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PubMedDate not supplied

Molar absorptivities of aflatoxins B1, B2, G1, and G2 in acetonitrile, methanol, and toluene-acetonitrile (9 + 1) (modification of AOAC Official Method 971.22): collaborative study.

Four laboratories participated in a mini-collaborative study of AOAC Official Method 971.22, Standards for Aflatoxins, Thin-Layer Chromatographic Method, to extend the method to 3 replacement solvents for benzene for calibration of standard aflatoxin solutions. Triplicate test sample vials, each containing 25 micrograms of the respective aflatoxin for each of the 4 aflatoxins and for each of the solvents, were prepared and sent to each collaborator. The collaborators dissolved the aflatoxin in each vial in 2 mL solvent, measured the UV spectrum, and reported the absorptivity maxima near 350 nm. The concentrations of the aflatoxins in the test samples were determined by dissolving identical test samples in benzene-acetonitrile (98 + 2) and following the procedure described in AOAC Official Method 971.22. These concentrations were, in turn, used to determine the molar absorptivities in the other 3 solvents (see Table 1). AOAC Official Method 971.22 has been modified to extend its applicability to 3 replacement solvents for benzene for calibration of standard aflatoxin solutions.

Absorption↗

PubMed2004

[Comparison between the post-column derivatization with bromine by HPLC and the fluorometric analysis for determination of aflatoxins in medicinal herbs and plant extracts].

AIM: To compare the post-column derivatization technique (IAC-PCD-HPLC) for the determination of aflatoxins B1, B2, G1 and G2 and the rapid procedure with fluorometric analysis (SFB) for the determination of total aflatoxins. METHODS: The method of post-column derivatization with bromine by HPLC consisted of extraction of the sample with MeOH-H2O (70:30) followed by clean-up of the extracts with immunoaffinity columns and finally, HPLC determination with fluorescence detection. Aflatoxins B1 and G1 were determined as their bromine derivatives, produced in an on-line post-column derivatization system. In SFB method, samples were ground and extracted with methanol-water (70:30). A portion of the extract was cleaned up by passage through a immunoaffinity column, One mL of purified extract was derivatized with a bromine reagent, and fluorescence of the solution was immediately quantified with a calibrated fluorometer containing a broad wavelength pulsed xenon light source. RESULTS: In IAC-HPLC method, the overall average recoveries for three different medicinal herbs spiked at levels of 1.3 and 2.6 ng x g(-1) of total aflatoxins ranged from 93% to 97%. The detection limit was 0. 06 microg x kg(-1) for both G2 and B2 and 0.20 microg x kg(-1) for both G1 and B1, based on a signal/noise 3:1 and the precision (within-laboratory relative standard deviation) ranged from 0.8% to 1.4%. Each of aflatoxins B1, B2, G1 and G2 in 39 kind medicinal materials were determined by IAC-PCD-HPLC, and the total aflatoxins were determined by SFB. CONCLUSION: The SFB method is not the suitable method for the determination of total aflatoxins in medicinal herbs and plant extracts.

Aflatoxin B1↗

PubMedDate not supplied

Mutagenic effect of aflatoxin G1 in comparison with B1.

Available data indicate structure activity relationships in toxicity and carcinogenecity of aflatoxins in the order of B1 greater than G1 greater than G2 greater than B2. This set of tools is useful for investigations in experimental chemical mutagenesis. The present study is the second in a series concerning the activity of this group of aflatoxins on human chromosomes, using the techniques of Geimsa banding and sister chromatid exchanges. The results showed that aflatoxin G1 is a mutagenic agent to human chromosomes. The distribution of breaks on individual chromosomes according to relative length was nonrandom. Chromosomes 1, 2, 3, 4, and 5, the largest chromosomes, have more breaks, whereas chromosomes 19, 20, 21, and 22, the smallest chromosomes, have less than the expected number of breaks. Comparing these results with that of aflatoxin B1, we found that (1) the mutagenic activity of B1 on human chromosomes is higher than that of G1, and (2) although chromosomes 2, 11, 19, and 20 were the most affected by aflatoxin B1, chromosomes 1, 2, 3, 4, and 5 were the most affected by aflatoxin G1. This result indicates structure activity relationships in mutagenecity that are in agreement with those of the toxicity and carcinogenecity of aflatoxins B1 and G1.

Aflatoxin B1↗

PubMedDate not supplied

A study on the inhibition of aflatoxin B1 induced hepatocarcinogenesis by the Rhizopus delemar.

The effect of Rhizopus delemar on the carcinogenicity in rats of Aflatoxin B1 was studied. The Aflatoxin B1 was administered in free drinks to each male wistar rat at 126 micrograms per week such that a total dose of 3.40 mg was given over a period of 27 weeks. The culture abstract of Rhizopus delemar was added simultaneously to a group of these rats by mixing the Aflatoxin B1 solution. Animals were killed separately during 18th, 30th, 38th and 52nd week. Liver cell altered foci and neoplasms were qualified by using light microscopic and electromicroscopic morphology, by the morphometry and by the enzymic reactions. In the group of Aflatoxin B1 the incidence of hepatocellular carcinoma was 71%. In the group receiving Rhizopus delemar together with Aflatoxin B1, the hyperplastic foci and pathological enzymic foci were decreased at all times pointed and atd at termination, and in none of the rats had liver neoplasms appeared. The result of this experiment showed that the Rhizopus delemar has intensive capacity in inhibiting the toxic damage and carcinogenicity of the liver by the Aflatoxin B1, because it is not only able to postpone the appearance of altered foci and to control their development but also to accelerate their withdraw in advance. The Rhizopus delemar can be used as a feasible and efficacious means to control the intoxication of Aflatoxin B1.

Aflatoxin B1↗

PubMed1986

A preliminary survey on aflatoxin exposure in Singapore.

Aflatoxins (naturally occurring chemicals of fungal origin) are powerful liver carcinogens, and increased incidence of hepatocellular carcinoma has been observed in areas where exposure to this mycotoxin is high (e.g., Africa, China). These areas also have a high incidence of HBV infection. It has been suggested that this environmental carcinogen interact with HBV in the aetiogenesis of hepatocellular carcinoma in these areas. The aim of this study was to determine the level of aflatoxin exposure in the local population. Fifty healthy adults were studied. Details of dinner taken the previous evening were obtained. Early morning urine was collected and aflatoxin quantitated by ELISA following purification on an antibody affinity column. Rabbit polyclonal antibody to aflatoxin B1 was used, and the mean of at least two assays were determined. Six individuals (12%) showed ELISA inhibition values of more than 25%, equivalent to aflatoxin levels of more than 100 pg/ml in urine. Levels ranged from 185 pg/ml to 2300 pg/ml aflatoxin B1 equivalents. All 6 individuals consumed fried food. The highest level was found in a medical student who had 'satay' (crushed peanut) sauce with dinner. This is in contrast to 52% individuals from Gambia with urine aflatoxin levels between 100 and 1000 pg/ml.

Adult↗

PubMedDate not supplied

Beta-cyclodextrin post-column fluorescence enhancement of aflatoxins for reverse-phase liquid chromatographic determination in corn.

beta-Cyclodextrin enhances the fluorescence of aflatoxins B1 and G1 in aqueous systems. This effect was utilized in developing a unique reverse-phase liquid chromatographic (LC) method for determination of aflatoxins B1, B2, G1, and G2 (B1 detection limit 1 ppb), without preparing derivatives of B1 and G1. The aflatoxins are dissolved in methanol or the mobile phase for injection onto the LC system. Using a mobile phase of methanol-beta-cyclodextrin (1 + 1), the aflatoxins are resolved on a C18 column. Fluorescence of the aflatoxins is enhanced by post-column introduction of an aqueous concentrated beta-cyclodextrin solution. All 4 aflatoxins elute within 10 min in the order G2, G1, B2, B1. Fluorescence responses for B1 and G1 standards were linear over the concentration range 0.5-10 ng, yielding correlation coefficients (r) of 0.9989 and 1.000, respectively. The average peak response ratio for G1:B1 for the mobile phase-enhancement solution described was 0.765 with a coefficient of variation (CV) of 0.98%. CVs were 6.2, 9.0, and 7.5% for multiple assays of aflatoxin B1 in 3 samples of naturally contaminated corn. For samples of corn spiked to a total B1 content of 8.3 ng/g, average B1 recovery was 90% (CV 11.7%).

Aflatoxin B1↗

PubMedDate not supplied

Negative ion chemical ionization mass spectrometric method for confirmation of identity of aflatoxin B1: collaborative study.

An interlaboratory study of a negative ion chemical ionization mass spectrometric (MS) confirmation procedure for aflatoxin B1 was conducted in laboratories in the United States, England, and West Germany. Twelve partially purified, dry film extracts from naturally and artificially contaminated roasted peanuts, cottonseed, and ginger root containing varying quantities of aflatoxin B1 were distributed to the participating laboratories. The extracts required additional cleanup before MS analysis, using either an acidic alumina column and preparative thin layer chromatography (TLC) or a 2-dimensional TLC procedure. Recovery of purified aflatoxin B1 was influenced by the degree of recovery of sample from acid alumina and/or the TLC plate and incomplete elution of aflatoxin B1 from silica gel. Factors affecting MS confirmation included the purity and recovery of aflatoxin and MS instrument sensitivity. Aflatoxin B1 identity was confirmed in 19.5, 90.9, and 100% of samples containing less than 5, 5-10, and greater than 10 ng aflatoxin B1/g product, respectively, by solid probe introduction using full mass scans. The MS method has been adopted official first action.

Aflatoxin B1↗

PubMedDate not supplied

Rapid quantitation and confirmation of aflatoxins in corn and peanut butter, using a disposable silica gel column, thin layer chromatography, and gas chromatography/mass spectrometry.

A simple, rapid, and solvent-efficient method for determining aflatoxins in corn and peanut butter is described. Aflatoxins B1, B2, G1, and G2 were extracted from 50 g sample with 200 mL methanol-water (85 + 15). A portion of the extract was diluted with 10% NaCl solution to a final concentration of 50% methanol, and then defatted with hexane. The aflatoxins were partitioned into chloroform. The chloroform solution was evaporated, and the residue was placed on a 0.5 g disposable silica gel column. The column was washed with 3 mL each of hexane, ethyl ether, and methylene chloride. Aflatoxins were eluted with 6 mL chloroform-acetone (9 + 1). The solvent was removed by evaporation on a steam bath, and the aflatoxins were determined using thin layer chromatography (TLC) with silica gel plates and a chloroform-acetone (9 + 1) developing solvent. Overall average recovery of aflatoxin B1 from corn was 82%, and the limit of determination was 2 ng/g. For mass spectrometric (MS) confirmation, aflatoxin B1 in the extract from 3 g sample (20 ng/g) was purified by TLC and applied by direct on-column injection at 40 degrees C into a 6 m fused silica capillary gas chromatographic column. The column was connected directly to the ion source. After injection, the temperature was rapidly raised to 250 degrees C, and the purified extract was analyzed by negative ion chemical ionization MS.

Aflatoxin B1↗

PubMed1981

Effect of boiling, frying, and baking on recovery of aflatoxin from naturally contaminated corn grits or cornmeal.

Corn grits naturally contaminated with aflatoxins were used for making boiled grits, and portions of the boiled grits were used for making pan-fried grits; cornmeal naturally contaminated with aflatoxins was used for making corn muffins. Procedures and recipes were derived from cookbook and market package recommendations. From analyses of the products for aflatoxins before and after preparation of the table-ready products, it was determined that 72 +/- 9% (n = 15) of the aflatoxin found in the original grits could be recovered after the grits were boiled. The recovery of aflatoxin B1 after the grits were fried was either 66 +/- 10% (n = 6) or 47 +/- 8% (n = 9), depending on whether 3 cups of water or 4 cups of water per cup of grits, respectively, were used for preparing the boiled grits before frying. Similarly, it was determined that 87 +/- 4% (n = 9) of the aflatoxin B1 found in the original cornmeal could be recovered from the baked muffins. No detectable aflatoxin B2 a was present in the extracts from any of the table-ready products.

Aflatoxin B1↗

PubMed1982

Effects of sex difference and dietary protein level on the binding of aflatoxin B1 to rat liver chromatin proteins in vivo.

The risk of aflatoxin-induced hepatocarcinoma is greater in males than in females and is similarly higher in animals fed 20% casein diets than in those fed 5%. In this study, groups of male and female F344 rats were fed either a 5 or 20% casein diet for 6 weeks. Two hr after a 1-mg/kg i.p. dose of [3H]aflatoxin B1, animals were killed and four protein fractions were sequentially extracted from the liver chromatin of each. Within each treatment group, aflatoxin binding to nonhistones was greater than to histones, both before and after dialysis. Comparing treatments, the higher-risk factors were associated with a greater liver content of aflatoxin as well as with increased binding of both nondialyzable and dialyzable aflatoxin to the various fractions. The high degree of correlation between total liver content and adduct formation implicates the former as a major determinant of the latter. Also associated with the higher-risk factors was a shift in the distribution of dialyzable aflatoxin toward greater adduct formation with one of the nonhistone fractions, suggesting the possibility of a role for noncovalent aflatoxin:protein adducts in hepatocarcinogenesis.

Aflatoxin B1↗

PubMed2000

Environmental and genetic determinants of aflatoxin-albumin adducts in the Gambia.

Aflatoxins together with chronic hepatitis B virus (HBV) infection contribute to the high incidence of hepatocellular carcinoma in developing countries. An understanding of the mechanism of interaction between these factors would provide a strong rationale for developing effective prevention strategies. In this study in The Gambia we examined the effect of environmental (place of residence and timing of sample collection) and host factors (age, sex, HBV status and interindividual variations in carcinogen metabolising enzymes) in determining blood aflatoxin-albumin adduct levels in 357 individuals of whom 181 were chronic HBV carriers. Samples were analysed for aflatoxin-albumin adducts, HBV status and genotypes of glutathione S-transferase (GST) M1, GSTT1, GSTP1 and epoxide hydrolase (EPXH). Urine samples were analysed for 6beta-hydroxycortisol:cortisol ratio as a marker of cytochrome P450 (CYP) 3A4 activity. Adduct levels were significantly higher in subjects resident in rural [geometric mean adduct level 34.9 pg aflatoxin B1-lysine equivalent (28.5-42.8; 95%CI)/mg albumin] than in periurban areas [22.2 pg (14.9-33.4)/mg] and were approximately twice as high in the dry season [mid-February to March; 83.2 pg (53.3-130.8)/mg] than the wet [July to August; 34.9 pg (28.5-42.8)/mg]. In contrast, HBV status, CYP3A4 phenotype, GSTT1, GSTP1 and EPXH genotypes were not associated with aflatoxin-albumin adduct level. However, mean adduct levels were significantly higher in non-HBV infected subjects with GSTM1 null genotype. The main factors which affect aflatoxin-albumin adduct levels in this population are environmental, notably place of residence and timing of sample collection. This study further emphasises the priority to reduce aflatoxin exposure in these communities by primary prevention measures.

Adolescent↗

PubMed1999

Fungal degradation of aflatoxin B1.

A number of fungal cultures were screened to select an organism suitable to be used in the detoxification of aflatoxin B1. They were co-cultured in Czapek-Dox-Casamino acid medium with aflatoxin B1 producing Aspergillus flavus. Several fungal cultures were found to prevent synthesis of aflatoxin B1 in liquid culture medium. Among these Phoma sp., Mucor sp., Trichoderma harzianum, Trichoderma sp. 639, Rhizopus sp. 663, Rhizopus sp. 710, Rhizopus sp. 668, Alternaria sp. and some strains belonging to the Sporotrichum group (ADA IV B14(a), ADA SF VI BF (9), strain 720) could inhibit aflatoxin synthesis by > or =90%. A few fungi, namely ADA IV B1, ADA F1, ADA F8, also belonging to the Sporotrichum group, were less efficient than the Phoma sp. The Cladosporium sp. and A. terreus sp. were by far the least efficient, registering <10% inhibition. The cultures which prevent aflatoxin biosynthesis are also capable of degrading the preformed toxin. Among these, Phoma sp. was the most efficient destroying about 99% of aflatoxin B1. The cell free extract of Phoma sp. destroyed nearly 50 microg aflatoxin B1 100 ml(-1) culture medium (90% of the added toxin), and this was more effective than its own culture filtrate over 5 days incubation at 28+/-2 degrees C. The degradation was gradual: 35% at 24 h, 58% at 48 h, 65% at 72 h, 85% at 96 h and 90% at 120 h. The possibility of a heat stable enzymatic activity in the cell free extract of Phoma is proposed.

Aflatoxin B1↗

PubMed1987

Aflatoxin exposure, hepatitis B virus infection and liver cancer in Swaziland.

A study was carried out in Swaziland to assess the relationship between aflatoxin exposure, hepatitis B infection, and the incidence of liver-cell carcinoma, which is the most commonly occurring malignancy among males in Swaziland. Levels of aflatoxin intake were evaluated in dietary samples from households across the country, and crop samples taken from representative farms. Prevalence of hepatitis B markers was estimated from the serum of blood donors, and liver cancer incidence was recorded for the years 1979-83 through a national system of cancer registration. Across 4 broad geographic regions, there was a more than 5-fold variation in the estimated daily intake of aflatoxin, ranging from 3.1 to 17.5 micrograms. The proportion of HBV-exposed individuals was very high (86% in men), but varied relatively little by geographic region; the prevalence of carriers of the surface antigen was 23% in men, and varied from 21 to 28%. Liver cancer incidence varied over a 5-fold range, and was strongly associated with estimated levels of aflatoxin. In an analysis involving 10 smaller subregions, aflatoxin exposure emerged as a more important determinant of the variation in liver cancer incidence than the prevalence of hepatitis infection. Aflatoxin estimates from crop samples appeared to be a reasonable surrogate for dietary measurements. A comparison with dietary aflatoxin levels measured in an earlier survey in Swaziland suggested that programmes aimed at reducing contamination levels had had some success.

Aflatoxins↗

PubMed1992

Aflatoxins isolated by immunoaffinity chromatography from foods consumed in The Gambia, West Africa.

An aflatoxin-specific, monoclonal antibody-based immunoaffinity chromatography method has been developed for the rapid isolation of aflatoxins from human foods. Aflatoxins were isolated by immunoaffinity chromatography from a variety of cooked foods, including maize, rice, millets, groundnut sauces, and leaf sauces, collected in The Gambia, West Africa. The aflatoxins were measured by direct fluorescence or high-pressure liquid chromatography. The highest levels were found for groundnut sauces, mean 162 ppb (range 18 to 943 ppb) for 18 positive samples, but aflatoxins were found in other foods; e.g., maize, mean 9.7 ppb (range 2 to 35 ppb) for nine positive samples. The food analysis results were used with records of the amounts of cooked food to estimate a mean daily intake for an individual of the order of 3.5 micrograms of aflatoxins per day. This approach for exposure assessment is considered in relation to other biomarkers of aflatoxin exposure using biological fluids.

Aflatoxins↗

PubMed1997

Relationship between aflatoxin biosynthesis and sporulation in Aspergillus parasiticus.

Regulation of aflatoxin biosynthesis during differentiation of Aspergillus parasiticus was analyzed by using a drug that inhibits the development of the fungus and mutants affected in sporulation. Diaminobutanone, a competitive inhibitor of ornithine decarboxylase, repressed spore germination. If added after spore germination had occurred, it blocked sporulation completely and suppressed aflatoxin biosynthesis, but was only partially inhibitory of mycelial growth. Putrescine partially counteracted the inhibitory effect of the drug on both sporulation and aflatoxin biosynthesis. Analysis of mutants affected in sporulation confirmed the existence of a relationship between sporulation and aflatoxin formation. A nonsporulating mutant was unable to synthesize aflatoxins. In a sectorial mutant, the sporulating sector synthesized aflatoxins normally, whereas the asporogenous sector was unable to do so. It is suggested that regulation of aflatoxin biosynthesis is correlated with the sporulation process.

Aflatoxins↗

PubMed1996

In situ absorption of aflatoxins in rat small intestine.

To evaluate the rate at which the four main aflatoxins (aflatoxins B1, B2, G1 and G2) are able to cross the luminal membrane of the rat small intestine, a study about intestinal absorption kinetics of these mycotoxins has been made. In situ results obtained showed that the absorption of aflatoxins in rat small intestine is a very fast process that follows first-order kinetics, with an absorption rate constant (ka) of 5.84 +/- 0.05 (aflatoxin B1), 4.06 +/- 0.09 (aflatoxin B2), 2.09 +/- 0.03 (aflatoxin G1) and 1.58 +/- 0.04 (aflatoxin G2) h-1, respectively.

Absorption↗

PubMed1990

Effect of peanut tannin extracts on growth of Aspergillus parasiticus and aflatoxin production.

Twenty-three peanut (Arachis hypogaea L.) genotypes were evaluated for kernel resistance to Aspergillus parasiticus Spear. colonization and aflatoxin contamination when incubated under high relative humidity. Also, tannin-containing extracts from kernel coats (testae) and cotyledons of these genotypes were prepared and tested for their effect on A. parasiticus growth and aflatoxin production in vitro. The lowest degree of colonization, less than 30%, was noted in kernels from the genotypes, Toalson x UF 73-4022 (selections TX-798731 and TX-798736), A72118, SN 55-437, PI337409, and Florunner. Genotypes with low levels of colonization also had the lowest aflatoxin contamination. The coefficient of correlation between infection frequency and aflatoxin contamination was 0.66. Higher levels of tannins were detected in the testae (23.9-97.2 mg g tissue) compared to the cotyledons (0.17-0.82 mg g tissue). Some of the methanol-extracted and water-soluble tannin extracts from testae and cotyledons, when incorporated in yeast extract sucrose liquid medium (100 mg l), significantly inhibited A. parasiticus growth and reduced the levels of aflatoxin produced. There was no overall correlation between the peanut genotypes and the influence of tannin extracts on A parasiticus growth and aflatoxin production. However, correlations were higher for specific genotypes. For example, the coefficient of correlation between the ability of tannin extracts from testae of genotypes PI337409 and TX-798736 to inhibit aflatoxin production was 0.93 and 0.85 respectively.

Aflatoxins↗

PubMed1989

Transformation of Aspergillus flavus to study aflatoxin biosynthesis.

Aflatoxin contamination of agricultural commodities continues to be a serious problem in the United States. Breeding for resistant genotypes has been unsuccessful and detoxification of food sources is not economically feasible. New strategies for control may become apparent once more is known about the biosynthesis and regulation of aflatoxin. Although the biosynthetic pathway of aflatoxin has been extensively studied, little is known about the regulation of the individual steps in the pathway. We have developed a genetic transformation system for Aspergillus flavus that provides a new and expedient approach to studying the biosynthesis of aflatoxin and its regulation. Through the use of this genetic transformation system, genes for aflatoxin biosynthesis can be identified and isolated by the complementation of aflatoxin negative mutants. In this paper we discuss molecular strategies for studying the regulation and biosynthesis of aflatoxin.

Aflatoxins↗