples before shipment. Zearalenone (25 ng/g), and nivalenol (120 ng/g) were detected in two out of 32 samples taken in Taiwan. The samples contained no detectable levels of either aflatoxins (> 0.5 ng/g) or deoxynivalenol (> 100 ng/g) before or after shipment.

Topics: Aspergillus; Aspergillus flavus; Carcinogens, Environmental; Cyclobutanes; Food Contamination; Food Microbiology; Fumonisins; Fungi; Fusarium; Mycotoxins; South Africa; Taiwan; Trichothecenes; Zea mays; Zearalenone

Peripheral blood lymphocytes were isolated from broiler chicks that had ingested feed amended with autoclaved Fusarium proliferatum culture material containing fumonisin B1 (FB1), fumonisin B2 (FB2) and moniliformin. Lymphocyte viability was determined for birds that were placed on amended rations at day 1 or day 7 of age at three different levels of mycotoxins, ranging from 61-546 ppm FB1, 14-94 ppm FB2 and 66-367 ppm moniliformin. Reduction of the tetrazolium salt, MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide], to yield MTT formazan, based on mitochondrial metabolic activity, was used to assess cell viability. Lymphocyte cytotoxic effects were observed in all treatment groups on day 21; chicks that started on amended feed at day 1 of age were affected more than those that started at day 7. Abnormal erythrocytes resembling early stages of erythroblasts were observed in peripheral blood from test chicks. Abnormally shaped red cells (poikilocytes) having a spindle-shape with one or both ends pointed were present. Some red cells appeared to be undergoing mitosis. Both reduced lymphocyte viability and abnormal erythrogenesis occurred in chicks given feed amended with F. proliferatum culture material containing FB1, FB2 and moniliformin.

Topics: Animal Feed; Animals; Carcinogens, Environmental; Cell Survival; Chickens; Cyclobutanes; Erythrocytes; Fumonisins; Fusarium; Lymphocytes; Male; Mycotoxins

Two hundred twenty-eight male chicks (Columbia x New Hampshire) were given feed amended with autoclaved culture material (CM) of Fusarium proliferatum Containing fumonisin B1 (FB1), fumonisin B2 (FB2) and moniliformin in 3 separate feeding trials. Purified FB1 and moniliformin were given separately and in combination in a fourth feeding trial. Birds were given amended rations at day 1 (Trial 1 and 4), day 7 (Trial 2), and day 21 (Trial 3) and their respective ration was given for 28 days (Trial 1), 21 days (Trial 2), 7 days (Trial 3), and 14 days (Trial 4). FB1 concentrations were 546, 193, and 61 ppm; FB2 were 98, 38 and 14 ppm; and moniliformin were 367, 193, and 66 ppm in the first 3 feeding trial regimens. Chicks in Trial 4 were given dietary concentrations of purified FB1 at 274 and 125 ppm, and moniliformin at 154 and 27 ppm. FB1 and moniliformin, both alone and in combination, produced dose-responsive clinical signs, reduced weight gains and mortality in chicks. Age of birds given amended feeds had little difference in the clinical response; however, those given the rations from days 7 or 21 were slightly less susceptible than those given rations beginning at 1 day of age. Additive effects were noted when the toxins were given in combination. When toxins were given separately, adverse effects took longer to occur. A system to monitor pattern and rate of defecation (RD) was developed for assessing the chicks' approach to feed, water and heat source as illness progressed. Our results indicate that chicks fed corn heavily infected with F. proliferatum under field conditions could suffer acute death similar to that described for 'spiking mortality syndrome' during the first 3 weeks of age.

Topics: Animal Feed; Animals; Chickens; Culture Media, Conditioned; Cyclobutanes; Fumonisins; Fusarium; Male; Mycotoxins; Poultry Diseases; Weight Gain

One hundred eight fertile eggs (Columbia x New Hampshire) were assigned to 10 groups of 10 eggs each (2 control groups had 14 eggs each). Five groups of eggs were inoculated on day 1 of incubation, while the other 5 groups were inoculated on day 10. The inoculum of the 4 treatment groups on both day 1 and 10 consisted of 1,10, or 100 microM purified fumonisin B1 (FB1) or a culture material extract (CME) of Fusarium proliferatum, having known amounts of FB1, FB2 and moniliformin (FB1 20 microM; FB2 4 microM and moniliformin 7 microM). Inoculum consisted of the respective toxin(s) dissolved in 100 microliters double distilled, autoclaved water (diluent). Control eggs were inoculated with diluent only. Mortality was both dose- and time-responsive in all treatments. Eggs inoculated on day 1 with 1 microM FB1 had 50% mortality; 10 microM FB1 had 70% mortality; 100 microM FB1 had 100% mortality; and CME had 100% mortality. Eggs inoculated on day 10 with 1,10 or 100 microM FB1 or CME had 30, 60, 90 and 80% mortality, respectively. Normal chicks were hatched from all control eggs. The median death times (MDT50) were inversely dose-responsive in all treatments, ranging from 3.0 to 7.4 days in embryos exposed on day 1 and from 3.2 to 9.0 days in those exposed on day 10. Early embryonic changes in exposed embryos included hydrocephalus, enlarged beaks and elongated necks. Pathologic changes were noted in liver, kidneys, heart, lungs, musculoskeletal system, intestines, testes and brain toxin-exposed embryos.

Topics: Animals; Chick Embryo; Culture Media, Conditioned; Cyclobutanes; Fumonisins; Fusarium; Mycotoxins; Poultry Diseases

The Fusarium moniliforme mycotoxins--fusarin C, fumonisin B1, moniliformin and bikaverin--were evaluated for genotoxicity by their ability to induce unscheduled DNA synthesis (UDS) in primary rat hepatocytes. Isolated hepatocytes were exposed to several concentrations of moniliformin (5.0-500 microM), bikaverin (1.0-500 microM), fumonisin B1 (0.5-250 microM), or fusarin C (1.0-100 microM). Aflatoxin B1, a known inducer of UDS, was included as a positive control. UDS was determined by autoradiography of cells after their exposure to [3H]thymidine. The highest doses of fusarin C and bikaverin caused cell death, but no cytotoxicity was observed in cells exposed to moniliformin or fumonisin B1. Fumonisin B1, moniliformin and bikaverin were not genotoxic in the UDS assay. The results of the UDS assay with fusarin C were inconclusive since a marginal effect on UDS was obtained.

Topics: Animals; Antineoplastic Agents; Culture Techniques; Cyclobutanes; DNA; Fumonisins; Fusarium; Liver; Male; Mutagens; Mycotoxins; Polyenes; Rats; Rats, Inbred Strains; Xanthenes; Xanthones