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PubMed1999

A colorimetric technique for detecting trichothecenes and assessing relative potencies.

We tested a novel colorimetric toxicity test, based on inhibition of beta-galactosidase activity in the yeast Kluyveromyces marxianus, for sensitivity to a range of mycotoxins. A variety of trichothecene mycotoxins could be detected. The order of toxicity established with this bioassay was verrucarin A > roridin A > T-2 toxin > diacetoxyscirpenol > HT-2 toxin > acetyl T-2 toxin > neosolaniol > fusarenon X > T-2 triol > scirpentriol > nivalenol > deoxynivalenol > T-2 tetraol. The sensitivity of detection was high, with the most potent trichothecene tested, verrucarin A, having a 50% effective concentration (concentration of toxin causing 50% inhibition) of 2 ng/ml. Other mycotoxins (cyclopiazonic acid, fumonisin B1, ochratoxin A, patulin, sterigmatocystin, tenuazonic acid, and zearalenone) could not be detected at up to 10 micrograms/ml, nor could aflatoxins B1 and M1 be detected at concentrations up to 25 micrograms/ml. This test should be useful for trichothecene detection and for studies of relevant interactions-both between trichothecenes themselves and between trichothecenes and other food constituents.

Biological Assay↗

PubMed1981

[Foreign substances in the meat and organs of bulls fed on a diet of swine and poultry fecal waste].

The meat and some organs of eight bulls given diet with 5% to 15% supplements of dried pig and poultry excrements for 175 days were subjected to examination for the presence of some foreign substances. The results were compared with samples from eight control bulls, fed the basal diet. Liver was not found to contain any aflatoxins B1 and M1. No statistically significant differences were found in the content of antimicrobial substances. The same can be said of the content of chlorinated pesticides. Residues of organo-phosphorus pesticides were not detected at all. As to chemical elements, the test bulls were found to have a significantly increased content of copper in liver and diaphragm. All the findings of the residues of foreign substances were within limits tolerated by veterinary regulations.

Animal Feed↗

PubMedDate not supplied

Simple, rapid cleanup method for analysis of aflatoxins and comparison with various methods.

A method is described for simple and rapid determination of aflatoxins in corn, buckwheat, peanuts, and cheese. Aflatoxins were extracted with chloroform-water and were purified by a Florisil column chromatographic procedure. Column eluates were concentrated and spotted on a high performance thin layer chromatographic (HPTLC) plate, which was then developed in chloroform-acetone (9 + 1) and/or ether-methanol-water (94 + 4.5 + 1.5) or chloroform-isopropanol-acetone (85 + 5 + 10). Each aflatoxin was quantitated by densitometry. The minimum detectable aflatoxin concentrations (micrograms/kg) in various test materials were 0.2, B1; 0.1, B2; 0.2, G1; 0.1, G2; and 0.1, M1. Recoveries of the aflatoxins added to corn, peanut, and cheese samples at 10-30 micrograms/kg were greater than 69% (aflatoxin G2) and averaged 91%, B1; 89%, B2; 91%, G1; 78%, G2; and 92%, M1. The simple method described was compared with the AOAC CB method, AOAC BF method, and AOAC milk and cheese method. These methods were applied to corn, peanut, and cheese composites spiked with known amounts of aflatoxins, and to naturally contaminated buckwheat and cheese. Recoveries were much lower for the BF method compared with our simple method and the CB method.

Aflatoxins↗

PubMed1984

Glucuronides in bile of rainbow trout (Salmo gairdneri) injected with [3H]aflatoxin B1 and the effects of dietary beta-naphthoflavone.

Rainbow trout Salmo gairdneri were fed a diet containing the mixed-function oxidase system inducer, beta-naphthoflavone or were fed a control diet. For the two respective diets, as much as 50 and 12% of an i.p.-injected dose of [3H]aflatoxin B1 was recovered in the bile. The major product in the bile of beta-naphthoflavone-fed trout was an aflatoxicol-M1 glucuronide, whereas the major product in the control bile was an aflatoxicol glucuronide.

Aflatoxin B1↗

PubMed1998

Systemic aspergillosis caused by an aflatoxin-producing strain of Aspergillus flavus.

The first case of human systemic infection by an Aspergillus flavus isolate demonstrated to produce aflatoxins in vitro and in vivo is described. The patient, a 41-year-old man with acute myelogenous leukaemia, developed a complication of suspected pulmonary Aspergillus infection during remission induction therapy. Antifungal chemotherapy brought about a considerable degree of improvement, but remission of the underlying disease was not attained. Bone marrow transplantation was also not effective. The patient showed recovery from neutropenia but died despite aggressive antifungal chemotherapy. The autopsy revealed lesions in the lungs, myocardium, kidneys, brain, thyroid gland and skin due to a suspected Aspergillus sp. A fungus isolated from the right lung and the skin lesions was identified as A. flavus. Aflatoxins B1, B2 and M1 were detected in culture filtrates of the isolated A. flavus, and in an extract of lung lesions. These aflatoxins are considered to have played an important role in damaging the immune system of the patient through their toxic effects.

Adult↗

PubMed1990

Effect of aflatoxins on rat peritoneal macrophages.

Phagocytosis, intracellular killing of Candida albicans, and superoxide production by rat peritoneal macrophages exposed to aflatoxins B1, B2, G1, G2, B2a, and M1 at several times and concentrations were analyzed to evaluate the intensity of a depressive effect for each mycotoxin. All aflatoxins used at very low concentrations had a depressive effect on the functions of macrophages. The biggest impairment of phagocytosis, intracellular killing, and spontaneous superoxide production was observed in macrophages exposed to aflatoxins B1 and M1.

Aflatoxins↗

PubMed1977

Comparative in vitro metabolism of aflatoxicol by liver preparations from animals and humans.

The metabolism of [14C]aflatoxicol by liver postmitochondrial and microsomal fractions from humans and eight other species was compared. A major metabolic pathway involves the dehydrogenation of aflatoxicol yielding aflatoxin B1. Human liver preparations were more active in this regard than preparations from any of the other species tested. The aflatoxicol dehydrogenase activity was mainly associated with the microsomal fraction and required a hydrogen acceptor (e.g., nicotinamide adenine dinucleotide phosphate), but was not inhibited by carbon monoxide, which implies that it was not dependent on the heme-containing microsomal drug-metabolizing system. It had a pH optimum of 8.0. Postmitochondrial liver fractions also oxidized aflatoxicol (and/or the aflatoxin B1 made from it) to at least five other metabolites that comigrated on thin-layer chromatography plates with authentic standards of aflatoxins Q1,P1,H1,M1, and B2a. None of these oxidative metabolites were formed in the presence of carbon monoxide. We also report on the in vitro reduction of aflatoxin B1 to aflatoxicol by the cytosol fractions from eight species. Most active in this regard were rabbit and trout preparations, while this activity was almost absent in the guinea pig. Preparations from humans and four other species were intermediate between these extremes.

Aflatoxins↗

PubMed1986

Mechanisms of anti-carcinogenesis by indole-3-carbinol: effect on the distribution and metabolism of aflatoxin B1 in rainbow trout.

Indole-3-carbinol (I3C), a component of cruciferous vegetables, was previously shown to inhibit aflatoxin B1 (AFB1) carcinogenesis in trout. The purpose of this study was to examine the effect of I3C on AFB1 metabolism and hepatic DNA adduct formation in vivo and in vitro. When fed at 0.2%, I3C produced a 70% reduction in average in vivo hepatic DNA binding of injected AFB1 over a 21-day period when compared to controls. A 24-h distribution study of injected tritiated AFB1 in I3C fish showed less total radioactivity in the blood and liver at all times examined, compared to controls. These reductions were due primarily to reduced levels of AFB1 bound to red blood cell DNA, reduced plasma levels of the primary metabolite aflatoxicol (AFL), and decreased levels of AFB1 and polar metabolites present in the liver of I3C fish. In contrast to blood, total radioactivity was significantly elevated in the bile of I3C fish resulting from a 7-fold increase in aflatoxicol-M1 glucuronide levels over controls. No difference was observed in concentration of AFL glucuronide, the primary conjugate present in control fish. There was no difference in total radioactivity remaining in the carcass of I3C or control fish. AFB1 metabolism in freshly isolated hepatocytes from I3C fish showed 20% less DNA binding in a 1-h assay, with a 2-fold increase in aflatoxin M1 production. Addition of I3C to control hepatocytes at levels of 1, 10 or 100 microM had no effect on AFB1 DNA binding. These findings indicate that I3C inhibition of AFB1 hepatocarcinogenesis in trout involves substantial changes in the pharmacokinetics of carcinogen distribution, metabolism and elimination, leading to significantly reduced initial hepatic-nuclear DNA damage in vivo.

Aflatoxin B1↗

PubMedDate not supplied

[Immunoenzyme test system for detection of aflatoxin B1].

Indirect enzyme immunoassay based on immobilized conjugate of aflatoxin B1 carboxymethyloxime with bovine serum albumin and polyclonal rabbit antibodies allows determining aflatoxin B1 with a low relative cross-reactivity against aflatoxin B2, G1, G2, M1, B2a and G2a and sterigmatocystin (15.5, 15.5, 1.7, 1.0, 0.03, 0.03 and 0.01%, respectively) with a sensitivity of 0.04 ng per well or 4.0 ng per ml organic solvent.

Aflatoxin B1↗

PubMed1983

Metabolic activation and bacterial mutagenicity of aflatoxin B1 in two different test systems.

The metabolism of aflatoxin B1 (AFB1) by liver post-mitochondrial supernatant fraction from phenobarbitone treated male albino rats in liquid suspension and soft-agar plate incorporation bacterial mutation assay systems has been studied. The AFB1 concentration used was in the range of those added to bacterial mutagenicity tests with this mycotoxin. Three oxidative metabolites of AFB1 viz the Tris derivative of AFB1 8,9-diol (derived from the 8,9-epoxide), aflatoxin Q1 (AFQ1) and M1 (AFM1) were observed. The metabolite profile and time course of formation were qualitatively similar in both assay systems. The rate and overall formation of metabolites in the soft-agar system was approximately one half that in the liquid suspension system which was reflected in decreased AFB1 induced bacterial mutation in the former system. The AFB1 metabolite profile in these in vitro systems did not mirror completely the reported in vivo profile seen in the rat, as aflatoxin P1 (AFP1) and a glutathione conjugate were not detected. No evidence was found for a prolongation of metabolism in the soft-agar system.

Aflatoxin B1↗

PubMedDate not supplied

Serum epoxide hydrolase (preneoplastic antigen) in human and experimental liver injury.

Reports of an increase in a serum epoxide hydrolase (sEH), immunochemically related to microsomal EH in humans and rats with hepatocellular carcinoma (HCC), suggested its use as a serum marker for this disease. We have now measured sEH levels (as either immunochemically determined content or enzyme activity) in a number of human and experimental models of liver disease. sEH was elevated above the normal range in at least 50% of individuals with HCC, including: 3 of 6 northern Californians; 4 of 7 Koreans with hepatitis B-associated HCC; hepatitis B-associated HCC in woodchucks; and male rats receiving chronic treatment with aflatoxin B1 or ciprofibrate. sEH was rarely elevated in other forms of chronic liver disease. Only 2 of 9 Koreans with hepatitis B-associated cirrhosis, 1 of 8 carriers, but none with chronic active hepatitis or infection with no apparent liver disease had elevated sEH. In addition, no elevations were found in woodchucks with noncancerous viral hepatitis. In aflatoxin B1- and M1-treated rats sEH was not elevated in those with only hyperplastic foci or hepatocellular adenomas, and in two rat initiation-promotion protocols sEH was elevated only in those rats which received the entire set of treatments. sEH was also increased during acute hepatotoxicity in rats treated with CCl4 or 1,2-dibromo-3-chloropropane. The mechanism of increase in sEH during hepatocarcinogenesis appears to be different from that of other markers of HCC, for in the Korean patients, there was no correlation between sEH concentrations and those of alpha-fetoprotein or ferritin, nor was there a correlation with alpha-fetoprotein concentrations in the aflatoxin-treated rats. Furthermore, the increase in sEH does not correlate with induction of microsomal EH in the liver of experimental animals. Studies to date indicate that sEH is selective for HCC and severe hepatonecrotic injury, and may be of some use in the diagnosis of HCC, particularly as a complement to other serum markers.

Animals↗

PubMed1991

[Use of chick embryos for prediction of embryotoxic effects of mycotoxins in mammals].

Embryotoxic effects of 25 mycotoxins were investigated in two-, three- and four-day chick embryos; the results were evaluated on the eighth day of development. The embryotoxicity ranged from 0.0001 to 0.1 microgram per embryo in T-2 toxin, aflatoxin B1, G1, B2 and M1, cytochalasin E, ochratoxin A and PR-toxin; from 0.1 to 1.0 microgram per embryo in sterigmatocystin, aflatoxin G2, vomitoxin (4deoxynivalenol), patulin, rubratoxin B, secalonic acid D, mycophenolic acid, and from 1.0 to 100 micrograms per embryo in penicillic acid, cyclopiazonic acid, tenuazonic acid, citrinine, brevianamide A, zearalenone, fusaric acid, griseofulvin, kojic acid and 8-methoxypsolaren. Acute cardiotoxic effects were observed in PR-toxin, patulin, rubratoxin B, penicillic acid, citrinine and zearalenone. Teratogenic effects with a spectrum of different embryonal malformations occurred in T-2 toxin, ochratoxin A, PR-toxin, patulin, secalonic acid D, mycophenolic acid and citrinine. The embryotoxic effects demonstrated in chick embryos correlated with the well-know literary data on mammals. Considering the different chemical composition and biological effects of mycotoxins, we suppose that the embryotoxicity test of chick embryos will also be suitable for testing other biologically active substances in the environment.

Animals↗

PubMed2001

Control of food and agro product contamination in Bulgaria.

The ban of organochlorine pesticides in Bulgaria (1969) has led to their significant drop below the maximum residue limits. The climate and the imperfect storage facilities benefit the production of Fusarium toxins desoxynivalenol (folytoxin), zearalenon (F-2), T-2, ochratoxin A and aflatoxins in grain products, M1 in milk products, and patulin in apple juices and nectars. Heavy metals are found in smaller concentrations than in industrially developed countries with the exception of lead, which may be due to the wide use of leaded gasoline. Bulgaria has 5 "hot spots" related to sources of heavy metals. An elaborated inventory PCB, PCDD, and PCDF sources suggests that there are no toxicologically significant environmental and food pollutions with these substances. Sanitary control is enforced by several laws and subordinate regulations on the national level, which, however, have failed to coordinate it with the relevant activities of the Ministries of Health and of Agriculture and Forestry.

Bulgaria↗

PubMed2005

Prevalence of aflatoxins in blood and urine of Egyptian infants with protein-energy malnutrition.

The aim of the present work was to study the presence of aflatoxins in blood and urine of infants with protein-energy malnutrition (PEM). The study was conducted on 60 infants, 30 with kwashiorkor and 30 with marasmus, with 10 age-matched healthy infants studied as a control group. Complete blood count, liver function tests, and determination of the level of aflatoxins (B1, B2, G1, G2, M1, M2, G2a, B3, GM1, P, and aflatoxicol R0) in blood and urine were carried out in all studied infants. Serum aflatoxins were detected in more infants with kwashiorkor (80%) than in those with marasmus (46.7%). The mean serum levels of total aflatoxins, AFB1, AFG1, and AFB2a, were significantly higher in infants with kwashiorkor (p <.001). Aflatoxin B1 (AFB1) was the most commonly detected type. The prevalence of aflatoxin excretion in the urine of infants with kwashiorkor was 80%, a higher value than that in infants with marasmus (46.7%). The mean urinary concentration of total aflatoxins followed the same pattern of distribution (p < .052). There were no significant differences between groups in the mean urinary concentrations of AFB1, AFG1, AFB2a, AFM1, and AFG2a. Aflatoxins were not detected in any of the serum or urine samples of the control group. Aflatoxins are highly prevalent in this study population and show a high degree of correlation with severe PEM.

Aflatoxins↗

PubMed1977

[Influence of cooling temperatures on aflatoxin formation in milk products (author's transl)].

In the literature several contradictionary results have been published on the aflatoxin formation at temperatures below 10 degrees C. Therefore experiments with pastes made from milk and cheese powder artificially contaminated with Aspergillus parasiticus, were performed at temperatures of 1 degree C, 5 degrees C, and 10 degrees C for 28 days at a relative humidity of 90--95%. Even at 1 degree C, the aflatoxins B1, B2, G1, G2, and M1 could be determined quantitatively. The lactose content did not have a significant influence on the aflatoxin values. Even storage of cheese (camembert and cottage cheese) in a 10% salt solution did not inhibit aflatoxin formation at 20 degrees C.

Aflatoxins↗

PubMed1998

Determination of aflatoxicol in human urine by immunoaffinity column clean-up and liquid chromatography.

A method for the determination of aflatoxicol in urine has been developed. The urine samples were cleaned up by an automated procedure using immunoaffinity columns before analysis by high-performance liquid chromatography and fluorescence detection. Post-column derivatization with bromine allowed the simultaneous determination of aflatoxicol and aflatoxins B1, B2, G1, G2, M1, and Q1. Average recovery of aflatoxicol was 99% in the range 4-40 pg ml-1 of spiked urine samples. The relative standard deviations were all between 1% and 3%. The limit of detection was 1 pg ml-1 urine. Authentic samples from exposed feed-factory workers were analysed, but aflatoxin levels were found to be below the detection limit.

Aflatoxins↗

PubMedDate not supplied

Identification of aflatoxins by quadrupole mass spectrometry/mass spectrometry.

MS/MS daughter experiments were recorded for aflatoxins B1, B2, G1, G2, M1, M2, and aflatoxicol, using 3 ionization modes. Daughters were recorded from the molecular ion (M+) using electron impact ionization (EI). Daughters from the protonated molecules (MH+) were recorded in the positive ion mode and the daughters from the molecular anion (M-) were recorded in the negative ion mode using chemical ionization (CI). These daughter spectra are all relatively simple. The EI daughters are quite similar to conventional EI spectra. The yield of (M-) is about 100 times greater than the yield of M+ in EI or MH+ in isobutane CI spectrum. Negative ion daughter spectra were used to demonstrate the feasibility of determining the presence of aflatoxin B1 in crude extracts of contaminated corn. Aflatoxin B1 could be detected at 10 ppb.

Aflatoxins↗

PubMed1986

Aflatoxin inhibition of rat liver mitochondrial cytochrome oxidase activity.

Aflatoxins B1, B2, G1, G2, and M1 have been evaluated for activity toward cytochrome oxidase in isolated rat liver mitochondria employing ferrocytochrome c and p-phenylene diamine as reductants. The aflatoxins inhibited the cytochrome oxidase activity to a greater extent when monitored by O2 uptake measurements than by substrate oxidation. AFG2 and AFM1 were the most potent (50-70%). Using oligomycin and 2,4-DNP as respiratory inhibitor and uncoupler, respectively, the aflatoxins appear to inhibit e- rather than energy transfer reactions. These toxins did not uncouple cytochrome oxidase activity.

Aflatoxins↗