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PubMedDate not supplied

Comparison of postcolumn derivatization-liquid chromatography with thin-layer chromatography for determination of aflatoxins in naturally contaminated corn.

Quantitation of aflatoxins by liquid chromatography with postcolumn iodine derivatization (LC-PCD) and fluorescence detection was compared with quantitation by the AOAC CB method, 968.22. Thirty-seven naturally contaminated corn samples were ground and then divided. One portion was extracted, and the extract was cleaned up and analyzed by thin-layer chromatography according to the CB method. The second portion was extracted and cleaned up in a similar fashion, but quantitation was by the LC-PCD method. For aflatoxin B1 concentrations ranging from 0 to 150 ng/g, results obtained by the 2 methods were fitted to a linear equation with the LC-PCD results as the dependent variable. The correlation coefficient was 0.99, the intercept was near 0, and the slope was near 1. For aflatoxin B2, the correlation coefficient was 0.97, and the intercept was near 0. However, the slope of the equation relating LC-PCD concentration to TLC concentration was only 0.5. We believe that this lack of equivalence between the methods for determination of aflatoxin B2 is due to overestimation by the TLC method because the low levels present are near the TLC detection limit for B2.

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↗

PubMedDate not supplied

Effects of mixed-function oxidase and aflatoxin B1 on lysogenic and indicator strains of Bacillus subtilis.

The present study was conducted to determine the effects of metabolized aflatoxin B1 (via a mammalian liver mixed-function oxidase system) and native aflatoxin B1 upon induction of bacteriophage in Bacillus subtilis and growth of B. subtilis. A lysogenic strain of B. subtilis (BDS-1, phi 105) and an indicator strain of this species (DBS-1) were utilized in the present experiment. Lysogenic cultures were incubated for various lengths of time in the presence of either native or metabolized toxin, and plaque-forming units were determined. Identical experiments were conducted with the indicator strain and colony-forming units were determined. At a native toxin concentration of 25 micrograms/ml of medium, the maximum number of plaque-forming units was induced in lysogenic cells. However, when cells were incubated in the presence of aflatoxin B1 and mixed-function oxidase, neither plaque-forming units nor colony-forming units could be detected from lysogenic or indicator cells, respectively. This organism is apparently much more susceptible to inhibition of cellular replication than to lysis via bacteriophage induction. Thus, from the present study and from previously reported research, differences in susceptibility to native and metabolized aflatoxin B1 exist among species of Bacillus.

Aflatoxin B1↗

PubMed1986

[Fluctuation in the concentration of sex steroids and aflatoxin B1 in the seminal plasma of boars and its relation to sperm production].

The concentration of testosterone, 17-beta oestradiol and aflatoxin B1 were studied in the semen plasma of 21 boars of four breeds for the period of twelve months. The following spermiological parameters were investigated: semen volume, sperm concentration, percentage of abnormal spermatozoa, and survival of spermatozoa. The fertilizing capacity of ejaculates was evaluated according to the conception rate of sows and gilts after the first insemination, according to the average number of piglets per litter and average number of live-born piglets per litter. The highest aflatoxin B1 residues in sperm were recorded in March to May and were related with aflatoxin concentration in feed ration. The group of boars with fertility disorders had more aflatoxin in their sperm (up to 100 pmol . l-1), lower sperm concentration, lower survival of spermatozoa, and a larger proportion of abnormal spermatozoa. The year season had a significant influence on the concentration of the hormones. The highest average value of testosterone (10.2 +/- 1.28 nmol) was obtained in autumn and lower values were recorded in winter. The changes in 17-beta estradiol concentration were similar to the changes in testosterone content, with the maximum value in November (0.249 nmol X 1(-1]. The boars with reproduction disorders had a significantly lower concentration of 17-beta oestradiol. Significant correlations were found between the concentration of the hormones, semen volume, and sperm concentration. 17-beta oestradiol also had a significant positive correlation to abnormal spermatozoa and to the activity of aspartate aminotransferase.

Aflatoxin B1↗

PubMedDate not supplied

Development of milk powder reference materials certified for aflatoxin M1 content (Part I).

The development of 3 full-cream milk powder reference materials, certified for their aflatoxin M1 content, is described. The materials were prepared and certified within the Reference Material Programme of the Community Bureau of Reference (BCR). The 3 reference materials, RMs 282, 284, and 285, contain aflatoxin M1 at concentrations of less than 0.05, 0.31 +/- 0.06, and 0.76 +/- 0.05 micrograms/kg, respectively. The preparation, testing for homogeneity, stability of the reference materials, and the certification exercise, which was preceded by 2 intercomparisons of methods, are discussed. Particular emphasis was placed on the independence of the measurements in the certification exercise and the control of errors associated with extraction efficiency and the aflatoxin M1 calibrant. Finally, some guidance is given on avoiding the principal sources of errors in the determination of aflatoxin M1. Details concerning the supply of the reference materials will be provided by BCR on request.

Aflatoxin M1↗

PubMed1988

Immunological detection of aflatoxin B1-DNA adducts formed in vivo.

Two monoclonal antibodies (6A10 and 12F5) were obtained after fusion of mouse P3X63-AG.8.653 myeloma cells with spleen cells isolated from BALB/c mice immunized with imidazole ring-opened aflatoxin B1 (AFB1)-DNA and characterized by competitive enzyme-linked immunosorbent assays. Both antibodies are highly specific for imidazole ring opened AFB1-DNA and show some cross-reactivity with AFB1-DNA and no cross-reactivity with 8,9-dihydro-8-(7-guanyl)-9-hydroxy-AFB1, AFB1 conjugated with bovine serum albumin, aflatoxin M1 conjugated with bovine serum albumin, AFB1, or aflatoxin G1. Antibody 6A10 was further characterized and showed no cross-reactivity with DNA modified by several other carcinogens. It could detect adducts with 4-fold higher sensitivity in highly modified DNA (2.5 adducts/100 nucleotides) than in low modified DNA (4 adducts/10(5) nucleotides). With low modified DNA the limit of sensitivity is 5 adducts/10(7) nucleotides. Antibody 6A10 reliably detected adducts formed in vivo in rats and mice treated with AFB1. In a pilot study, AFB1 adducts were detected in liver tissues from individuals living in areas with suspected exposure to AFB1. Monitoring adduct levels in human tissue may provide information not only on carcinogen exposure but also on the relationship among infection with hepatitis B virus, dietary exposure to aflatoxin B1, and liver cancer.

Aflatoxin B1↗

PubMedDate not supplied

Development of milk powder reference materials certified for aflatoxin M1 content (Part II): Certification of milk powder RM 283.

The development of a full cream milk powder reference material, certified for its aflatoxin M1 content (target concentration: 0.1 microgram/kg), is described. The material (RM 283) was prepared and certified within the Reference Material Programme of the Community Bureau of Reference, along with other members of a series of milk powder reference materials. Homogeneity, evaluated by determining the aflatoxin M1 content of 30 units, was found to be acceptable (coefficient of variation of analysis results: 9.1%); stability has been demonstrated in a long-term study. The certification exercise involved 7 laboratories. Calibration, control of recoveries, blank values, and independence of the replicate measurements were emphasized. All sets of results of the certification exercise were accepted for statistical evaluation. A certified value for the aflatoxin M1 content: 0.09(+0.04)(-0.02) micrograms/kg was derived. The certification of RM 283 completes the series of 4 milk powder reference materials having certified aflatoxin M1 contents.

Aflatoxin M1↗

PubMed1988

[Influence of aflatoxin B1 on growth of rats under various nutritional conditions].

The effect of the addition of aflatoxin B1 was studied in 48 male, Sprague-Dawley rats weaned at 21 days of age. The animals of the experimental group received one of the following diets to which aflatoxin B1 was added (5 mg/kg ration), a protein-free diet, the regional basic diet of Northeast Brazil (RBD) containing 9.07% protein, and commercial casein diets (at 10 and 20%). The control groups were fed the same diets without aflatoxin B1. To detect possible body alterations, the body weight and food intake, as well as protein and aflatoxin B1 intakes were recorded. Significant alterations were detected in the experimental groups, especially in the protein-depleted animals, and in those fed the RBD and 10% commercial casein diets, when compared to their controls.

Aflatoxin B1↗

PubMed1985

Clinical and biochemical effects of aflatoxin in feed ration of chicks.

Aflatoxin carcinogenesis appears to relate to multiple factors. This includes bulky adduct formation at DNA guanine N-7. The process also requires more extensive physiological degradation, possibly by the toxin alone as the active principle, but in instances also involving other assaults (e.g., hepatitis B virus). Since aflatoxin carcinogenesis involves complex effects, we have undertaken to define the range of influence of this common food contaminant upon a susceptible model, the broiler-type chick. Aflatoxicosis in two treated groups was indicated by jaundice, coagulopathy, dehydration of combs and shanks, retardation of body weight, and decrease in bursa weight. Blood clotting time, hemoglobin content, erythrocyte and packed-cell volume were affected. Hepatocytes were swollen and had undergone fatty degeneration. Bile duct hyperplasia was evident. Total serum protein, alkaline phosphatase, creatine, lactate dehydrogenase, serum glutamic oxalacetic transaminase and glutamyl transpeptidase were similarly abnormal in birds receiving the contaminated (0.5 and 2.5 micrograms/g aflatoxin B1) feed rations. The aflatoxin B1 and its metabolites were isolated by HPLC from chick serum, liver and muscle.

Aflatoxin B1↗

PubMedDate not supplied

[Various aspects of the effect of nutritional factors on the metabolism and biological action of aflatoxin B1 in the rat liver].

Interrelationships between the quality of nutrition, oxidative hydroxylation of aflatoxin B1 and lipid peroxidation were studied in biomembranes of hepatocyte endoplasmic reticulum of growing male rats of the WAG strain. Activity of the liver microsomal monooxygenase, lipid peroxidation as well as metabolism of aflatoxin B1 were shown to depend on presence of three essential amino acids (lysine, methionine and threonine) and vitamins A, E and C. Deficiency of these compounds altered the aflatoxin metabolism causing formation of highly reactive metabolites, which might accelerate the carcinogenic effect of the xenobiotic. However, formation of free toxic metabolites of aflatoxin was stimulated under conditions of balanced nutrition as a result of which its toxic effect might be increased.

Aflatoxin B1↗

PubMed1981

Effects of aflatoxins in young ponies.

Sixteen clinically normal, healthy ponies were randomly assigned to 4 groups and given aflatoxin B1 in doses of 0.045, 0.030, 0.015, and 0 (control) mg/kg of body weight per day for 21 days (or total doses of 0.945, 0.630, 0.315, and 0 mg/kg). The animals were allowed to recover for 3 months and then were reassigned to 4 treatment groups such that each group during the 2nd trial included a pony from each of the groups of the 1st trial. The animals in the new groups were intubated and were given aflatoxin in doses of 0.4, 0.2, 0.1, and 0 (control) mg/kg/day for 5 days ( or total doses of 2.0, 1.0, 0.5, and 0 mg/kg). Venous blood samples were drawn every other day to monitor for toxicosis; examinations were made for RBC and WBC counts, hemoglobin concentration, PCV, serum urea nitrogen, prothrombin time, and serum concentrations of aspartate aminotransferase, iditol dehydrogenase, alkaline phosphatase, albumin, gamma-glutamyl transferase, and arginase. There were no significant differences between treatment groups and controls (given no aflatoxin) in the toxicologic values examined for during the 1st trial. During the 2nd experiment, 2 of the ponies in the large-dose treatment gorup (2.0 mg/kg) demonstrated increased serum enzyme activities. These animals had been in the large-dose (0.945 mg/kg) and median-dose (0.63 mg/kg) groups during the 1st trial. Arginase, iditol dehydrogenase, and gamma-glutamyl transpeptidase activities became increased on the 4th day of treatment and continued to increase until the 6th day of the experiment (1 day after treatment was terminated). These enzymes approached control group values at 10 days after cessation of treatment. These increases were indicative of hepatocellular toxicity. It was concluded that the possibility of equine aflatoxicosis exists although ponies given high quality rations appear to be less susceptible than some other species. Prior exposure to aflatoxins may predispose to clinical toxicity on subsequent exposure, despite lack of expression of clinical signs.

Aflatoxin B1↗

PubMed1982

Linear dose-response curve for the hepatic macromolecular binding of aflatoxin B1 in rats at very low exposures.

The possibility of a low dose threshold for rat liver macromolecular binding of aflatoxin B1 was investigated. Doses in ng/kg of radiolabeled aflatoxin B1 produced measurable covalent binding of aflatoxin to DNA, RNA, and protein, and the extent of this binding increased linearly over a dose range of 10 to 1000 ng/kg. Macromolecular adduct formation was observed at the lowest dose used (10 ng/kg) which is within the human exposure range. Although diethyl maleate caused a reduction in hepatic glutathione from 5 to 2.3 mumol/g of liver and a slight increase in macromolecular adduct levels, the dose-response curve for macromolecular adduct formation remained linear in both diethyl maleate-pretreated and control groups. These results indicate that macromolecular binding of aflatoxin B1 is essentially a linear function of dose at low exposures and that hepatic glutathione offers little if any protection against this binding.

Aflatoxin B1↗

PubMed1983

Aflatoxin and Reye's syndrome.

This study indicates the association of a mycotoxin (aflatoxin B1) with Reye's syndrome. The presence of aflatoxin B1 in livers from 4 girls and 1 boy aged from 3 to 11 months was detected using two different techniques: a) direct chemical titration of aflatoxin B1 in liver extracts; and b) fluorescence microscopy of unstained liver sections. Our results suggest the existence of acute intoxication by aflatoxin in these children.

Aflatoxin B1↗

PubMed1983

[Aflatoxin M1 - isolation of a toxin-producing strain of the mold Aspergillus flavus].

A strain of Aspergillus flavus producing aflatoxins B1, G1 and M1 was obtained. Aflatoxin M1 constitutes about 5% of the total amount of aflatoxins produced. Aflatoxin M1 was isolated from a crude chloroform extract and was identified by thin silica-gel layer chromatography (TLC), by high-performance liquid chromatography (HPLC) and spectral analysis.

Aflatoxin M1↗

PubMed1984

Fluorometric studies on the binding of aflatoxin B1 to bovine serum albumin.

The quenching of dansylated BSA fluorescence by Aflatoxin B1 at the dansyl emission peak provided a useful method to study Aflatoxin B1 - BSA interaction, making evident one binding site with hydrophobic characteristics. The Ka = 4.0 X 10(4) M-1 at 18 degrees C could assing to this site a role in Aflatoxin B1 transport, but not in storage in the systemic circulation. Evidence supporting the presence of more binding sites, probably of similar characteristics as the former, was obtained from the study of the displacement of ANS bound to BSA by Aflatoxin B1, in spite of the fact that this interaction cannot be explained as a simple competition between ligands.

Aflatoxin B1↗

PubMed1981

Comparison of radioimmunoassay and enzyme-linked immunosorbent assay for determining aflatoxin M1 in milk.

Using a highly specific antibody against aflatoxin M1, a radioimmunoassay (RIA) and an enzyme-linked immunosorbent assay (ELISA) were developed for the quantitation of M1 in milk. RIA was sensitive in the range of 5-50 ng per assay but was subject to interference by whole milk. Extraction and cleanup were therefore necessary for the detection of M1 in milk at 0.5 ng/mL. An ELISA procedure was developed by using an aflatoxin M1-carboxymethyl-horseradish peroxidase conjugate as the ligand. Competitive assays revealed that this system was relatively more sensitive for M1 than for B1, and had a much lower degree of cross-reactivity for aflatoxins B2, G1, G2, B2a, and aflatoxicol. As low as 0.25 ng M1/mL in artificially contaminated milk (raw, whole, skim) could be detected by ELISA in 3 h without extraction or cleanup. Because of its simplicity, sensitivity, and specificity, ELISA is the preferred method for monitoring aflatoxin M1 in milk.

Aflatoxin M1↗

PubMed1981

[Analysis of aflatoxin Ml in fresh milk].

Seventy-seven samples of cow's milk were examined by the method after Stubble-field (1979) for the presence fo aflatoxin M1; 34 of these samples came directly from farms and 43 were mixed, being taken from tank trucks. Aflatoxin M1 was found in five samples from farms and in none of the mixed samples. In the positive cases, concentrations were determined semiquantitatively and were found to range from a trace amount up to 0.38 microgram aflatoxin M1 per litre of milk. Hence the aflatoxin M1 concentration levels never exceeded tha admissible limit value.

Aflatoxin M1↗

PubMed1981

Improved fluorometric-iodine method for determination of aflatoxin in corn.

Several innovations in the fluorometric-iodine (FL-I) method for determining aflatoxin in corn made the procedure faster and more convenient than the original method. Ground corn was packed into a chromatographic column and the aflatoxins were extracted with methylene chloride. Sep-Pak C18 cartridges were used for sample cleanup. A 5 min thin layer chromatographic slide analysis confirmed the presence of aflatoxin, which was quantitated by fluorometric determinations of the iodine derivative of aflatoxin B1.

Aflatoxin B1↗