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PubMed1980

[Method for the simultaneous determination of aflatoxins B1 and M1 in the liver of slaughter animals].

The method used by Egmond et al. (1979) was chosen from a number of methods recommended for the determination of aflatoxins in raw materials of animal origin. This method is described in detail to facilitate its use in practice in cases of forced slaughters of animals suspected of aflatoxicosis. The sensitivity of the method for aflatoxin B1 and M1 is about 0.05 micrograms . kg-1. On the whole, 88 liver samples were examined for the presence of the aflatoxins B1 and M1. The samples had been obtained from the slaughtered pigs (52), bulls (23), cows (6), calves (5), and from deceased pigs (2). Positive findings were obtained in five of sixteen pork liver samples and in two of the tested five samples of calf liver. All of these animals were suspected of aflatoxicosis. At current slaughter, only one case of 36 examined pigs was found to be positive. Aflatoxin M1 was found more frequently than aflatoxin B1. However, the findings never exceeded the concentration of 100 ng . kg-1; this is less by 1.5 orders than the proposed tolerated concentration for adult animals (5 micrograms . kg-1).

Aflatoxins↗
PubMedDate not supplied

Past and future in mycotoxin toxicology research.

Before 1960 the toxicology of mycotoxins was mainly of concern to veterinarians, because outbreaks of mycotoxicoses resulted occasionally in considerable loss of livestock. By a wider use of biotests, preferably in mammals, a further decline of such intoxications probably will occur. Following the discovery of the carcinogenicity of some aflatoxins, the focus turned to human health. Screening tests for carcinogenicity are still in development. The test used most frequently is the Ames test on microorganisms. Unfortunately, many problems still must be resolved before an extrapolation of results from these tests to man is possible. Examination of the carcinogenic activity of mycotoxins in long-term animal experiments is often difficult due to lack of resources, lack of test material, and the toxicity of the compounds, which precludes administration of sufficiently high dose levels. The available data regarding a possible carcinogenic activity of several important mycotoxins, such as the trichothecenes or patulin, do not fulfill currently used criteria. Therefore further studies are needed. A new approach is determination of the binding capacity to DNA of suspected carcinogens, which seems to correlate well with carcinogenic potency. By this method, a high carcinogenicity of aflatoxin M1 can be deduced. However, the macromolecular-bound residues of aflatoxin B1, which may occur in tissues of domestic animals, most probably do not show carcinogenic activity. Although many questions are still unanswered, it seems that the numerous mycotoxins identified since 1960 are less toxic or carcinogenic and occur less frequently in food than do aflatoxins.

Aflatoxins↗
PubMedDate not supplied

Aflatoxin, a human carcinogen: determination in foods and biological samples by monoclonal antibody affinity chromatography.

We have used monoclonal antibody technology to produce antibodies that recognize aflatoxins in order to develop noninvasive methods in conjunction with other chemical analytical techniques to monitor human exposure to environmental carcinogens. These methods require the ability to quantitate aflatoxins and their metabolites, including DNA and protein adducts, in readily accessible compartments such as serum and urine. The techniques permit efficient analysis of many samples in a relatively short time. Also, these monoclonal antibody affinity columns have been extremely useful for rapid isolation of aflatoxins from food and grain samples, as well as aflatoxin M1 from milk. Monoclonal antibody affinity methods are nondestructive to the aflatoxin molecule, so the sample aliquot can be used for confirmation. The use of monoclonal antibody preparative affinity columns represents a major, substantive breakthrough for analytical chemists and will be a generally applicable technology for isolation of many different substances.

Aflatoxins↗
PubMed1982

Enhanced hepatotoxicity of aflatoxin B1 by pretreatment of rats with ethanol.

Hepatotoxicity of aflatoxin B1 (2.0 and 4.0 mg/kg i.p.) as determined by plasma enzyme activities (GPT and GOT), liver triglycerides and histopathologic changes was enhanced in rats pretreated with four oral doses of ethanol (4.0 g/kg each) at 48, 45, 24 and 21 hrs prior to aflatoxin B1 administration. Pretreatment with ethanol (4.0 g/kg) slightly increased liver weight without changing hepatic microsomal protein contents. Also it caused an increase in microsomal aniline hydroxylase but a decrease in p-nitroanisole-o-demethylase, 48 hrs after the first ethanol dose. In the rats pretreated with ethanol, aflatoxin B1 was metabolized at a higher extent to aflatoxins M1 and Q1. These results suggest that an increased hepatotoxicity of aflatoxin B1 after pretreatment with ethanol may presumably due to an increase in microsomal formation of active aflatoxin B1 metabolite.

Aflatoxin B1↗
PubMed1991

Evaluation of a commercial immunoassay system for sulfamethazine and aflatoxin detection in biological fluids and feeds.

Commercial immunoassay systems produced by International Diagnostics to analyze for sulfa drugs and aflatoxin residues have been evaluated with milk, urine, feed and serum samples. Neither system produced satisfactory results with feeds. The sulfa test reproducibility was good enough to provide semiquantitative results on milk (40 ul sample) and urine, but should be regarded as qualitative on urine or feed. The reproducibility of the aflatoxin test was acceptable for semiquantitative use on serum, but should be regarded as qualitative on urine and semiquantitative on milk with a solid phase concentration. The overall reproducibility was at least +/- 10% if the test was used semiquantitatively. The sensitivity of the test was 10 ng for both sulfamethazine and aflatoxin B1. The range of the color change was very narrow (0-20 ng). The aflatoxin test was designed for aflatoxin B1 and was roughly twice as sensitive to B1 as to M1 aflatoxin. These procedures can be used on appropriate matrices at suitable sensitivities to rapidly screen samples for sulfa drugs and aflatoxin residues. The use of proper standards to demonstrate effectiveness in each matrix is very important.

Aflatoxins↗
PubMed1977

[Influence of raw milk processing on the aflatoxin M content of milk products (author's transl)].

Several contracdictory results in the literature lead us to the conclusion, that the influence of raw milk processing on aflatoxin content should be tested under as close as possible practical conditions. Even though storage at 5 degrees C for 1-3 days does not greatly influence aflatoxin content (11-25% reduction), this might still be important for food inspection. Although experiments on exposure to light resp. oxygen were repeated ten times, the results could not be definitely be shown as due to oxidation. Part of the contradictory literature references also in the case of freeze drying in our opinion caused by the way in which aflatoxins was added. The loss was less pronounced when milk was contaminated naturally than when it was added artificially. Heating of milk, depending on the conditions, caused a decrease of the aflatoxin-content of between 12 and 35% when making butter from naturally contaminated cream 23% (18-28%) of the aflatoxin M1 appeared in the butter, whereas the buttermilk contained the major amount of aflatoxin.

Aflatoxins↗
PubMed1995

Retention and distribution of aflatoxin in tissues of chicks fed aflatoxin-contaminated poultry rations amended with soil.

The effects of silty clay loam on aflatoxin B1 (AFB1) retention and distribution were investigated when added to diets of chicks fed aflatoxin-contaminated rations. One hundred 14-d-old White Leghorn chicks were fed a control ration (clean corn), a low aflatoxin-contaminated ration (120 ng AFB1/g), a high aflatoxin-contaminated ration (700 ng AFB1/g), or a high aflatoxin-contaminated ration (700 ng AFB1/g) + 10% or 25% soil. Livers, crops and breast muscles in each group were pooled and analyzed for AFB1 and metabolites. The addition of soil significantly reduced the AFB1 levels in the livers, although the reduction was less when 10% soil was fed compared with the 25% soil feeding. AFB1 concentrations in the crops of chicks fed high aflatoxin-contaminated ration without soil was statistically indistinguishable from the chicks in the other groups. AFB1 concentrations were significantly reduced in the breast muscles of chicks fed 10% or 25% soil compared to chicks fed the high aflatoxin-contaminated ration without soil. Aflatoxin B2 was detected only in livers, crops and breast muscles from chicks fed aflatoxin-contaminated ration without soil. Aflatoxin M1 (AFM1) was detected only in livers and crops of chicks fed aflatoxin-contaminated ration without soil and only in breast muscles of chicks fed the low aflatoxin-contaminated ration and high aflatoxin-contaminated ration + 25% soil. AFM1 concentration was significantly higher in the crops of chicks fed high aflatoxin-contaminated ration without soil.

Aflatoxin B1↗
PubMed1979

Distribution of aflatoxins B1 and M1 in contaminated calf and pig livers.

The determination of aflatoxins B1 and M1 in multiple sections of livers from 4 calves and 1 pig exposed to high levels of aflatoxins showed a uniform distribution of the aflatoxins in each liver, within the precision of the analytical method used. The thin layer chromatographic method has an expected within-laboratory coefficient of variation of 15%.

Aflatoxins↗
PubMed1984

Failure of plant tissues to metabolize aflatoxin B1?

After exposure of peas and wheat kernels to aflatoxin B1 solutions the following aflatoxins could not be detected in seed extracts: aflatoxins M1, B2a, Q1, aflatoxicol and tetrahydrodeoxyaflatoxin B1.

Aflatoxin B1↗
PubMed1982

Determination and thin layer chromatographic confirmation of identity of aflatoxins B1 and M1 in artificially contaminated beef livers: collaborative study.

An international collaborative study involving 13 laboratories was conducted to test methods for the determination and thin layer chromatographic (TLC) confirmation of identity of aflatoxins B1 and M1 in beef liver. For the determination, each collaborator furnished fresh or frozen beef liver. Samples were artificially contaminated by adding solutions containing various concentrations of aflatoxins B1 and M1 (0.032-0.69 ng/g). Two TLC confirmation methods were tested with extracts obtained from the determination. Two measurement methods using 2-dimensional TLC were evaluated. In the first, sample extracts were compared directly with B1 and M1 standards on TLC plates; in the second, internal standards plus sample extracts were compared with B1 and M1 standards on the plates. Average within-laboratory coefficients of variation (CV) for the direct method were 26% for B1 and 26% for M1 compared with 24 and 26%, respectively, for the internal standard method. The average between-laboratory CV values were 39% for B1 and 41% for M1 by the direct method and 36% for B1 and 39% for M1 by the internal method and 36% for B1 and 39% for M1 by the internal standard method. Recoveries ranged from 64 to 90% for B1 and from 72 to 86% for M1. These data indicate that the more convenient direct method was sufficient, and internal standards were unnecessary. An analysis of variance was calculated from combined sample data to determine components of variance. The within-laboratory CV values were 27.0 and 32.3% for B1 and M1, respectively, and the between-laboratory CV values were 47.1 and 53.2%, respectively. Both TLC confirmation methods gave satisfactory results and have been adopted official first action, along with the determination method.

Aflatoxin B1↗
PubMedDate not supplied

Application of immunoaffinity columns to mycotoxin analysis.

Immunoaffinity columns (IACs) are widely used for cleanup and isolation of mycotoxins extracted from foods and biological fluids, particularly aflatoxins, ochratoxin A, and fumonisins. The columns are prepared by binding antibodies specific for a given mycotoxin to a specially activated solid-phase support and packing the support suspended in aqueous buffer solution into a cartridge. The mycotoxin in the extract or fluid binds to the antibody, impurities are removed with water or aqueous solution, and then the mycotoxin is desorbed with a miscible solvent such as methanol. Further separation can be performed with IAC, followed by liquid chromatographic (LC) quantitation, either off-line or on-line in an automated system, or by fluorometry. IACs have been used by laboratories that developed the antibodies but are also available commercially for aflatoxins, ochratoxin A, fumonisins, zearalenone, and deoxynivalenol. Among commercial IACs, Aflatest P is used as the cleanup step in an LC method and in a solution fluorometry method for corn, peanuts, and peanut butter that was adopted as an AOAC INTERNATIONAL Official Method after evaluation by an international collaborative study. As part of a fluorometer-based test kit, aflatest P was further certified by the AOAC Research Institute to measure total aflatoxins in 10 grains and grain products. IACs can concentrate the analyte from a large amount of sample, allowing detection limits at low parts-per-trillion levels in some cases (e.g., for aflatoxin M1 and ochratoxin A in liquid food matrixes). Regeneration of IACs for reuse in aflatoxin, ochratoxin A, fumonisin, and zearalenone analyses has been investigated.

Aflatoxins↗
PubMed1988

Modification of aflatoxin B1 biotransformation in vitro and DNA binding in vivo by dietary broccoli in rats.

Cruciferous vegetables have been shown to have anticarcinogenic effects in animals but biochemical mechanisms have not been completely elucidated. The effects of dietary broccoli on in vivo DNA binding of the hepatocarcinogen aflatoxin B1 (AFB) and in vitro formation of the putative carcinogenic intermediate, AFB-8,9-epoxide, as well as detoxification of the epoxide by conjugation with glutathione (GSH), were examined in this study. Animals were fed a purified diet, a purified diet plus 25% freeze-dried broccoli, or standard rodent chow for 3 wk. In vivo binding of AFB to hepatic DNA was determined. Biotransformation of AFB in vitro (microsomal oxidation to AFB-8,9-epoxide, as well as hydroxylated metabolites, and cytosolic GSH conjugation of AFB-8,9-epoxide generated in situ) was measured by an HPLC method that allows specific and direct determination of AFB metabolites and thus, the rates of their formation. Microsomal mixed-function oxidase and epoxide hydrolase activities and cytosolic glutathione S-transferase activities were also measured with commonly used surrogate substrates. The rate of cytosolic conjugation of AFB-8,9-epoxide was increased 2.8-fold by the broccoli diet and 2.2-fold by the chow diet. These changes were not fully reflected by increases in activity with surrogate substrates. The chow diet did not affect epoxide hydrolase activity nor glutathione S-transferase activity toward 3,4-dichloronitrobenzene or benzo[a]pyrene 4,5-oxide, whereas these activities were significantly increased by the broccoli diet. Microsomal formation of AFB-8,9-epoxide was unaffected by the dietary treatments, whereas formation of aflatoxin M1 was increased. The chow diet, but not the broccoli diet, increased the amount of aflatoxin Q1 formed from AFB. Binding of AFB to DNA in vivo was significantly lower in the broccoli group but not in the chow-fed animals. These results indicate that broccoli contains substances that cause a reduction in the binding of AFB metabolites to DNA, possibly through the induction of glutathione S-transferase(s). Broccoli and rodent chow differ in their constituents that increase levels of xenobiotic biotransformation enzymes relative to a purified diet. The results also indicate the limitations of reliance on measurements of biotransformation pathways using surrogate substrates instead of carcinogenic compounds of interest.

Aflatoxin B1↗
PubMed1987

Metabolic basis for the protective effect of the antioxidant ethoxyquin on aflatoxin B1 hepatocarcinogenesis in the rat.

The effect of dietary administration of 0.5% ethoxyquin (EQ) on the in vivo induction of enzymes and effect on aflatoxin B1 (AFB1)-DNA binding in liver and the consequent in vitro metabolism of AFB1 by male Fischer F344 rat liver-derived fractions have been examined. EQ increased microsomal cytochrome P-450s, in particular those isozymes classed as phenobarbital inducible, and the in vitro rate of metabolism of AFB1. The formation of the presumed detoxified metabolites, aflatoxins M1 and Q1, was enhanced to a greater extent than was the formation of the active metabolite, aflatoxin B1-8,9 epoxide (assessed by the level of aflatoxin B1-8,9-dihydrodiol). Prolonged feeding with EQ was accompanied eventually by a reduction in the initially elevated cytochrome P-450 content, but this was not reflected in any significant decrease in the rate of AFB1 metabolism in vitro. EQ increased the glutathione S-transferase activity of the liver cytosol fractions as assessed with the model substrate 1-chloro-2,4-dinitrobenzene. The capacity of these fractions specifically to catalyze the conjugation of AFB1 with glutathione was induced to a far greater extent than was the conjugation of 1-chloro-2,4-dinitrobenzene. gamma-Glutamyl transpeptidase was induced in the periportal areas of the liver lobule. Reduced in vivo binding of [3H]AFB1 to DNA of liver and kidney was found to result from EQ treatment. It is concluded that the reduced hepatocarcinogenesis which results from feeding EQ simultaneously with AFB1 is due to the reduction in DNA-adduct formation which in turn is due at least in part to increased detoxifying metabolism in the microsomal, cytosolic, and plasma membrane compartments of the liver cells.

Aflatoxin B1↗
PubMed1977

[Methods for assessing permissible levels of intentional and unintentional food additives (author's transl)].

Foods may contain intentional and unintentional additives. The former group includes, for example, flavours, colouring substances and preservatives, while the latter includes pesticides and mycotoxins. To determine the amount of these substances that are admissible in man, extensive toxicological tests have to be performed with experimental animals to establish a no toxic effect level. Based on the no toxic effect level and applying a safety factor an "acceptable daily intake" (ADI) can be calculated for human beings. The problems outlined in the article are illustrated by several examples, such as the presence of DDT and aflatoxin M1 in milk and of mercury in fish.

Aflatoxins↗
PubMed1977

Aflatoxin in Tunisian foods and foodstuffs.

1076 samples of different commodities were screened for aflatoxin contamination. Samples were taken from storage houses and dealers throughout the country. 14 of these samples contained aflatoxin (as much as 62 microgram/kg). Corn was found to be the most contaminated agricultural product followed by sorghum and peanuts. Wheat and barley showed no contamination. 1 out of 19 pistachio samples contained 22 microgram/kg of aflatoxin B1. Fluid milk showed no contamination while only 2 out of 248 cheese samples were found contaminated with aflatoxin M1 (10.6 microgram/kg).

Aflatoxins↗
PubMed1985

Characterization of water-soluble glucuronide and sulphate conjugates of aflatoxin B1. 1. Urinary excretion in monkey, rat and mouse.

Water-soluble aflatoxin conjugates prepared from urine samples from rats, mice and rhesus monkeys dosed with [14C]aflatoxin B1 (AFB1) ip or iv were hydrolysed by enzymes (beta-glucuronidase and sulphatase), acid or a combination of both treatments. Different amounts of AFB1 and its metabolites were found in hydrolysates from different sources, indicating the presence of glucuronide, sulphate and possibly mercapturate conjugates of aflatoxins. In addition to aflatoxins M1, P1, Q1 and B2a, AFB1 was frequently identified in the products released from the hydrolysates. These water-soluble aflatoxin conjugates were not mutagenic to Salmonella typhimurium TA98 in the presence of rat-liver S-9 mix. However, chloroform extracts of the hydrolysates from beta-glucuronidase and sulphatase treatment showed mutagenic activity in these bacteria in the presence of S-9 mix. Although very low levels of AFB1 radioactivity were detected in the hydrolysates, the potent mutagenic activity of AFB1 contributed to the high numbers of revertant colonies. AFP1 was detected in urine samples from monkeys that were pretreated with phenobarbital before an iv dose of AFB1. No mutagenic activity was detected in the enzymatic hydrolysate of the sample from these monkeys. The results thus indicate that AFB1 can form glucuronide and/or sulphate conjugate(s) directly and be excreted in the urine.

Aflatoxin B1↗
PubMed1990

Detection and detoxification of aflatoxins: prevention of aflatoxicosis and aflatoxin residues with hydrated sodium calcium aluminosilicate.

Our recent findings demonstrate that HSCAS can prevent aflatoxicosis in chickens and swine and significantly decreases the level of aflatoxin M1 residues in the milk of lactating dairy cattle. The basic mechanism for this action appears to involve sequestration of aflatoxin in the gastrointestinal tract and chemisorption (i.e., tight binding) to HSCAS which results in a reduction in aflatoxin bioavailability. Research is in progress to elucidate the specificity of HSCAS action and to construct a series of selective chemisorbents for mycotoxin control in livestock and poultry.

Aflatoxins↗
PubMed1978

In vitro metabolism of aflatoxin B2 by animal and human liver.

The metabolism of aflatoxin B2 by postmitochondrial supernatant fractions of duck, rat, mouse, and human livers was studied in an in vitro system. Duck liver had a much higher level of activity than had tissues from other species. Postmitochondrial supernatant equivalent to 0.2 g whole liver metabolized 40 to 80% of the initial substrate in 30 min, compared to less than 6% for the other species. Among several metabolites formed by duck liver, aflatoxin B1 was produced in amounts equivalent to 2 to 8% of the initial substrate, and metabolites having chromatographic properties postualted for aflatoxicols 1 and 2 and aflatoxins M1 and M2 were also formed in small amounts. In contrast, rat, mouse, and human liver preparations produced no detectable aflatoxin B1 and only small amounts of compounds thought to be aflatoxins Q2 and P2. The greater susceptibility of duck liver to the toxicity of aflatoxin B2 may be attributable to its ability to form aflatoxin B2 may be attributable to its ability to form aflatoxin B1, which could then be activated through further metabolism.

Aflatoxins↗