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PubMed1986

In vitro activity of alpha, beta, gamma human interferons and Aspergillus terreus mycotoxins on cell proliferation.

The in vitro effect of different doses of alpha, beta and gamma human interferons and their interaction on the proliferation rate of human erythroleukemic cell line (K-562) and other cell lines has been evaluated. The results show that the stronger activity is exerted by beta HIF in comparison with alpha HIF. The action is selective and species-specific. beta HIF never elicited an "enhancing" effect on cell proliferation; on the contrary this phenomenon has been observed to occur with alpha and gamma HIF. In our cell system, the interaction between beta and gamma HIF gave a synergistic effect; on the contrary, no interaction has been observed to take place when beta HIF and directly cytotoxic mycotoxins extracted from A. terreus are associated.

Cell Division↗

PubMed1989

Risk assessment of the mycotoxin ochratoxin A.

Ochratoxin A (OA) is a mycotoxin which has been found to occur in foods of plant origin, in edible animal tissues, as well as in human blood sera and tissues. The ability of OA to move up the food chain is aided by its long half-life in certain edible animal species. In this report, an evaluation of the health risks to Canadians due to the presence of OA in food products is presented. The first part of the report deals with the physicochemical aspects, mycology, laboratory production, analytical methods, and natural occurrence in plant products, animal products, and human tissues. The stability of OA in foods and feeds, the effects of food processing, and the removal from foods and feeds by physiochemical means are also discussed. From these data, the worst case estimate for the daily exposure of Canadians to OA, from the consumption of pork-based food products and cereal foods, is approximately 5 ng OA/kg body wt (mean of eaters) for young children, the highest consumption group on a body weight basis. The second part of the report deals with the metabolic disposition as well as the available toxicity database for OA in laboratory animals, farm animals, and humans. The major target for OA toxicity in all mammalian species tested is the kidney, and endemic nephropathies affecting livestock as well as humans have been attributed to OA. OA is also teratogenic, and in the fetus the major target is the developing central nervous system. Recent studies have provided "clear evidence" of the carcinogenicity of OA in two rodent species. OA was found to be nonmutagenic in various microbial and mammalian gene mutation assays, but weak genotoxic activity to mammalian cells was noted. In addition, OA was found to suppress immune function. Based on the NTP carcinogenicity study with OA in rats, the estimated tolerable daily intake in humans ranges from 0.2 to 4.2 ng OA/kg body wt, depending on the method of extrapolation used. In view of the toxic properties of OA, it is recommended that exposure to OA be kept to a minimum. In Canada, further monitoring programs are required to better define the overall residue profile of OA in cereal grains, animal feeds, animal food products, and human blood. Such data are required to better assess dietary exposure and to ascertain the need for regulatory controls or other control mechanisms.

Abnormalities, Drug-Induced↗

PubMedDate not supplied

Mycotoxin analysis by fast atom bombardment tandem mass spectrometry.

Positive fast atom bombardment tandem mass spectrometry is demonstrated to be an effective technique for determination of crude aflatoxins and sterigmatocystin-related compounds. The molecular ion was selected by the first system and bombarded to produce characteristic daughter ions that could be used to identify mycotoxins in mixtures and with the same molecular weight.

Aflatoxins↗

PubMedDate not supplied

Isolation and characterization of 4'-hydroxy T-2 toxin, a new metabolite of the trichothecene mycotoxin T-2.

Biotransformation of the trichothecene mycotoxin T-2 by the hepatic S-9 fraction prepared from phenobarbital-treated rats yielded a new metabolic product designated RLM-3. The metabolite was purified from the hepatic preparation using preparative HPLC. The structural analysis of RLM-3 was carried out using gas chromatography/mass spectrometry and 1H and 13C NMR. RLM-3 was identified as 4'-hydroxy T-2. The toxicity of RLM-3 in comparison to T-2 toxin and 3'-hydroxy T-2 was assessed using a rat skin bioassay technique. The metabolite 4'-hydroxy T-2 was shown to be deacylated at the C-4 position to yield 4'-hydroxy HT-2 when incubated with rat hepatic S-9 preparations.

Animals↗

PubMedDate not supplied

Metabolic conversions of trichothecene mycotoxins: biotransformation of 3-acetyldeoxynivalenol into fusarenon-X.

The trichothecene mycotoxin 3-acetyldeoxynivalenol was transformed by cultures of the diacetoxyscirpenol producer Fusarium sp. strain C37410-90 into four compounds, identified as deoxynivalenol, 15-acetyldeoxynivalenol, 3,15-diacetyldeoxynivalenol and fusarenon-X. The major transformations are the result of specific esterification and de-esterification processes, but the production of fusarenon-X involves in addition a novel 4 beta-hydroxylation of the trichothecene ring system itself.

Biotransformation↗

PubMed1988

Effects of T-2 mycotoxin ingestion on phagocytosis of Aspergillus fumigatus conidia by rabbit alveolar macrophages and on hematologic, serum biochemical, and pathologic changes in rabbits.

Rabbits were given T-2 mycotoxin orally at 0, 0.25, 0.5, and 0.75 mg/kg of body weight/day for 21 days. Only rabbits in the 0.75 mg/kg/day group (4 of 5 rabbits) died. Alveolar macrophages were harvested on day 22 and used for in vitro phagocytosis of killed Aspergillus fumigatus conidia. Cultures included sera from untreated rabbits or rabbits treated with T-2. Phagocytosis was significantly (P less than 0.01) reduced in cultures that used serum from rabbits treated with 0.5 mg of T-2/kg/day and alveolar macrophages from untreated rabbits or rabbits treated with T-2. There was little reduction in phagocytosis when alveolar macrophages from rabbits treated with T-2 and normal serum were used. Ingestion of 0.5 mg of T-2 toxin/kg/day significantly (P less than 0.05) reduced weight gain, serum alkaline phosphatase activity, serum sorbitol dehydrogenase activity, and serum bacteriostasis. Similar changes were found in the 0.75 mg/kg/day group, as well as a significant (P less than 0.05) reduction in PCV, total WBC, and differential leukocyte counts. Neutrophil counts decreased, but not significantly (0.05 less than P less than 0.10). Significant changes were not detected in alanine transaminase activity, aspartate transaminase activity, blood urea nitrogen concentration, or complement hemolytic activity. Histopathologic changes consisting of centrilobular hepatocellular swelling, mild portal and periportal fibrosis and lymphocyte necrosis within secondary lymphoid tissues developed in most rabbits treated with T-2. Thymic atrophy, bile duct reduplication, and lymphocyte depletion of secondary lymphoid tissues developed in the group given 0.75 mg/kg/day.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1988

Pathologic, hematologic, and serologic changes in rabbits given T-2 mycotoxin orally and exposed to aerosols of Aspergillus fumigatus conidia.

The influence of immunosuppression by T-2 mycotoxin on the fungal disease aspergillosis was investigated in rabbits. Four groups of rabbits (groups 1A, 1B, 3A, and 3B) were given 0.5 mg of T-2 toxin/kg of body weight/day, PO; in addition, rabbits of groups 3A and 3B were exposed to aerosols of Aspergillus fumigatus conidia from days 7 through 16. Rabbits of groups 2A and 2B were exposed to A fumigatus aerosols, but were not given T-2 toxin, and rabbits of group 0 served as controls. Two rabbits of group 1A, 1 rabbit of group 1B, and 1 rabbit of group 3A died before scheduled necropsy. Rabbits of groups 1A, 2A, and 3A were killed and necropsied on day 17, and the remaining rabbits (groups 0, 1B, 2B, and 3B) were killed and necropsied on day 28. Changes caused by T-2 toxin included leukopenia, marginal anemia, and increased number of and morphologic changes in nucleated erythrocytes by day 21, followed by a regenerative hematologic response. Serum alkaline phosphatase and sorbitol dehydrogenase activities and antibody response to A fumigatus (as measured by an indirect hemagglutination test) were decreased by T-2 toxin ingestion. Rabbits with aspergillosis had leukocytosis, increased PCV, and increased antibody response to A fumigatus. Histologic lesions consisting of centrilobular hepatocellular swelling, portal and periportal fibrosis, and lymphocyte necrosis and/or depletion within secondary lymphoid tissue were observed in most rabbits treated with T-2 toxin. Normal defense mechanisms against A fumigatus infection were compromised by T-2 treatment, as evidenced by the severity and extent of lung lesions, greater number of hyphal elements observed, and greater number of colonies of A fumigatus isolated from rabbits of groups 3A and 3B. There were no significant changes in group-0 rabbits.

Administration, Oral↗

PubMed1988

[Radioimmunologic determination of the mycotoxin ochratoxin A--a new diagnostic method in Czechoslovakia].

A new radioimmunological method was developed for the determination of the mycotoxin ochratoxin A. The specific antibodies used in this method had been prepared by the immunization of rabbits by means of administration of ochratoxin A conjugate with bovine serum albumin. Their effective affinity constant was Ka = 5.1 X 10(-9) l. Mol-1. The substance used as radioligand was 125I-ochratoxin with a high specific radioactivity (Czechoslovak patent PV 6136, 1986). The average sensitivity of determination (ED 85%) was 10 to 15 picograms per 0.1 ml of sample. The range of the calibration curve was mostly from 5 to 360 picograms.

Animals↗

PubMed1988

Targeting of mycotoxins to reticuloendothelial system of mice with carrier erythrocytes.

The tricothecene mycotoxin, T-2 toxin, was encapsulated in bovine erythrocytes for in vivo delivery of T-2 toxin to macrophages. Intraperitoneal injection of bovine carrier erythrocytes (5 X 10(8) cells) containing T-2 toxin saturated mouse liver uptake of erythrocytes by 6 h postinjection. At 24 h postinjection, 20% of the injected carrier cells containing toxin were localized in the liver of mice. Saturation of the liver uptake of bovine carrier cells was independent of encapsulated or free T-2 toxin. A dose of T-2 toxin sufficient to inhibit 50% of the macrophage protein synthesis was targeted to the liver via the carrier erythrocytes. A methodology for delivery of highly toxic molecules to liver macrophages is described.

Animals↗

PubMedDate not supplied

Isolation and liquid chromatographic determination of the cyclic peptide mycotoxin cyclosporin A from rice.

A simple method for determination and quantitation of a cyclic peptide mycotoxin, cyclosporin A, in rice is presented. Rice inoculated with Trichoderma polysporum (Link ex Pers.) was extracted with methylene chloride after 4 weeks of incubation. Cyclosporin A was isolated from extracts by using open bed gel filtration column chromatography (LH-20, acetonitrile) and monitored with thin layer chromatography and reverse phase liquid chromatography coelution with a standard. Preliminary thin layer chromatographic methods were developed. Cyclosporin A was detected by iodine and after partial acid hydrolysis by ninhydrin and UV light. A liquid chromatographic method was developed that used a reverse phase disposable cartridge cleanup and isocratic chromatography with a reverse phase octadecylsilica column and a UV detector set at 212 nm. Recovery of cyclosporin A from spiked rice samples (mg/g range) was 85%.

Chromatography, Liquid↗

PubMedDate not supplied

Detection and quantitation of T-2 mycotoxin in rat organs by radioimmunoassay.

A standard radioimmunoassay was compared with radiochromatography for the ability to detect unlabeled T-2 mycotoxin in organs from exposed animals. When 10% of HT-2, the only known metabolite that cross-reacts with T-2, was included and expressed as T-2 equivalents in the radiochromatographic detection, correlation between toxin detection in liver, spleen, and kidney by the 2 techniques was r = 0.98. An unknown metabolite was detected in heart extract by radiochromatography. Inclusion of this material in the T-2 equivalents detected by radiochromatography indicated a near-perfect correlation (r = 0.95; p greater than 0.05; slope = 0.82; y = intercept = 72) among all 4 tissues.

Animals↗

PubMedDate not supplied

Use of solid-phase extraction systems to improve the sensitivity of Artemia bioassays for trichothecene mycotoxins.

Solid-phase extraction was used to preconcentrate trichothecene mycotoxins from rivers and streams in order to develop and improve a rapid and sensitive bioassay using the brine shrimp Artemia salina. For T-2 toxin, HT-2 toxin, and 4,15-diacetoxyscirpenol, LC50 values obtained were 172, 600, and 700 micrograms/L, respectively. The LC50 for 4-deoxynivalenol was 21 mg/L. A more than 5-fold increase in sensitivity was observed when solid-phase extraction (SPE) was used in conjunction with the Artemia bioassay. For T-2 toxin, HT-2 toxin, and 4,15-diacetoxyscirpenol, LC50/SPE values after solid-phase extraction were 21, 83, and 130 micrograms/L. The use of river and stream waters and chlorinated water did not seem to interfere with the bioassay.

Animals↗

PubMedDate not supplied

Liquid chromatographic determination and stability of the Fusarium mycotoxin moniliformin in cereal grains.

Moniliformin is a mycotoxin produced by Fusarium subglutinans and other Fusarium species. A rapid, liquid chromatographic method for its determination in corn and wheat is described. Samples are extracted in acetonitrile-water (95 + 5); following defatting with n-hexane, an aliquot of the extract is evaporated and cleaned up on small C18 and neutral alumina columns successively. Reverse-phase liquid chromatography (LC) is conducted on a C18 column with 10 or 15% methanol or acetonitrile in aqueous ion-pair reagent as mobile phase, with detection by ultraviolet absorption at 229 and 254 nm. Average recoveries of moniliformin (potassium salt) added to ground corn and wheat at levels of 0.05-1.0 micrograms/g were 80% (n = 20) and 85% (n = 12), respectively, and the limit of detection was ca 0.01-0.18 micrograms/g, depending on LC conditions. Analysis of 24 samples of wheat, 4 samples of rye, and 12 samples of corn showed moniliformin in only 2 corn samples (0.06 and 0.2 micrograms/g). Moniliformin was also detected in a sample of artificially damaged (slashed) corn (0.2 micrograms/g) and selected kernels of corn that were field-inoculated with F. subglutinans and F. moniliforme (50 micrograms/g and 0.5 micrograms/g, respectively). In stability studies, moniliformin (potassium salt, 1 microgram/g) in ground corn and ground wheat heated at 50, 100, and 150 degrees C for 0.5-2 h decomposed moderately, e.g., 55% remained in corn after 0.5 h at 100 degrees C.

Chromatography, Liquid↗

PubMed1986

Acute toxicity of T2 mycotoxin to the guinea-pig by inhalation and subcutaneous routes.

The acute inhalation and subcutaneous toxicity of T2 mycotoxin has been investigated in guinea-pigs. The toxicity by the two routes was quantitatively and qualitatively similar. The LCt50 was 5749 mg min m-3 and the subcutaneous LD50 1-2 mg kg-1. Histological changes in the decedents which were similar by both routes of administration were most marked in the lymphoreticular system but also occurred in the gut. Lymphocytolysis and phagocytosis occurred in both the cortex of the thymus and of the lymph nodes. Lymph nodes were more severely affected in the decedents among the animals dosed with T2 by the subcutaneous route. The small intestine exhibited dead and dying cells throughout the lamina propria after T2 by either route.

Aerosols↗

PubMed1985

[Developments in research on mycotoxins].

Since the early 1960's attention has been paid to mycotoxins by various disciplines of the National Institute of Public Health and Environmental Hygiene (RIVM) (Analytical Chemistry, Microbiology, Toxicology). A major part of the work is carried out at the request of the Chief Medical Office. The activities undertaken on behalf of the Chief Veterinary Officer concern investigations on the causes of fungal growth and toxin production as well as on the presence of aflatoxin B1 and the analytical possibilities of determining aflatoxin B1 in feeds and aflatoxin M1 in milk. Because of its structural relationship with aflatoxin B1, aflatoxin M1 is suspected of having carcinogenic properties. In order to be able to do chronic toxicity studies in rats, efforts are being made to synthesize approximately 25 g. of aflatoxin M1 in co-operation with the State University of Utrecht, which was found to be a time-consuming and extremely difficult job. From the point of view of the Chief Veterinary Officer, it is expected that the analytical and toxicological features of aflatoxin M1 will continue to be of interest in the near future.

Aflatoxin B1↗

PubMed1979

Protein synthesis inhibition in rat liver by the mycotoxin patulin.

Patulin, a carcinogenic mycotoxin, inhibits in vivo and in vitro protein synthesis in rat liver. The in vivo inhibition culminates 5 h after toxin administration and reaches a maximum of 65% with regard to control values; a breakdown of polysomes is associated with the translational blockage. However in in vitro systems, the cellular fractions obtained from patulin-treated rats appear equally as active in protein synthesizing ability and as sensitive to the toxin action as those prepared from control animals. The in vitro inhibition by patulin is dose related. The postmitochondrial system is less sensitive than that functioning with isolated polysomes and pH 5 enzyme. This difference might be due to the presence of soluble factor(s) that counteract patulin action. We propose that the inhibition of protein synthesis by patulin may result from an interaction of the drug with active SH groups at the membrane level (amino acid transport, ion equilibrium) and/or at the cytoplasmic level (enzymes and factors involved in the translational process).

Amino Acids↗

PubMed1983

Genotoxicity of Fusarium mycotoxins (nivalenol, fusarenon-X, T-2 toxin, and zearalenone) in Chinese hamster V79-E cells in vitro.

The mycotoxins nivalenol, fusarenon-X, T-2 toxin and zearalenone were checked for clastogenic damage, induction of SCEs and cell cycle delay in Chinese hamster V79-E cells in vitro. The trichothecenes nivalenol, fusarenon-X and T-2 toxin provoked a marked toxicity as especially expressed by cell cycle delay. As compared to toxicity, they are weak clastogens. Addition of S9 mix toxified nivalenol, detoxified T-2 toxin and had no marked influence on fusarenon-X activity. SCE values were slightly increased. It is suggested that the effects observed are unspecific and are caused by inhibition of protein synthesis. Zearalenone was inactive in the three assays. Problems of genotoxicity and carcinogenicity of Fusarium toxins are discussed.

Animals↗

PubMed1994

[Ochratoxin A, ubiquitous mycotoxin contaminating human food].

Ochratoxin A (OTA) a mycotoxin produced by molds of the Aspergillus and Penicillium genera, contaminates animal feeds and human foods. It has been shown to induce renal adenomas and hepatocellular carcinomas in rodents. OTA is implicated in Balkan endemic nephropathy, a disease followed by a high incidence of urinary tract tumours. Concerning the genotoxicity of OTA, we have recently shown, using the [32P]-phosphate postlabelling method, that several DNA-adducts are formed in four mice organs treated with OTA. Some of the adducts were specific of every analyzed tissue. These results, allow us to state that OTA metabolism in different from organ to organ. The influence of OTA metabolism on its genotoxic effect was studied. Preliminary results have shown the possibilities of oxidative pathways in OTA metabolism leading to genotoxic compounds. Effects of some vitamins such as retinol (A), ascorbic acid (C) and tocopherol (E), which are known to act as superoxide anion scavengers, were tested on genotoxicity of OTA. Pretreatment of mice by vit E induced a decrease of the DNA-adducts by 80% in kidney, and by 55% in liver. Vit A and vit C decreased DNA-adduct levels by 70% in kidney. In liver, DNA adduct level was essentially decreased by vit C (90%). Vit A decreased only the level by 25% in this organ. The involvement of oxidative metabolism in the genotoxicity of OTA led us to investigate the effect of prostaglandin H synthase (PHS) which is known to cooxidase xenobiotics. Aspirin and indomethacin which inhibit this enzyme were given prior to OTA administration to mice in order to test this metabolic pathway. The decrease observed with aspirin was of about 90% and 30% in kidney and liver respectively, and of 90% and 80% with indomethacin in kidney and liver. These results confirmed that OTA is activated to genotoxic metabolites by cooxydation by the prostaglandin synthase route. Human bronchial epithelial cells (BEAS-2B) expressing or not human cytochrome P450s (CYP) (1A2, 2A6, 2D6, 2E1 and 3A4) were incubated with 0.5 microM OTA for 24 h. DNA-adducts were detected in all cells. Total DNA-adduct levels ranged from 4 to 85 adducts per 10(9) nucleotides. Some adducts were common to all cell types including cells expressing only normal phase II enzymes, but no cytochromes P450. Some other DNA-adducts were only induced by specific CYPs. The highest DNA-adduct level was found in cells where CYP 1A2 was expressed. Nevertheless, more different types of DNA-adducts were formed in cells expressing CYP 2D6.(ABSTRACT TRUNCATED AT 400 WORDS)

Abnormalities, Drug-Induced↗