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PubMed2005

Suppressive effect of deoxynivalenol, a Fusarium mycotoxin, on bovine and porcine neutrophil chemiluminescence: an in vitro study.

We evaluated the immunotoxicity of deoxynivalenol (DON), a Fusarium mycotoxin, on bovine and porcine neutrophils in vitro by using two function parameters, luminol-dependent chemiluminescence and random migration under agarose. A 2-hr DON treatment suppressed the chemiluminescence of bovine and porcine cells by 42% and 35% (on average) at 10(-5)M, and by 19% and 26% at 10(-6)M. Slight suppression was observed at concentrations lower than 10(-6)M. However, after an 18-hr DON treatment, random migration of neutrophils of both species remained unaffected, even at the highest concentration (10(-5)M). Although further extensive studies are needed, to our knowledge this is the first study to have revealed in vitro that DON can affect neutrophil function.

Animals↗

PubMedDate not supplied

Metabolic conversions of trichothecene mycotoxins: de-esterification reactions using cell-free extracts of Fusarium.

A crude cell-free extract from cultures of Fusarium sp. strain C37410-90 possessed significant esterase activity and hydrolyzed the trichothecene mycotoxin 3-acetyldeoxynivalenol (3-AcDON) to deoxynivalenol (DON) in high yield. Smaller amounts of 15-acetyl- and 3,15-diacetyl-esters of DON were also formed. The extract was capable of hydrolyzing a range of natural and semisynthetic trichothecene esters, and showed a high degree of regioselectivity towards position 3. 3,4,15-Triacetylscirpentriol (TAS) was efficiently hydrolyzed to 4,15-diacetoxyscirpenol (DAS), and no further transformation was observed. The enzyme activity was partially purified.

Biotransformation↗

PubMedDate not supplied

Determination of the acute 50% lethal dose T-2 toxin in adult bobwhite quail: additional studies on the effect of T-2 mycotoxin on blood chemistry and the morphology of internal organs.

Three experiments were conducted to assess mortality rate, blood chemistry, and histologic changes associated with acute exposure to T-2 mycotoxin in adult bobwhite quail. In Experiment 1, adult quail were orally dosed with T-2 toxin to determine the lethal dose that resulted in 50% mortality of the affected population (LD50), and that dose was determined to be 14.7 mg of T-2 toxin per kilogram of body weight (BW). A second experiment was performed to study the effects of 12-18 mg/kg BW T-2 toxin on blood chemistry and liver enzyme profiles. Posttreatment uric acid, aspartate aminotransferase, lactic dehydrogenase, and gamma glutamyltransferase increased as compared with pretreatment values. In contrast, posttreatment plasma total protein, cholesterol, and triglyceride levels numerically decreased as compared with pretreatment values. Changes in blood chemistry values were consistent with liver and kidney damage after T-2 toxin exposure. In Experiment 3, histologic analyses of bone marrow, spleen, liver, small intestine, kidney, and heart were conducted on birds dosed in Experiment 2. Marked lymphocyte necrosis and depletion throughout the spleen, thymus, bursa, and gut-associated lymphoid tissue in the small intestine were observed in birds dosed with 15 and 18 mg/kg BW T-2 toxin. Necrosis of liver and lipid accumulation as a result of malfunctioning hepatocytes were also observed. Little or no morphologic change was observed in bone marrow and heart tissue. The LD50 for adult bobwhite quail as found in this study is two to three times higher than that reported for other species of commercial poultry. Results from these data confirm previous reports of immunosuppressive and/or cytotoxic effects of T-2 toxin in other mammalian and avian species. T-2 toxin may have a negative impact on the viability of wild quail populations.

Acute Disease↗

PubMed1991

Comparative fate of the tritiated trichothecene mycotoxin, T-2 toxin, in chickens and ducks.

A tritiated preparation of the trichothecene mycotoxin, T-2 toxin, was administered as a single oral dose to 21-day-old male broiler (Hubbard x Hubbard) chickens and White Pekin ducks. There were few significant differences between the two species in metabolism, tissue retention, and excretion of T-2 toxin and its metabolites. On the basis of the data obtained, the differences in toxicological sensitivity to T-2 toxin known to exist between these two species cannot likely be attributed to differences in the metabolism or elimination of T-2 toxin from the body.

Animals↗

PubMed1989

Fusarium mycotoxins from peanuts suspected as a cause of sandhill crane mortality.

An estimated 9,500 sandhill cranes (Grus canadensis) died in Gaines County, Texas and Roosevelt County, New Mexico between 1982 and 1987. The predominant clinical sign observed in sick cranes was their inability to hold their heads erect, both while standing and flying. Multiple muscle hemorrhages and submandibular edema were the most common lesions seen at necropsy. Mycotoxins produced by Fusarium sp. growing during cold, wet weather on peanuts left in the field after harvest, the predominant foods of the dead cranes at the time of these mortality events, were identified as the most likely cause of this mortality. Rendering moldy peanuts inaccessible to the cranes by conventional tillage resulted in reduced crane mortality in these areas.

Animals↗

PubMedDate not supplied

[Effect of the mycotoxin zearalenone on the metabolism of membrane phospholipids of rat lymphocytes].

The data obtained have shown that a single intravenous administration of 1 ml of mycotoxin zearalenon alcohol solution (15 mg/ml) to rats leads to the formation of pronounced abnormalities in lymphocyte membranes phospholipid (PL) metabolism. These changes are conditioned by activation of phospholipase A2, which catalyses the deacylation of PL-glycerides predominantly phosphatidylcholines with the formation of high concentrations of lysophosphatidylcholines. On the other hand, intensification of deacylation processes of PL, which accompanied by the liberation of high quantities of unsaturated fatty acids leads to the active incorporation of its into the processes of lipids free radical peroxidation with the formation of significant quantities of lipid peroxides. Intraperitoneal administration of 1 ml 10% sol of sodium thiosulfate no later then 1-2 h after zearalenon toxic action leads to the normalization of disorders observed.

Animals↗

PubMed2001

Agonistic and antagonistic effects of zearalenone, an etrogenic mycotoxin, on SKN, HHUA, and HepG2 human cancer cell lines.

Zearalenone (ZEA) is a nonsteroidal estrogenic compound mainly produced by the molds Fusarium graminearium and Fusarium culmorum found in a variety of host plants and soil debris around the world. ZEA is usualy non-lethal to animals but is important to livestock producers because its hyperestrogenic effects adversely influence the reproductive performance of animals. There have been suggestions of possible involvement of ZEA in the progression of breast malignancies and tumors of the female reproductive tract in humans. The toxic or stimulatory effects of ZEA and its metabolites alpha-zearalenol and 17-beta-estradiol on SKN, HHUAand HepG2 cells were studied using rapid colorimetric MTT assay. In general, both concentrations of 17-beta-estradiol (100M and 10 nM) were toxic to SKN and HHUA cell cultures. Both ZEA and alpha-zearalenol stimulated the proliferation of SKN and HHUA cells. On HepG2 cells, lower concentrations (10 nM) of 17-beta-estradiol and higher concentrations (100 microM) of ZEA exhibited toxic effects, whereas treatment with higher concentrations of 17-beta-estradiol and lower concentration of ZEA did not show toxic effects. A dose dependent antagonistic effect was observed when the cell cultures were pre-incubated with ICI 182,780, a synthetic estrogen receptor blocker, before estradiol or mycotoxin treatments.

Adenocarcinoma↗

PubMed2002

Suppressive effect of zearalenone, an estrogenic mycotoxin, on bovine neutrophil chemiluminescence.

The effects of zearalenone (ZEA), an estrogenic mycotoxin produced by Fusarium fungi, on bovine neutrophils were investigated in vitro using chemiluninescence, a bactericidal parameter. ZEA suppressed luminol-dependent, phorbol 12-myristate 13-acetate (PMA)-elicited chemiluminescence in a dose-dependent manner at concentrations of 10(-4) M and 10(-5) M. No significant suppression was observed at concentrations lower than 10(-6) M. The possible mode ofaction of 10(-4) M ZEA on the cell activity was investigated with special reference to intracellular Ca2+ ([Ca2+]i) release and estrogen receptors. The 10(-4) M ZEA treatment significantly impaired [Ca2+]i release. When pretreated with a low dose (10(-6) M) of PMA, the cells resisted the ZEA-induced chemiluminescence suppression. However, pretreatment of the cells with the estrogen receptor blockers Tamoxifen and ICl 182,780 (both at 10(-6) M) did not annul the suppressive ZEA action. Considering that PMA is an activator of protein kinase C (PKC), a signal transducing enzyme, and in association with a rise in [Ca2+]i causes cytosolic PKC to shift to the plasma membrane where the activated PKC triggers a varied array of cellular responses, the pharmacological dose of ZEA might have suppressed chemiluminescence by hindering the release of [Ca2+]i and the PKC shift. The results of pretreatment with estrogen receptor blockers, however, did not support the suggestion that the ZEA treatment affected the cells via estrogen receptor pathways.

Animals↗

PubMed2000

Genetic determination of variability of barley doubled haploids inoculated with Fusarium culmorum (W.G.Sm.) Sacc. with regard to mycotoxin accumulation and reduction in yield traits.

The genetic determination of variability of barley doubled haploid (DH) lines in regard of their susceptibility to Fusarium head blight caused by Fusarium culmorum was studied. The susceptibility was evaluated in 3-year field experiment on the basis of reduction in yield traits and myotoxin accumulation in infected kernels. The following traits were analysed in inoculated and control plants: kernel number and weight per ear, 1000-kernel weight, percentage of plump kernels (>2.5 mm), deoxynivalenol (DON) content and nivalenol (NIV) content of kernels. On the basis of the obtained data, heritability coefficient (ratio of genotypic to phenotypic variance) was assessed, and genetic parameters as well as the number of effective factors were estimated. Heritability coefficients calculated from two-way analysis of variance, i.e.regarding the influence of years and year x genotype interaction, appeared to be exceptionally low and ranged from 5.2% for the reduction in plump kernels to 38.2% for the reduction in 1000-kernel weight. In the case of mycotoxin accumulation about 60% of the observed variability in NIV concentrations and 30% in DON concentration resulted form genetic differences among lines. Additive effects of genes were important for all the analysed traits. Significant effects of dominance and dominance x dominance were observed for 1000-kernel weight and percentage of plump kernels. Moreover, it was found that the observed variability in yield trait reduction resulted from segregation of 5-6 effective factors, DON contents from 4 factors, while NIV content from 5 factors.

Journal Article↗

PubMed2005

[Histogenesis of lung adenocarcinoma induced by oral adminstration of mycotoxins in mice].

OBJECTIVE: To study the histogenesis and the putative mechanisms of adenocarcinoma induced by AFG1 and ST in NIH mice. METHODS: Thirty-four cases of lung adenocarcinomas induced by AFG1 and ST in NIH mice were included in this study and 12 cases of normal lung tissues were used as control. The phenotype of the lung adenocarcinomas was determined by immunohistochemical expression of SP-C and CC-10 at protein level. The expression of P53, Ras P21 and PCNA was studied with immunohistochemical staining. RESULT: The positive expression of SP-C was found in all the lung adenocarcinomas, while no expression of CC-10 could be seen. The labelling index of PCNA in the adenocarcinomas were significantly higher than that of control (P < 0.01). No positive expression of mutant P53 and Ras at protein level could be found. CONCLUSION: The lung adenocarcinomas induced by the two mycotoxins in NIH mice arise from alveolar type II cells and no expression of mutant P53 and Ras at protein level was found in the lung adenocarcinomas.

Adenocarcinoma↗

PubMed2005

Mycological analysis of cereal samples and screening of Fusarium strains' ability to form deoxynivalenole (DON) and zearalenone (ZEA) mycotoxins--a pilot study.

Filamentous fungi are cosmopolitan microorganisms found in almost all environments. It should be pointed out that occurance of moulds on food or feed may cause health disorders in humans and animals. Mycoflora appears as a source of toxic methabolites, mycotoxins, which hepatotoxic, genotoxic, nefrotoxic and carcinogenic abilities were already proven in several studies. Hense mycological analysis of cereal grains raises as an important manner in evaluation of food and feed health features. Among the most frequent cereal contaminants Alternaria, Aspergillus, Fusarium and Penicillium strains are mentioned. Due to their ability to grow on cereals during both its field growth and storage, Fusarium moulds occure to be an important contamination factors in food and feed industry. In this study Fusarium strains isolates from wheat and maize were examined in order to recognize their abilities to produce two toxins: zearalenon (ZEA) and deoxynivalenole (DON). Mycological analysis shown differentiation within fungal microflora occuring in samples of different storage conditions, where Fusarium strains represented aproximately 20-70% of all mould species present. In purpose of Fusarium strains species evaluation, isolates were mycologically analysed. In the second step of the project, toxicological screening of isolates was performed using Thin Liquid Chromatography (TLC) evaluating toxigenic potential of single strains' production of ZEA and DON. This data gives the possibility of pointing the most toxigenic strains and also shows differentiations in their occurance in cereals. This paper presents introductory research data, which can be useful in recognition of cereal contamination with moulds and their toxic methabolites.

Chromatography, Thin Layer↗

PubMed1991

[Changes in the hemostatic system after administration of the mycotoxin deoxynivalenol (vomitoxin) to rhesus monkeys].

The toxic effect of deoxynivalenol was studied in experiments on 8 test and 3 control Macaca rhesus monkeys. It has been found that differences in the hemostasis parameters depend on the frequency of deoxynivalenol administration. Normalization of the blood coagulation process is recorded after 1.5-2 months. Early diagnosis of intoxication with mycotoxins, deoxynivalenol in particular, is of great prognostic significance and may help prevent the development of irreversible changes in the body.

Animals↗

PubMed1991

[Immunoenzyme detection of the mycotoxin, ochratoxin A].

Indirect, enzymoimmunological assays of the mycotoxin ochratoxin A were developed. In this technique a polyclonal (rabbit) antibody to ochratoxin A was used, along with the other, peroxidase-labelled (pig anti rabbit) antibody. The sensitivity of this method ranged around 75 pg of ochratoxin A per pit. The range of calibration curve was from 10 to 1000 pg per pit. The cross reactions with other ochratoxins made 1.4% (ochratoxin C). The ELISA test of ochratoxin A can be used as an expeditious screening method for a preliminary examination of the greater number of samples.

Enzyme-Linked Immunosorbent Assay↗

PubMed1991

Modulation of mycotoxin and nitrosamine carcinogenesis by indole-3-carbinol: quantitative analysis of inhibition versus promotion.

The value of chemopreventive agents for reducing human response to mycotoxins and N-nitrosamines remains uncertain, especially since many such agents also can act as tumour promoters. Indole-3-carbinol (I3C) from cruciferous vegetables can inhibit DNA adduction and hepatocarcinogenesis induced by aflatoxin B1 (AFB1) or N-nitroso-diethylamine in trout if given before and with the carcinogen but promotes carcinogenesis when given after initiation. Similar results have been obtained with I3C and AFB1 in rats. In detailed studies using 10,000 trout, inhibition of AFB1 carcinogenesis was found to be saturable at high doses of I3C, approximately proportional to dose of I3C through the range of human intake and, within this range, quantitatively predicted by I3C-mediated reduction of AFB1-DNA adduction in liver. In a second study, post-initiation promotion of AFB1 carcinogenesis was approximately proportional to I3C dose, increased with duration of exposure, decreased with delayed onset of exposure, and reduced but still significant when I3C was given on alternate months or weeks or twice per week only. Hence, promotion by this common component of cruciferous vegetables required prolonged exposure but not necessarily on a daily basis.

Aflatoxin B1↗

PubMedDate not supplied

[Mycotoxins of Fusarium spp. in rotten fruits from Cucurbita ficifolia].

Swine acute toxicosis with hemorrhages was recognized after feeding on decayed chayotes (C. ficifolia fruits). In order to elucidate the origin of this pathology, chayotes spoiled by fusaria were analyzed. The mycotoxins (T-2 toxin, fusarenon X) identified in decayed chayotes, the mice alterations and the isolated species (F. equiseli, F. graminearum, F. heterosporum, F. sambucinum var. coeruleum and F. solani), suggest that the effects on swine may be due to trichothecenes produced by fusaria within fruits, and that eating damaged chayotes is dangerous for animals.

Food Contamination↗

PubMedDate not supplied

[The effect of the trichothecene mycotoxin deoxynivalenol (vomitoxin) on calcium homeostasis, vitamin D metabolism and receptors in rats].

Metabolism of calcium and vitamin D was studied in young rats administered with trichothecene-related mycotoxin deoxynivalenol (vomitoxin) at a daily dose of 10 mg/kg perorally within 7 days. The vomitoxin treatment caused a moderate hypocalcemia, a decreased absorption of calcium in small intestine as well as led to decrease of alkaline phosphatase activity in blood and small intestine mucosal membrane. Density and saturation of bone tissue with minerals were not altered. Concentration of 25-OHD in blood and activity of vitamin D3(25)-hydroxylase in liver tissue were decreased by 40% and 30%, respectively. Development of 1,25(OH)2D3 and 24,25(OH)2D3 as well as concentration of total and free 1,25(OH)2D3 receptors were not altered in kidney. At the same time, these impairments of calcium and vitamin D metabolism were prevented by providing high content of vitamin D in the ration--0.25 mg/kg of food. Impairments in calcium metabolism caused by vomitoxin may be partially related to development of a secondary deficiency in vitamin D.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗

PubMed1990

Reversal of intracellular toxicity of the trichothecene mycotoxin T-2 with monoclonal antibody.

The trichothecene mycotoxin T-2 is a potent inhibitor of intracellular protein synthesis. We have previously shown that a mouse immunoglobulin G1 monoclonal antibody (15H6) specific for T-2 toxin can neutralize the in vitro protein synthesis inhibitory effect of the toxin in human B-lymphoblastoid cultures, and protect rats from lethal toxemia. We now report that these monoclonal antibodies can induce the net efflux of [3H]-T-2 toxin from poisoned human B-lymphoblastoid cells in vitro, and restore protein synthesis. Administration of the monoclonal antibodies (250 mg/kg) 30 min before infusion of a lethal dose (1 mg/kg) of T-2 toxin causes the sequestration of the toxin in the plasma compartment. When administered 35 min after T-2 toxin, a time when the bulk of toxin is in the tissues, the monoclonal antibodies facilitate the migration of toxin back into the plasma compartment. These data demonstrate that monoclonal antibodies can be of therapeutic value against an intracellular toxin.

Animals↗

PubMed1979

Inhibition of electrogenic sodium transport across toad urinary bladder by the mycotoxin patulin.

The effects of the mycotoxin patulin (4-hydroxy-4H-furo[3,2c]pyran-2(6H)-one) on short circuited intact toad bladder and on Na+-K+, activated ATPase were examined in an attempt to elucidate the relationship between toxin, the Na+-K+ ATPase enzyme system and associated active sodium transport. Patulin inhibited transbladder short circuit current and Na+-K+ ATPase from isolated bladder preprations. The effect was exponentially dependent on time. A significantly slower rate of inhibition was achieved within 15-30 min. The results are compatible with the assumption that Na+-K+ ATPase is associated with the pump mechanism since patulin inhibited enzyme activity and concomitantly reduced the rate of electrogenic Na+ transport. A significant correlation suggested a cause-effect relationship.

Animals↗