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PubMed1982

Association of aflatoxin B1 with plasma components in vitro.

The in vitro association of [3H]aflatoxin B1 with plasma from man, pig and rat was compared. The uptake of aflatoxin B1 into plasma was rapid and did not differ between species. Its association with lipoprotein fractions was minimal when incubated with whole plasma; column chromatography of plasma from all 3 species resulted in the elution of the aflatoxin B1 with the low Mr plasma proteins. It is concluded that although aflatoxin B1 is a hydrophobic compound, it does not partition into the plasma lipoproteins and that its in vitro uptake into plasma does not differ among the 3 species studied. Plasma transport is probably not one of the factors determining species specificity for carcinogenesis by aflatoxin B1.

Aflatoxin B1↗

PubMedDate not supplied

The effect of indole-3-carbinol, an aflatoxin B1 hepatocarcinoma inhibitor, and other indole analogs on the rainbow trout hepatic mixed function oxidase system.

Rainbow trout were fed diets containing 3.4 mmol of indole-3-carbinol, indole-3-ethanol, indole-3-aldehyde, or indole-3-acetic acid in 100 g salmon oil/kg diet for 3 weeks. The indoles did not increase hepatic microsomal cytochrome(s) P-450 or P-448 nor induce the associated mixed function oxidase enzyme activities as measured by ethoxyresorufin-O-deethylase (EROD) and benzphetamine-N-demethylase activities. Indole-3-carbinol did not alter the in vitro metabolism of aflatoxin B1 to aflatoxicol and aflatoxin M1; but the other indoles did suppress the formation of aflatoxin M1 from aflatoxin B1. The results suggest that the mechanism by which indole-3-carbinol protected rainbow trout from aflatoxin B1 (AFB1) hepatocarcinogenesis was not via the alteration of the mixed function oxidase system.

Aflatoxin B1↗

PubMed2005

Safety and efficacy evaluation of aqueous citric acid to degrade B-aflatoxins in maize.

Chemical inactivation of aflatoxin B1 (AFB1) and aflatoxin B2 (AFB2) in maize grain by means of 1N aqueous citric acid was confirmed by the AFLATEST immunoaffinity column method, high performance liquid chromatography (HPLC), and the Ames test (Salmonella-microsomal screening system). The AFLATEST assay showed that aflatoxins in the maize grain with an initial concentration of 29 ng/g were completely degraded and 96.7% degradation occurred in maize contaminated with 93 ng/g when treated with the aqueous citric acid. Aflatoxin fluorescence strength of acidified samples was much weaker than untreated samples as observed in HPLC chromatograms. On the other hand, the Ames test results indicated that the mutagenic activity of acidified samples was greatly reduced compared with that of untreated samples based on his- --> his+ reversions in the Salmonella TA100 strain. Chemical inactivation appears to be a promising method of removing aflatoxin from food commodities.

Aflatoxin B1↗

PubMed2006

Incidence of aflatoxins in Iran pistachio nuts.

Aflatoxins (AF) are highly toxic and carcinogenic secondary fungal metabolites and have been detected in various food commodities including pistachio nuts. Pistachio nuts were produced in Iran during March 2002-February 2003 analyzed for aflatoxin B1 (AFB1), aflatoxin B2 (AFB2), aflatoxin G1 (AFG1) and aflatoxin G2 (AFG2) using immunoaffinity column and quantitated by HPLC and/or TLC-scanner. In this regard, 3356 pistachio nut samples were collected. After dividing samples to sub-samples, 10,068 AF analyses were done. Among 10,068 samples analyzed, AFB1 was detected in 3699 samples (36.7% of the total) with the mean and median of 5.9 (+/-41.7) ng/g and 0.1 ng/g, respectively. Total AF (AFT) was detected in 2852 samples (28.3% of the total) with the mean and median of 7.3 (+/-53.2)ng/g and 0.4 ng/g, respectively. AFB1 level in 1191 samples (11.8%) was above the maximum tolerated level (MTL) of AFB1 in pistachio nut in Iran (5 ng/g). Regarding AFT, the mean contamination level (7.3 ng/g) was lower than MTL of AFT in pistachio nut in Iran as well as lower than the proposed draft maximum level of Codex Committee on Food Additives and Contaminants for AFT (15 ng/g), and only 7.5% of samples had levels above the MTL.

Aflatoxin B1↗

PubMed1998

Interaction between cyclodextrins and aflatoxins Q1, M1 and P1. Fluorescence and chromatographic studies.

The fluorescence properties of the aflatoxins M1, Q1, P1 in solution and the effect of various cyclodextrins (alpha-, beta-, gamma-, hydroxypropyl-beta- and alpha-beta-heptakis-di-O-methyl-beta-) on their fluorescence emission were studied. Among the aflatoxins, a substantial enhancement of the fluorescence emission of aflatoxin Q1 in the presence of aqueous solutions of alpha-, beta-, hydroxypropyl-beta, and alpha-beta-heptakis-di-O-methyl-beta-cyclodextrin, was observed. On the contrary, gamma-cyclodextrin proved to be inefficient to enhance the fluorescence properties of this compound. No important fluorescence enhancement was found for aflatoxins P1 or M1 for any of the cyclodextrin derivatives tested. The complex formation constant (Kf) of these compounds with beta-cyclodextrin was chromatographically determined, and from the results obtained, we can conclude that Kf cannot be used alone to explain the fluorescence increase. Thermodynamic studies showed that delta-H and delta-S parameters, associated with the partition of aflatoxins in RP-HPLC, increased when beta-cyclodextrin was added to the eluent.

Aflatoxin M1↗

PubMed2001

Natural co-occurrence of aflatoxin and cyclopiazonic acid in peanuts grown in Argentina.

Natural occurrence of aflatoxins and cyclopiazonic acid (CPA) contamination in peanuts was investigated. Co-occurrence of CPA and aflatoxins was detected in two of 50 samples analysed. The levels of these toxins found in positive samples were 4300 and 493 microg kg(-1) for CPA, 625 and 435 microg kg(-1) for aflatoxin B1 (AFB1), and 625 and 83 microg kg(-1) for aflatoxin G1 (AFG1), respectively. Levels of CPA contamination in the positive samples were similar to those registered in other substrates. This is the first report of natural co-occurrence of CPA and aflatoxins in Argentina.

Aflatoxin B1↗

PubMed2002

Comparison of nixtamalization and extrusion processes for a reduction in aflatoxin content.

Traditional nixtamalization and an extrusion method for making the dough (masa) for corn tortillas that requires using lime and hydrogen peroxide were evaluated for the detoxification of aflatoxins. The traditional nixtamalization process reduced levels of aflatoxin B(1) (AFB(1)) by 94%, aflatoxin M(1) (AFM(1)) by 90% and aflatoxin B(1)-8,9-dihydrodiol (AFB(1)-dihydrodiol) by 93%. The extrusion process reduced levels of AFB(1) by 46%, AFM(1) by 20% and AFB(1)-dihydrodiol by 53%. Extrusion treatments with 0, 0.3 and 0.5% lime reduced AFB(1) levels by 46, 74 and 85%, respectively. The inactivation of AFB(1), AFM(1) and AFB(1)-dihydrodiol in the extrusion process using lime together with hydrogen peroxide showed higher elimination of AFB(1) than treatments with lime or hydrogen peroxide alone. The extrusion process with 0.3% lime and 1.5% hydrogen peroxide was the most effective process to detoxify aflatoxins in corn tortillas, but a high level of those reagents negatively affected the taste and aroma of the corn tortilla as compared with tortillas elaborated by the traditional nixtamalization process.

Aflatoxin B1↗

PubMed2004

Occurrence of aflatoxins and fumonisins in preharvest maize from south-western Nigeria.

A survey was conducted on the incidence of fungi, and the natural occurrence of aflatoxins and fumonisins in preharvest maize from fields in south-western Nigeria. Mycological examinations revealed the predominance of F. verticillioides (Zea mays) (syn. F. moniliforme), occurring in 89.3% of samples with a mean kernel infection of 49.4%, while Aspergillus flavus was isolated from 65% of samples having a mean kernel infection of 6.8%. Aflatoxin B1 was detected in 18.4% of samples with a mean of 22 micrograms kg-1, while aflatoxins B2, G1 and G2 were present in 7.8, 2.9 and 1% of the samples with mean levels of 10, 8 and 7 micrograms kg-1, respectively, in contaminated samples. Total aflatoxins ranged from 3 to 138 micrograms kg-1 in positive samples, with a mean of 28 micrograms kg-1. Fumonsin B1 was the predominant toxin detected in terms of frequency (78.6% of samples) and quantity (concentration range 70-1780 micrograms kg-1, mean = 495 micrograms kg-1). Fumonisin B2 was detected in 68 samples (66%) with a mean of 114 micrograms kg-1. Fifteen samples were contaminated with both aflatoxins and fumonisins.

Aflatoxin B1↗

PubMed2004

Degradation of aflatoxins in peanut kernels/flour by gaseous ozonation and mild heat treatment.

Aflatoxins occur naturally in many agricultural crops causing health hazards and economic losses. Despite improved handling, processing and storage, they remain a problem in the peanut industry. Therefore, new ways to detoxify contaminated products are needed to limit economic/health impacts and add value to the peanut industry. The study was conducted (1) to evaluate the effectiveness of ozonation and mild heat in breaking down aflatoxins in peanut kernels and flour, and (2) to quantify aflatoxin destruction compared with untreated samples. Peanut samples were inoculated with known concentrations of aflatoxins B1, B2, G1 and G2. Samples were subjected to gaseous ozonation and under various temperatures (25, 50, 75 degrees C) and exposure times (5, 10, 15 min). Ozonated and non-ozonated samples were extracted in acetonitrile/water, derivatized in a Kobra cell and quantified by high-performance liquid chromatography. Ozonation efficiency increased with higher temperatures and longer treatment times. Regardless of treatment combinations, aflatoxins B1 and G1 exhibited the highest degradation levels. Higher levels of toxin degradation were achieved in peanut kernels than in flour. The temperature effect lessened as the exposure time increased, suggesting that ozonation at room temperature for 10-15 min could yield degradation levels similar to those achieved at higher temperatures while being more economical.

Aflatoxin B1↗

PubMedDate not supplied

Aflatoxin M1 occurrence in dairy products marketed in Italy.

In 1984, 313 samples of imported liquid milk and 159 samples of imported cheese were checked for aflatoxin M1; 225 of the milk samples came from FR Germany and 88 from France, while 82 of the cheese samples came from France, 34 from FR Germany and 43 from the Netherlands. The number of positive samples was small both for German (13.8%) and for French (12.5%) milks, and the contamination levels were very low (maximum 23 ng/l). As regards the cheeses, aflatoxin M1 was detected in 19.5, 26.5 and 53.5% of the French, German and Dutch samples respectively, but only 2 French samples exceeded 250 ng/kg, the limit set by Swiss law. In 1985, two surveys were carried out on 276 milk samples mostly obtained from individual farms and on 416 cheese samples taken from all parts of the country. As regards the milk samples, 70 (25.3%) contained aflatoxin M1, but generally at very low levels; in fact only 7 (2.5%) of the samples exceeded 50 ng/l. Aflatoxin M1 was found in 130 (31.3%) of the cheese samples, but here again only 9 (2.2%) exceeded 250 ng/kg. There was no significant difference in aflatoxin M1 levels between Italian, German and French cheese samples but these were significantly lower (P less than 0.01) than in Dutch samples.

Aflatoxin M1↗

PubMedDate not supplied

Long-term administration of low doses of mycotoxins to poultry. 1. Residues of aflatoxin B1 and its metabolites in broilers and laying hens.

A study was performed to determine aflatoxin residues in tissues and organs of male broilers and hens that had been fed a diet contaminated with 50 micrograms/kg aflatoxin B1 (AFB1). Residue levels of AFB1, aflatoxicol (Ro), aflatoxin M1 (AFM1) and aflatoxin B2a (AFB2a) were determined by an HPLC method and, with the exception of AFB2a, were detected in the liver, kidney and thigh of both male broilers and hens. The highest levels found were for Ro in liver (1.10 and 0.60 micrograms/kg for male broilers and hens, respectively). On the other hand no detectable amounts of aflatoxins were found in any tissue after withdrawal periods of 14 and 33 days for male broilers and laying hens respectively.

Aflatoxin B1↗

PubMedDate not supplied

A simple quantitative HPLC method for determination of aflatoxins in cereals and animal feedstuffs using gel permeation chromatography clean-up.

A simple and sensitive procedure is described for the analysis of aflatoxins B1, B2, G1 and G2 in cereal and animal feedstuff samples. Aflatoxins are extracted with dichloromethane:water (10:1). Gel permeation chromatography (GPC) using a column packed with Bio-beads S-X3 and dichloromethane:hexane (3:1) as the eluent is used for clean-up of extracts prior to separation and quantification of aflatoxins by HPLC. The eluent fraction containing the aflatoxins is concentrated by evaporation under reduced pressure and the aflatoxins separated by reverse phase HPLC on an ODS column. Quantitative results have been obtained at levels down to 1 microgram/kg, and average recoveries from samples of wheat, maize and compound feed spiked at levels of 10 and 40 micrograms/kg were greater than 80%, 70% and 65% respectively.

Aflatoxin B1↗

PubMedDate not supplied

Methods for determination of aflatoxin M1 in milk and milk products--a review of performance characteristics.

Among numerous methods that have been published for determination of aflatoxin M1 in milk and milk products, the following have been selected for review of performance characteristics: methods for which interlaboratory testing has been carried out, methods proposed in support of national (Swiss) regulations following inclusion in check sample series, and methods that report detection limits for milk of less than or equal to 5 ng/l (less than or equal to 0.005 microgram/l) or less than or equal to 10 ng/kg (less than or equal to 0.01 microgram/kg) for cheese. It is practical to determine aflatoxin M1 in milk with good accuracy and precision down to low ng/l concentrations using thin-layer chromatography, high-performance liquid chromatography or enzyme-linked immunosorbent assay for quantitation. However, measurement at such low levels has not been tested by a true collaborative study. Confirmation of identity of aflatoxin M1 at low ng/l levels has also been reported. Recent evidence suggests that consideration should be given to inclusion of aflatoxin M4 in methods for aflatoxin M1.

Aflatoxin M1↗

PubMedDate not supplied

Determination of aflatoxin B1 levels in peanut butter using an immunoaffinity column clean-up procedure: inter-laboratory study.

Ten United Kingdom laboratories participated in an evaluation of an immunoaffinity column sample preparation procedure used to prepare aflatoxin B1 containing extracts obtained from peanut butters contaminated by aflatoxins. Each laboratory was sent seven randomly numbered samples of roasted peanut butter which included two sets of undisclosed triplicates. These two peanut butters were naturally contaminated with aflatoxin B1 at levels of about 12 and 35 micrograms/kg. The other sample was a nominal blank peanut butter containing approximately 2 micrograms/kg of aflatoxin B1 which was also employed by participants for recovery experiments. Participating laboratories were instructed to follow a protocol regarding the use of the immunoaffinity columns for extract preparation, but were allowed a free choice of instrumental technique for quantification of aflatoxin levels. Mean recovery for spikes was 72%. Coefficients of variation for the results from the 10 participants for the two contaminated roasted peanut butters were, respectively, 45% (on a mean of 13.6 micrograms/kg) and 36% (on a mean of 37.2 micrograms/kg).

Aflatoxin B1↗

PubMed1984

Aflatoxin and dimethyl sulfoxide influence on radiomanganese distribution and retention in neonate mice.

The LD50 (7 d) for aflatoxin B1 (AFB1) in CD-1 neonate mice (3.1 g; 5 d of age) was determined to be 13.3 mg/kg. The vehicle was dimethyl sulfoxide (DMSO), given intraperitoneally, at 0.01 ml/animal (7 mg/kg). The solvent was nontoxic and caused no significant change in body weight in animals during an 11-d experimental period (17 d of age). Aflatoxin B1 at 5.0 mg/kg and above caused reduced body weight gain. DMSO animals had a mean loss of more than 17% of the radiolabel over a 9-d period. Aflatoxin treatments reversed the DMSO loss of 54Mn in a concentration-related fashion, and generally, AFB1 caused a conservation of the radioisotope. The radiolabel was redistributed into the following organs/tissues: liver greater than brain greater than bone greater than muscle = lungs greater than blood. Aflatoxin-treated animals showed a twofold increase of radiolabel in the liver as compared to controls. The DMSO itself failed to influence 54Mn influx into the liver. In general, control neonate mice, by 17 d of age, were retaining and redistributing the 54MnCl2 and had not reached the time for sudden emergence of excretion common in rodents. DMSO was found not to be the most satisfactory solvent to use in the administration of aflatoxins, especially when manganese metabolism is being studied. Generally, both DMSO and AFB1 influenced radiomanganese distribution, DMSO having a substantial influence.

Aflatoxin B1↗

PubMed2003

Dietary aflatoxin exposure and chemoprevention of cancer: a clinical review.

Exposure to dietary aflatoxins is considered to be an important risk factor for the development of hepatocellular carcinoma in certain regions of the world. Significant advances have recently been made in understanding the clinical toxicology of aflatoxins. These include the development and validation of biomarkers of exposure and genotoxic effect. These biomarkers are currently being utilized to explore the potential that pharmaceutical interventions may have in modifying the toxicokinetics of dietary aflatoxin exposure. Preliminary results of clinical trials with the drug oltipraz suggest that it may modify the genotoxic effects of aflatoxin B1 by inhibiting bioactivation pathways and stimulating detoxification pathways. More recent results of a clinical trial with chlorophyllin suggest that this drug may have a role in preventing dietary exposure to aflatoxin B1 by reducing its oral bioavailability. The preliminary results of these chemoprevention studies may ultimately have implications for cancer prevention in high-risk populations in the future.

Aflatoxins↗

PubMed1990

Aflatoxin-DNA adduct formation in chronically dosed rats fed a choline-deficient diet.

Nutritional modulation of male Fischer rats by a choline-deficient/methionine-low diet dramatically increases hepatocarcinogenesis and reduces time to first tumors induced by aflatoxin B1 (AFB1). The effect of this diet on hepatic aflatoxin-DNA adduct burden in male Fischer rats dosed with a carcinogenic regimen of AFB1 was examined in this study. After 3 weeks of ingestion of a choline-deficient/methionine-low diet or control semi-purified diet, rats were administered a carcinogenic regimen of 25 micrograms [3H]AFB1 for 5 days a week over 2 weeks. Six choline-deficient and four control diet rats were killed 2 h after each dose, and liver DNA isolated. In addition, hepatic DNA was isolated from animals 1, 2, 3, and 11 days after the last [3H]AFB1 administration. At all time points HPLC analysis of aflatoxin-DNA adducts was performed to confirm radiometric determinations of DNA binding levels. No significant quantitative differences in AFB1-DNA adduct formation between the dietary groups were observed following the first exposure to [3H]AFB1; however, total aflatoxin-DNA adduct levels in the choline-deficient animals were significantly increased during the multiple dose schedule. When total aflatoxin-DNA adduct levels were integrated over the 10 day dose period, a 41% increase in adduct burden was determined for the choline-deficient animals. While this increase in DNA damage is consistent with the hypothesis that DNA damage is related to tumor outcome, the biochemical basis for this effect still needs to be elucidated.

Aflatoxin B1↗

PubMed1990

Transplacental transfer of aflatoxin in humans.

This study quantified aflatoxin (AFB1, AFG1 and AFQ1) by enzyme-linked immunosorbent assay in human cord sera obtained at birth and in serum obtained immediately after birth from the mother. The subjects of the study were residents of Songkhla, Thailand. Of the 35 samples of cord sera, 17 (48%) contained aflatoxin in concentrations from 0.064 to 13.6, mean 3.1 nmol/ml. By comparison only two (6%) of 35 maternal sera contained aflatoxin (mean 0.62 nmol/ml). These results demonstrate transplacental transfer and concentration of aflatoxin by the feto-placental unit which may be of biological importance. Aflatoxins are mutagenic, carcinogenic and teratogenic and cause immunosuppression in animals. The implications of these findings are potentially profound and deserve further study.

Aflatoxin B1↗