PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Mycotoxin”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 325 records · Page 18Linked to original sources

Effects of feeding blends of grains naturally contaminated with Fusarium mycotoxins on performance and metabolism of laying hens.

An experiment was conducted to evaluate the effects of feeding laying hens grains naturally contaminated with a combination of Fusarium mycotoxins. Parameters measured included performance, organ weights, and plasma chemistry. One hundred and forty-four, 45-wk-old laying hens were fed diets including: (1) control, (2) contaminated grains, and (3) contaminated grains + 0.2% polymeric glucomannan mycotoxin adsorbent (GMA) for a 12-wk period. The feeding of contaminated grains decreased feed consumption compared with controls in the first 4 wk. Feed consumption increased, however, from 4 to 8 wk and from 8 to 12 wk. The efficiency of feed utilization (feed consumption/egg mass) decreased compared with controls in the periods from 4 to 8 and from 8 to 12 wk when birds were fed contaminated grains. Supplementation with GMA decreased feed consumption and increased the efficiency of feed utilization in the period from 8 to 12 wk. Egg production and egg mass decreased in wk 4 and 8 compared with controls when contaminated grains were fed, whereas egg and eggshell weights decreased in the fourth wk. Plasma uric acid concentrations increased throughout the experiment and relative kidney weights increased at the end of the experiment compared with controls when birds were fed contaminated grains. The feeding of GMA prevented the elevation in uric acid concentrations and relative kidney weights. It was concluded that layer performance and metabolism were adversely affected by chronic feeding of a combination of Fusarium mycotoxins, and that GMA prevented many of these effects.

Adsorption↗

Effects of feeding grains naturally contaminated with Fusarium mycotoxins on performance and metabolism of broiler breeders.

A study was conducted to investigate the effects of feeding grains naturally contaminated with Fusarium mycotoxins on performance and metabolism of broiler breeders. Forty-two 26-wk-old broiler breeder hens and nine 26-wk-old roosters were fed the following diets: (1) control, (2) contaminated grains, and (3) contaminated grains + 0.2% polymeric glucomannan mycotoxin adsorbent (GMA) for 12 wk. The major contaminant was deoxynivalenol (12.6 mg/kg of feed), with lesser amounts of zearalenone and 15-acetyl-deoxynivalenol. Feed consumption and BW were not affected by diet. The feeding of contaminated grains did not significantly affect egg production. Decreased eggshell thickness was seen, however, at the end of wk 4, and dietary supplementation with GMA prevented this effect. There was no effect of diet on other egg parameters measured. There was a significant increase in early (1 to 7 d) embryonic mortality in eggs from birds fed contaminated grains at wk 4, but mid- (8 to 14 d) and late- (15 to 21 d) embryonic mortalities were not affected by diet. There were no differences in newly hatched chick weights or viability. The ratio of chick weight to egg weight was not affected by the feeding of contaminated grains. Weight gains of chicks fed a standard broiler starter diet at 7, 14, and 21 d of age were not significantly affected by previous dietary treatments for the dam. It was found that rooster semen volume and sperm concentration, viability, and motility were not affected by the feeding of contaminated diets. There was no effect of diet on the relative weights of liver, spleen, kidney, and testes. The feeding of contaminated grains decreased antibody titers against infectious bronchitis virus at the end of wk 12, and this was prevented by dietary supplementation with GMA. There was no effect of the diet on serum antibody titers against Newcastle disease virus. It was concluded that the feeding of blends of grains contaminated with Fusarium mycotoxins could affect performance and immunity in broiler breeder hens.

Animal Feed↗

Metabolism of mycotoxins, intracellular functions of vitamin B12, and neurological manifestations in patients with chronic toxigenic mold exposures. A review.

This paper evaluates the possible reasons for consistent vitamin B12 deficiency in chronic toxigenic mold exposures and the synergistic relationships with the possible mycotoxic effects on one-carbon metabolism that lead to the manifestations of clinical neuropathological symptomology. Vitamins are first defined in general and the nutritional sources of vitamin B12 are evaluated in particular. Since patients with chronic exposures to toxigenic molds manifest vitamin B12 deficiencies, the role of mycotoxins in vitamin B12 metabolism is assessed, and since vitamin B12 plays important biochemical roles in one-carbon metabolism, the synergistic effects with mycotoxins on humans are reviewed. An outline of the proposed mechanism by which mycotoxins disrupt or interfere with the normal functions of vitamin B12 on one-carbon metabolism is proposed. The overall functions of vitamin B12 as a source of coenzymes, in intracellular recycling of methionine, in methionine synthase reaction, in the prevention of chromosome breakage, in methylation, and in maintaining a one-carbon metabolic balance are reviewed. Signs, symptoms, and clinical neurological indications of vitamin B12 deficiency are also cited. By implication and derivation, it is likely that the interruption of the structure and function of vitamin B12 would in turn interfere with the one-carbon metabolism leading to the neurological manifestations. This review is an attempt to formulate a basis for an ongoing research investigation on the subject.

Animals↗

Molecular biology of mycotoxin biosynthesis.

Mycotoxins are secondary metabolites produced by many important phytopathogenic and food spoilage fungi including Aspergillus, Fusarium and Penicillium species. The toxicity of four of the most agriculturally important mycotoxins (the trichothecenes, and the polyketide-derived mycotoxins; aflatoxins, fumonisins and sterigmatocystin) are discussed and their chemical structure described. The steps involved in the biosynthesis of aflatoxin and sterigmatocystin and the experimental techniques used in the cloning and molecular characterisation of the genes involved in the pathway are described in detail. The biosynthetic genes involved in the fumonisin and trichothecene biosynthetic pathways are also outlined. The potential benefits gained from an increased knowledge of the molecular organisation of these pathways together with the mechanisms involved in their regulation are also discussed.

Cloning, Molecular↗

Natural occurrence of mycotoxins in some cereals.

Thirty samples each of wheat and rice and 22 of maize were screened qualitatively and quantitatively for the presence of mycotoxins out of which 13, 15 and 7 samples respectively were found to be contaminated with different mycotoxins. Aflatoxin was present in 37.4% samples and besides aflatoxin, ochratoxin A, sterigmatocystin, citrinin, rubratoxin and zearalenone were also present in the cereals. The quantity of aflatoxin was highest in rice samples in comparison to wheat and maize. During the preliminary bioassay no external changes were observed in the mice except for slight weight loss when fed with grain samples, while a high rate of mortality was observed when treated with lethal doses of mycotoxins.

Animals↗

Fungal contamination and mycotoxin detection of powdered herbal drugs.

Forty-nine powdered herbal drugs were analyzed for their mold profile and for the potential presence of three mycotoxins (aflatoxin, sterigmatocystin, ochratoxin A). Aspergillus and Penicillium species were predominant, but Rhizopus, Mucor, Cladosporium, and Aureobasidium spp. were also found in a few samples. Mycotoxins were not detected in any samples, and only one isolated culture was found to be a mycotoxin producer on laboratory media.

Aflatoxins↗

Bacterial bioluminescence as a bioassay for mycotoxins.

The use of bacterial bioluminescence as a toxicological assay for mycotoxins was tested with rubratoxin B, zearalenone, penicillic acid, citrinin, ochratoxin A, PR-toxin, aflatoxin B1, and patulin. The concentrations of mycotoxins causing 50% light reduction (EC50) in Photobacterium phosphoreum were determined immediately and at 5 h after reconstitution of the bacteria from a freeze-dried state. Generally, less toxins were required to obtain an EC50 at 5 h. The effects of the above mycotoxins on bioluminescence were determined after 5, 10, 15, and 20 min of incubation with the bacterial suspensions. The concentration of rubratoxin B necessary to elicit an EC50 increased with time, whereas the concentration of citrinin, penicillic acid, patulin, and PR-toxin necessary decreased with time. There was very little change in the concentration of zearalenone, aflatoxin B1, and ochratoxin A required to elicit an EC50 with time. The bacterial bioluminescence assay was most sensitive to patulin and least sensitive to rubratoxin B.

Biological Assay↗

Simple screening method for molds producing intracellular mycotoxins in pure cultures.

A simple screening method for molds producing the intracellular mycotoxins brevianamide A, citreoviridin, cyclopiazonic acid, luteoskyrin, penitrem A, roquefortine C, sterigmatocystin, verruculogen, viomellein, and xanthomegnin was developed. After removing an agar plug from the mold culture, the mycelium on the plug is wetted with a drop of methanol-chloroform (1:2). By this treatment the intracellular mycotoxins are extracted within seconds and transferred directly to a thin-layer chromatography plate by immediately placing the plug on the plate while the mycelium is still wet. After removal of the plug, known thin-layer chromatographic procedures are carried out. The substrate (Czapek yeast autolysate agar) and growth conditions (25 degrees C for 7 days) used by Penicillium taxonomists proved suitable for the production of the mycotoxins investigated when 60 known toxigenic isolates and 865 cultures isolated from foods and feedstuffs were tested with this screening method.

Aspergillus↗

Classification of terverticillate penicillia based on profiles of mycotoxins and other secondary metabolites.

Strains of available terverticillate penicillium species and varieties were analyzed for profiles of known mycotoxins and other secondary metabolites produced on Czapek yeast autolysate agar (intracellular metabolites) and yeast extract-sucrose agar (extracellular metabolites) by using simple thin-layer chromatography screening techniques. These strains (2,473 in all) could be classified into 29 groups based on profiles of secondary metabolites. Most of these profiles of secondary metabolites were distinct, containing several biosynthetically different mycotoxins and unknown metabolites characterized by distinct colors and retardation factors on thin-layer chromatography plates. Some species (P. italicum and P. atramentosum) only produced one or two metabolites by the simple screening methods. The 29 groups based on profiles of secondary metabolites were known species or subgroups thereof. These species and subgroups were independently identifiable by using morphological and physiological criteria. The species accepted, the number of isolates in each species investigated, and the mycotoxins they produced were: P. atramentosum, 4; P. aurantiogriseum, 510 (group I: penicillic acid and S-toxin and group II: penicillic acid, penitrem A [low frequency], terrestric acid [low frequency], viomellein, and xanthomegnin); P. brevicompactum, 81 (brevianamid A and mycophenolic acid); P. camembertii group I, 38, and group II, 114 (cyclopiazonic acid); P. chrysogenum, 87 (penicillin, roquefortine C, and PR-toxin); P. claviforme, 4 (patulin and roquefortine C); P. clavigerum, 4 (penitrem A); P. concentricum group I, 10 (griseofulvin and roquefortine C), and group II, 3 (patulin and roquefortine C); P. crustosum, 123 (penitrem A, roquefortine C, and terrestric acid); P. echinulatum, 13; P. expansum, 91 (citrinin, patulin, and roquefortine C); P. granulatum, 6 (patulin, penitrem A, and roquefortine C [traces]); P. griseofulvum, 21 (cyclopiazonic acid, griseofulvin, patulin, and roquefortine C); P. hirsutum, 100 (group I: terrestric acid; group II: citrinin, penicillic acid , roquefortine C, and terrestric acid; and group III: roquefortine C and terrestric acid), P. hirsutum group IV, 2 (chaetoglobosin C); P. isariiforme, 1; P. italicum, 41; P. mali, 104; P. roquefortii, 78 (group I: mycophenolic acid, PR-toxin, and roquefortine C and group II: mycophenolic acid, patulin, penicillic acid [low frequency], and roquefortine C); P. viridicatum group I, 634 (brevianamid A [low frequency], penicillic acid, viomellein, and xanthomegnin), P. viridicatum group II and III, 494 (citrinin and ochratoxin A), P. viridicatum group IV, 12 (griseofulvin and viridicatumtoxin). It is proposed that profiles of secondary metabolites be strongly emphasized in any future revision of the penicillia.

Mycotoxins↗

Trichothecene mycotoxins in aerosolized conidia of Stachybotrys atra.

Stachybotrys atra is the etiologic agent of stachybotryotoxicosis, and this fungus and its trichothecene mycotoxins were recently implicated in an outbreak of unexplained illness in homes. S. atra was grown on sterile rice, autoclaved, dried, and then aerosolized by acoustic vibration. The distribution of particles (mass and number) was monitored on an aerodynamic particle sizer interfaced with a computer. Dust was collected on preweighed glass-fiber filters and extracted with 90% aqueous methanol. Extracts were tested for the ability to inhibit protein synthesis in rat alveolar macrophages, the ability to inhibit the proliferation of mouse thymocytes, and the presence of specific trichothecene mycotoxins. Virtually all of the particles were less than 15 micron in aerodynamic diameter, and the mass median diameter was 5 micron. Thus, most of the particles were respirable. Microscopic analysis of the generated dust revealed that ca. 85% of the dust particles were conidia of S. atra, another 6% were hyphal fragments, and the remainder of the particles were unidentifiable. Thus, greater than 90% of the particles were of fungal origin. The extracts strongly inhibited protein synthesis and thymocyte proliferation. Purified satratoxin H was also highly toxic in the same systems. Each of the individual filters contained satratoxin H (average, 9.5 ng/mg of dust). Satratoxin G and trichoverrols A and B were found in lesser amounts in some, but not all, of the filters. The limit of analysis is ca. 50 ng. These results establish that the conidia of S. atra contain trichothecene mycotoxins. In view of the potent toxicity of the trichothecenes, the inhalation of aerosols containing high concentrations of these conidia could be a potential hazard to health.

Aerosols↗

Detection of airborne Stachybotrys chartarum macrocyclic trichothecene mycotoxins on particulates smaller than conidia.

Highly respirable particles (diameter, <1 microm) constitute the majority of particulate matter found in indoor air. It is hypothesized that these particles serve as carriers for toxic compounds, specifically the compounds produced by molds in water-damaged buildings. The presence of airborne Stachybotrys chartarum trichothecene mycotoxins on particles smaller than conidia (e.g., fungal fragments) was therefore investigated. Cellulose ceiling tiles with confluent Stachybotrys growth were placed in gas-drying containers through which filtered air was passed. Exiting particulates were collected by using a series of polycarbonate membrane filters with decreasing pore sizes. Scanning electron microscopy was employed to determine the presence of conidia on the filters. A competitive enzyme-linked immunosorbent assay (ELISA) specific for macrocyclic trichothecenes was used to analyze filter extracts. Cross-reactivity to various mycotoxins was examined to confirm the specificity. Statistically significant (P < 0.05) ELISA binding was observed primarily for macrocyclic trichothecenes at concentrations of 50 and 5 ng/ml and 500 pg/ml (58.4 to 83.5% inhibition). Of the remaining toxins tested, only verrucarol and diacetylverrucarol (nonmacrocyclic trichothecenes) demonstrated significant binding (18.2 and 51.7% inhibition, respectively) and then only at high concentrations. The results showed that extracts from conidium-free filters demonstrated statistically significant (P < 0.05) antibody binding that increased with sampling time (38.4 to 71.9% inhibition, representing a range of 0.5 to 4.0 ng/ml). High-performance liquid chromatography analysis suggested the presence of satratoxin H in conidium-free filter extracts. These data show that S. chartarum trichothecene mycotoxins can become airborne in association with intact conidia or smaller particles. These findings may have important implications for indoor air quality assessment.

Air Microbiology↗

Effect of chlorine dioxide gas on fungi and mycotoxins associated with sick building syndrome.

The growth of indoor molds and their resulting products (e.g., spores and mycotoxins) can present health hazards for human beings. The efficacy of chlorine dioxide gas as a fumigation treatment for inactivating sick building syndrome-related fungi and their mycotoxins was evaluated. Filter papers (15 per organism) featuring growth of Stachybotrys chartarum, Chaetomium globosum, Penicillium chrysogenum, and Cladosporium cladosporioides were placed in gas chambers containing chlorine dioxide gas at either 500 or 1,000 ppm for 24 h. C. globosum was exposed to the gas both as colonies and as ascospores without asci and perithecia. After treatment, all organisms were tested for colony growth using an agar plating technique. Colonies of S. chartarum were also tested for toxicity using a yeast toxicity assay with a high specificity for trichothecene mycotoxins. Results showed that chlorine dioxide gas at both concentrations completely inactivated all organisms except for C. globosum colonies which were inactivated an average of 89%. More than 99% of ascospores of C. globosum were nonculturable. For all ascospore counts, mean test readings were lower than the controls (P < 0.001), indicating that some ascospores may also have been destroyed. Colonies of S. chartarum were still toxic after treatment. These data show that chlorine dioxide gas can be effective to a degree as a fumigant for the inactivation of certain fungal colonies, that the perithecia of C. globosum can play a slightly protective role for the ascospores and that S. chartarum, while affected by the fumigation treatment, still remains toxic.

Chaetomium↗

Mycotoxin-producing potential of mold flora of dried beans.

To evaluate the potential for mycotoxin production by molds in dried beans, the mold flora of 114 samples was determined both before and after surface disinfection of the beans with 5% NaOCl. Surface disinfection substantially reduced mold incidence, indicating that contamination was mainly on the surface. The flora, both before and after disinfection, was dominated by species of the Aspergillus glaucus group, the toxicogenic species A ochracues, Penicillium cyclopium, and P. viridicatum, and species of Alternaria, Cladosporium, and Fusarium. The toxicogenic species Aspergillus flavis, A. versicolor, Penicillium Citrinum, P. expansum, P. islandicum, and P. urticae were encountered less frequently. Of 209 species of Aspergillus and Penicillium screened for mycotoxin production on sterile rice substrate, 114 produced one or more of the following mycotoxins: A. flavus, aflatoxins; A. ochraceus, ochratoxins; A. nidulans, A. unguis, and A. versicolor, sterigmatocystin; P. cyclopium, penicillic acid; P. citrinum and P. viridicatum, citrinin; P. urticae, patulin and griseofulvin. Sterigmatocystin production by A. unguis is reported for the first time.

Aflatoxins↗

Mycotoxins.

Mycotoxins are secondary metabolites produced by microfungi that are capable of causing disease and death in humans and other animals. Because of their pharmacological activity, some mycotoxins or mycotoxin derivatives have found use as antibiotics, growth promotants, and other kinds of drugs; still others have been implicated as chemical warfare agents. This review focuses on the most important ones associated with human and veterinary diseases, including aflatoxin, citrinin, ergot akaloids, fumonisins, ochratoxin A, patulin, trichothecenes, and zearalenone.

Aflatoxins↗

Alteration of immune function following dietary mycotoxin exposure.

Mycotoxins are a group of structurally diverse fungal secondary metabolites that elicit a wide spectrum of toxicologic effects. Of particular interest is the capacity of some mycotoxins to alter normal immune function when present in foods at levels below observable overt toxicity. Aflatoxin, patulin, citrinin, and zearalenone experimentally alter immunity, and recent evidence suggests that the immunologic effects of ochratoxin A and trichothecenes may have particular significance to human and animal health. For example, the capacity of ochratoxin A to inhibit natural killer cell activity and increase growth of transplantable tumour cells has been associated with renal and hepatic carcinomas in mice and might similarly contribute to human cancer. Impaired resistance to pathogenic microorganisms occurs after exposure to the trichothecenes T-2 toxin and vomitoxin. This may predispose food animals to infectious disease and could result in decreased productivity as well as increased animal-to-human transmission of pathogens such as Salmonella and Listeria. Vomitoxin also alters normal mucosal immune function, specifically at the level of regulation of development, differentiation, and homing of IgA-producing plasma cells. Interestingly, vomitoxin-induced enhancement of IgA production in the systemic compartment contributes to manifestations in the mouse that are highly analogous to human IgA nephropathy, the most common form of human glomerulonephritis worldwide. Over the long term, the extrapolation of mycotoxin-induced immunologic effects observed in inbred mice to actual disease in livestock and humans will require investigations that both simulate natural exposure conditions as well as improve understanding of the cellular and molecular bases for these effects among different species.

Animals↗

Uncertainties in the risk assessment of three mycotoxins: aflatoxin, ochratoxin, and zearalenone.

The risk assessment of mycotoxins is made up of two major components: an exposure assessment and a hazard assessment. There are many uncertainties in both of these components. This paper will briefly discuss the various aspects of the risk assessment process as it applies to mycotoxins and will then focus mainly on some of the uncertainties in the hazard assessment component of several carcinogenic mycotoxins. To arrive at an estimated "safe dose" (end point of the hazard assessment), we have previously used two major approaches: the no observed effect level (NOEL) divided by a safety factor approach and a mathematical (robust linear) extrapolation to a "virtual safe dose." Both of these approaches use only points from the no observed effect region of the dose-response curve and ignore valuable data from the response region. It is proposed to use the dose at which 50% of the animals would have developed tumors (the TD50) divided by a large safety factor of 50,000 as an additional estimate of "safe dose". For many studies, the TD50 lies within the observed response region of the dose-response curve and may have more validity. It is also suggested in certain cases that some of the uncertainties regarding the NOEL can be reduced if one uses a statistically derived no effect level (NEL).

Aflatoxins↗

Experimental IgA nephropathy induced by a low-dose environmental mycotoxin, nivalenol.

Based on the hypothesis that IgA nephropathy (IgAN) is triggered by some exogenous antigen(s) which induces dysregulation of the mucosal immune system, we developed an experimental model of orally induced IgAN by an environmental mycotoxin, nivalenol (NIV), which often contaminates agricultural products in Southeast Asia and Japan. In the present study, low doses of oral NIV reproducibly induced significant IgA deposits in the glomerular mesangium and elevated serum IgA levels in mice irrespective of the strain; the degree of immunopathological changes analogous to human IgAN was associated with the dose and duration of NIV treatment. Furthermore, a competitive enzyme-linked immunosorbent assay with an NIV analogue-protein conjugate disclosed that the IgA antibody in the sera from the NIV model mice had a higher affinity to the mycotoxin. Conclusively, these findings suggest that NIV induces some pathological changes in mice which resemble those in human IgAN, and that this mycotoxin is associated with pathogenesis in some types of glomerulonephritis.

Animals↗

Toxigenic fungi and mycotoxins.

Growth of commonly occurring filamentous fungi in foods may result in production of toxins known as mycotoxins, which can cause a variety of ill effects in humans, from allergic responses to immunosuppression and cancer. The most important mycotoxins are aflatoxins, ochratoxin A, fumonisins, trichothecenes and zearalenone. Aflatoxins are potent carcinogens and, in association with hepatitis B virus, are responsible for many thousands of human deaths per annum, mostly in non-industrialised tropical countries. Ochratoxin A is a probable carcinogen, and may cause urinary tract cancer and kidney damage in people from northern and eastern Europe. Fumonisins appear to be the cause of oesophageal cancer in southern Africa, parts of China and elsewhere. Trichothecenes are highly immunosuppressive and zearalenone causes oestrogenic effects in animals and man. Currently available records and statistics do not reflect the major role played by mycotoxins in mortality attributable to food-borne micro-organisms.

Food Microbiology↗