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PubMed1978

Degradation of aflatoxin by lactoperoxidase.

Three concentrations of lactoperoxidase, 5, 50, and 500 units/ml of reaction mixture, degraded aflatoxin in the presence of 225 micrometer NaCl and 50 micrometer H2O2 at 28 degrees C. Increasing the amount of lactoperoxidase from 50 to 500 units/ml of reaction mixture resulted in increasing the rate of degradation of aflatoxin B1 from 3.6 to 5.1%/24 h. When comparable amounts of lactoperoxidase were present, aflatoxin G1 was degraded approximately 1.5 times faster than was aflatoxin B1. At a given concentration of lactoperoxidase, aflatoxin degradation was independent of initial aflatoxin concentration. Derivatives that cochromatographed with aflatoxin B2a and derivatives that were water soluble were the major degradation products of aflatoxin B1. Similar derivatives, but in greater proportions, were noted as degradation products that resulted from activity of a blendure of mycelia of Aspergillus parasiticus.

Aflatoxins↗

PubMed2003

Quantitative trait loci for low aflatoxin production in two related maize populations.

Aflatoxin B(1) formed by Aspergillus flavus Fr:Link has been associated with animal disease and liver cancer in humans. We performed genetic studies in progenies derived from maize inbred Tex6, associated with relatively low levels of aflatoxin production, crossed with the historically important inbred B73. (Tex6 x B73) x B73 BC(1)S(1) and Tex6 x B73 F(2:3) mapping populations were produced and evaluated in 1996 and 1997 in Champaign, Ill. Ears were inoculated 20 to 24 days after midsilk using a pinboard method and a mixture of conidia of A. flavus Link:Fr. isolates. Aflatoxin B(1) levels in harvested ears were determined using an indirect competitive ELISA. Molecular markers were assayed on the populations and used to generate maps. Molecular marker - QTL associations for lower levels of aflatoxin production were determined using multiple regression (MR) and composite interval analysis with multiple regression (CIM MR). MR revealed sets of markers associated with lower aflatoxin production in 1996 and 1997, and CIM MR detected a smaller subset of loci significant in 1997. QTLs for lower aflatoxin were attributed to both Tex6 and B73 parental sources. Environment strongly influenced the detection of QTLs for lower aflatoxin production in different years. There were very few chromosome regions associated with QTLs in more than 1 year or population with MR analysis, and none with CIM MR analysis. In 1997, QTLs for lower aflatoxin were detected with CIM MR in bins 5.01-2 and 5.04-5 in the BC(1)S(1) population, and in bins 3.05-6, 4.07-8 and 10.05-10.07 in the F(2:3) population. These QTL associations appear the most promising for further study.

Aflatoxins↗

PubMed2006

Biochemical analysis of oxidative stress in the production of aflatoxin and its precursor intermediates.

The relevance of oxidative stress in the production of aflatoxin and its precursors was examined in different mutants of Aspergillus parasiticus, which produce aflatoxin or its precursor intermediates, and compared with results obtained from a non-toxigenic strain. In comparison to the non-toxigenic strain (SRRC 255), an aflatoxin producing strain (NRRL 2999) or mutants that accumulate aflatoxin precursors such as norsolorinic acid (by SRRC 162) or versicolorin (by NRRL 6196) or O-methyl sterigmatocystin (by SRRC 2043) had greater oxygen requirements and higher contents of reactive oxygen species. These changes were in the graded order of NRRL 2999 > SRRC 2043 > NRRL 6196 > SRRC 162 > SRRC 255, indicating incremental accumulation of reactive oxygen species, being least in the non-toxigenic strain and increasing progressively during the ternary steps of aflatoxin formation. Oxidative stress in these strains was evident by increased activities of xanthine oxidase and free radical scavenging enzymes (superoxide dismutase and glutathione peroxidase) as compared to the non-toxigenic strain (SRRC 255). Culturing the toxigenic strain in presence of 0.1-10 muM H(2)O(2 )in the medium resulted in enhanced aflatoxin production, which could be related to dose-dependent increase in [(14)C]-acetate incorporation into aflatoxin B(1) and increased acetyl CoA carboxylase activity. The combined results suggest that formation of secondary metabolites such as aflatoxin and its precursors by A. parasiticus may occur as a compensatory response to reactive oxygen species accumulation.

Acetyl-CoA Carboxylase↗

PubMed1990

Aflatoxin production by entomopathogenic isolates of Aspergillus parasiticus and Aspergillus flavus.

Fourteen isolates of Aspergillus parasiticus and 2 isolates of Aspergillus flavus isolated from the mealybug Saccharicoccus sacchari were analyzed for production of aflatoxins B1, B2, G1, and G2 in liquid culture over a 20-day period. Twelve Aspergillus isolates including 11 A. parasiticus and 1 A. flavus produced aflatoxins which were extracted from both the mycelium and culture filtrate. Aflatoxin production was detected at day 3 and was detected continually for up to day 20. Aflatoxin B1 production was greatest between 7 and 10 days and significantly higher quantities were produced by A. flavus compared to A. parasiticus. Aflatoxin production was not a stable trait in 1 A. parasiticus isolate passaged 50 times on agar. In addition to loss of aflatoxin production, an associated loss in sporulation ability was also observed in this passaged isolate, although it did maintain pathogenicity against S. sacchari. An aflatoxin B1 concentration of 0.16 micrograms/mealybug (14.2 micrograms/g wet wt) was detected within the tissues of infected mealybugs 7 days after inoculation. In conclusion, the ability of Aspergillus isolates to produce aflatoxins was not essential to the entomopathogenic activity of this fungus against its host S. sacchari.

Aflatoxins↗

PubMed1976

Mutation induction by rodent liver microsomal metabolities of aflatoxins B1 and G1 in Neurospora crassa.

The mutagenic activities of aflatoxins B1 and G1 were studied in the ad-3 test system of Neurospora crassa by treatment of conidia with aflatoxin and liver homogenate for 2 h. No significant increase in the ad-3 mutation frequency over the spontaneous frequency was observed when either aflatoxin or mammalian liver homogenate was omitted from the test system. The ad-3 mutation frequencies increased to between 29 and 87/10(6) survivors, which is a 73- to 217-fold increase over the average spontaneous ad-3 mutation frequency (0.4/10(6) survivors), after conidia of N. crassa were treated with 0.67 mM aflatoxin B1, hamster liver homogenate, and a NADPH generating system. A 9- to 15-fold increase in the mutation frequency over the spontaneous mutation frequency was found when 0.67 mM of aflatoxin G1 instead of aflatoxin B1 was used in the test system. Treatment of conidia with 0.44 mM aflatoxin B1 mice liver homogenate and a NADPH generating system caused a small, but significant increase in the ad-3 mutation frequencies. No significant increase in the mutation frequency was found when a single sample of human liver homogenate was used in the test system. These studies show that metabolic activation is necessary for the expression of the mutagenic activity of aflatoxins B1 and G1 in N. crassa.

Aflatoxins↗

PubMed1983

Effects of long-term feeding of ammoniated, aflatoxin-contaminated corn to Fischer 344 rats.

The effectiveness of ammonia treatment in reducing the chronic toxicity of aflatoxin-contaminated corn was determined. Fischer 344 rats were fed semi-purified rations containing 20% w/w corn that was either free of aflatoxin or naturally contaminated with 880 micrograms/kg total aflatoxin and was either treated with ammonia gas or was not treated. Therefore the rats that were fed the aflatoxin-contaminated diet received 176 ppb total aflatoxins. Body weight and food consumption were recorded throughout the study; hematological measurements were made after 87 weeks of feeding; and after 91 weeks the rats were killed and histopathological abnormalities were noted. Signs of chronic toxicosis in rats fed aflatoxin-contaminated corn included increased mortality, decreased hematocrit and hemoglobin levels, elevated serum alkaline phosphatase activities, and a 100% incidence of liver neoplasia. These signs did not occur in rats in the other dietary treatment groups, including those fed ammoniated, aflatoxin-contaminated corn. The results provide further evidence that the atmospheric ammoniation process effectively reduces the toxicity of aflatoxin-contaminated corn.

Aflatoxins↗

PubMed1994

Growth of and aflatoxin production by Aspergillus flavus in peanuts stored under modified atmosphere packaging (MAP) conditions.

The combined effects of water activity (aw), storage temperature, headspace oxygen and carbon dioxide concentrations on the growth of, and aflatoxin production by Aspergillus flavus on sterile peanuts were examined using a process optimization technique termed response surface methodology (RSM). Regression analysis of the data indicated that aw, storage temperature and initial headspace oxygen concentration were all significant factors (P < 0.001) affecting the growth of, and aflatoxin production by A. flavus. Extensive growth and aflatoxin production occurred during the first week of storage in most treatment combinations. Maximum growth occurred in peanuts with an aw of 0.97, a storage temperature of 25 degrees C and headspace oxygen of 10% (balance 60:40 carbon dioxide:nitrogen), after 21 days of storage while maximum aflatoxin production occurred at a lower aw of 0.94, after 21 days under similar storage/gaseous conditions. In several treatment combinations, where high levels of aflatoxin (> 20 ng/g) were initially detected, aflatoxin concentration decreased during storage to levels less than the current regulatory limit of 20 ng/g. This study has shown that A. flavus can grow and produce aflatoxin in carbon dioxide enriched atmospheres in the presence of oxygen. It also emphasizes the combined effect of several 'barriers' to inhibit and reduce aflatoxin in MAP products containing various levels of residual oxygen.

Aflatoxins↗

PubMed1986

Aflatoxin carryover and clearance from tissues of laying hens.

A feeding trial was conducted to determine the levels of aflatoxins deposited in the tissues of hens fed a diet contaminated with 3310 micrograms AFB1/kg and 1680 micrograms AFB2/kg for 4 wk. At the end of aflatoxin feeding, the livers were pale, enlarged and haemorrhagic and the ovaries were significantly smaller than those from control hens and contained only small ova. Only a small fraction of the aflatoxins consumed was deposited in the tissues, either as the original compounds or as their metabolites, which were widely distributed in all tissues. The highest levels of aflatoxins were detected in the gizzard, kidneys and liver, with average total concentrations of less than 3 micrograms/kg. The lowest residue levels were detected in the breast, blood serum and leg, with breast muscle having a total concentration of less than 0.1 microgram/kg. Two days after removal of the contaminated feed, aflatoxin residues in all tissues had decreased markedly, with no aflatoxins being detected in the heart or spleen. No aflatoxin residues were detected in the breast, leg, gizzard and ovaries of hens killed 8 days after withdrawal, or in the kidneys and blood at 16 days. However, one of seven hens had measurable amounts of AFB2 in the liver 32 days after withdrawal. Although few residues were detected in most tissues after 8 days on the aflatoxin-free diet, variation existed between tissues and between individual hens in the amount of time required to achieve tissue clearance.

Aflatoxins↗

PubMed2006

Surface binding of aflatoxin B1 by Saccharomyces cerevisiae strains with potential decontaminating abilities in indigenous fermented foods.

Saccharomyces cerevisiae constitutes one of the most important microorganisms involved in food fermentations throughout the world. Aflatoxin B(1) binding abilities of S. cerevisiae strains isolated from indigenous fermented foods from Ghana, West Africa were tested in vitro. Results show that aflatoxin binding was strain specific with 7 strains binding 10-20%, 8 strains binding 20-40% and 3 strains binding more than 40% of the added aflatoxin B(1) when grown and incubated under standard conditions. Binding by two of the strains was further characterized. Highest binding capacity was seen with cells collected at the exponential growth phase with the strains A18 and 26.1.11 binding 53.0 and 48.8% of the total toxin respectively and the binding reduced towards the stationary phase. Aflatoxin B(1) binding increased steadily when the cells were incubated with 1 to 20 microg/ml of aflatoxin B(1). Binding was not affected by the cells grown at temperatures ranging from 20 to 37 degrees C, but was significantly reduced at 15 degrees C. Binding seems to be a physical phenomenon with cells treated at 52, 55 and 60 degrees C for 5 and 10 min or 120 degrees C for 20 min binding significantly higher quantities (more than 2-fold in 120 degrees C treated cells) of aflatoxin B(1) than their viable counterpart. Similarly, when the cells were treated with 2 M HCl for 1 h, up to 2-fold increase in binding was observed. The results obtained show that some strains of S. cerevisiae, viable or non-viable, are effective aflatoxin binders and these properties should be considered in the selection of starter cultures for relevant indigenous fermented foods where high aflatoxin level is a potential health risk.

Aflatoxin B1↗

PubMed1999

Co-mutagenicity of coumarin (1,2-benzopyrone) with aflatoxin B1 and human liver S9 in mammalian cells.

Coumarin (1,2-benzopyrone), a natural dietary constituent and drug currently under evaluation for treatment of certain cancers and lymphedema, reduces polycyclic aromatic hydrocarbon-induced neoplasms in rodents. Because most rodents metabolize coumarin through 3,4-epoxidation, whereas 7-hydroxylation predominates in humans, their suitability as a model for coumarin effects in humans has been questioned. We examined coumarin chemoprotection against the promutagen and dietary contaminant aflatoxin B1 with human liver S9 bioactivation in the Chinese hamster ovary cell/hypoxanthine-guanine phosphoribosyltransferase mutation assay. Coumarin in the absence of aflatoxin B1 was not mutagenic or cytotoxic up to 500 microM. When included with either 1 or 10 microM aflatoxin B1, coumarin produced a dose-dependent increase in mutant frequency and cytotoxicity. At concentrations greater than 50 microM, coumarin stimulated human liver S9 bioactivation of aflatoxin B1 to the mutagenic 8,9-epoxide. This increase was 12- and fivefold at 500 microM coumarin with 1 and 10 microM aflatoxin B1, respectively, compared with incubations with aflatoxin B1 alone. These findings differ from previous results with liver S9 from other species, and indicate that coumarin co-mutagenicity with aflatoxin B1 and human liver S9 is through increased aflatoxin B1 bioactivation.

Aflatoxin B1↗

PubMed1999

Evaluation of the mycological status of luncheon meat with special reference to aflatoxigenic moulds and aflatoxin residues.

The luncheon meat samples analyzed, which were produced locally by the two main luncheon meat producing companies in Egypt were relatively highly contaminated either by moulds and yeasts in general, aflatoxigenic species and aflatoxin residues in particular. The most frequently encountered fungi from the samples were yeasts, Aspergillus niger, A. flavus, Penicillium chrysogenum, Rhizopus stolonifer, Mucor circinelloides. Less common were Cladosporium sphaerospermum, Alternaria alternata, Mycosphaerella tassiana, P. aurantiogriseum and P. oxalicum. The most important aflatoxigenic species, A. flavus, was isolated frequently. It was 10% of the total fungal isolates from both samples of the two companies. Seven luncheon meat samples out of 50 analyzed were positive for aflatoxin B1 or B1 and G1, while all samples were negative for aflatoxins B2, G2, M1 and M2. Aflatoxin B1 was detected only in 4 and 3 samples out of 25 analyzed from each of company A and B, respectively. The highest detectable level, 11.1 ppb, was recorded in a sample from company B and the least, 0.5 ppb, in a sample from company A. Aflatoxin G1, at concentration of 3.2 ppb, was detected in only one sample of the aflatoxin B1--contaminated 3 samples of company B: this sample also had the highest level of aflatoxin B1. Some luncheon meat samples had higher numbers of aflatoxigenic A. flavus than others, however these samples were negative for aflatoxins. The hazardous potential of such contamination will be discussed.

Aflatoxins↗

PubMed2002

Association of aflatoxin biosynthesis and sclerotial development in Aspergillus parasiticus.

Secondary metabolism in fungi is frequently associated with asexual and sexual development. Aspergillus parasiticus produces aflatoxins known to contaminate a variety of agricultural commodities. This strictly mitotic fungus. besides producing conidia asexually, produces sclerotia, structures resistant to harsh conditions and for propagation. Sclerotia are considered to be derived from the sexual structure, cleistothecia. and may represent a vestige of ascospore production. Introduction of the aflatoxin pathway-specific regulatory gene, aflR, and aflJ, which encoded a putative co-activator, into an O-methylsterigmatocystin (OMST)-accumulating strain, A. parasiticus SRRC 2043, resulted in elevated levels of accumulation of major aflatoxin precursors, including norsolorinic acid (NOR), averantin (AVN), versicolorin A (VERA) and OMST. The total amount of these aflatoxin precursors, NOR, VERA, AVN and OMST, produced by the aflR plus aflJ transformants was two to three-fold that produced by the aflR transformants. This increase indicated a synergistic effect of aflR and aflJ on the synthesis of aflatoxin precursors. Increased production of the aflatoxin precursors was associated with progressive decrease in sclerotial size, alteration in sclerotial shape and weakening in the sclerotial structure of the transformants. The results showed that sclerotial development and aflatoxin biosynthesis are closely related. We proposed that competition for a common substrate, such as acetate, by the aflatoxin biosynthetic pathway could adversely affect sclerotial development in A. parasiticus.

Aflatoxins↗

PubMed2002

Effects of neem leaf extract on production of aflatoxins and activities of fatty acid synthetase, isocitrate dehydrogenase and glutathione S-transferase in Aspergillus parasiticus.

The relationship between the activities of 3 cytosolic enzymes with aflatoxin biosynthesis in Aspergillus parasiticus cultured under different conditions has been investigated in order to find out the role of each enzyme in aflatoxin biosynthesis. Basically the activity of isocitrate dehydrogenase (IDH) was higher in non-toxigenic strains as compared to its counterpart toxigenic fungi (p < 0.05). In contrast, the activities of fatty acid synthase (FAS) as well as glutathione S-transferase (GST) were higher (P < 0.05) in toxigenic strains than that of the non-toxigenic fungi. Aflatoxin production was inhibited in fungi grown in presence of various concentrations of neem leaf extract. Aflatoxin was at its lowest level (>90% inhibition) when the concentration of neem extract was adjusted to 50% (v/v). No significant changes in FAS and IDH activities were observed when aflatoxin synthesis was under restraints by neem (Azadirachta indica) leaf extract. During a certain period of time of culture growth, when aflatoxin production reached to its maximum level, the activity of FAS was slightly induced in the toxigenic strains fed with a low concentration (1.56% v/v) of the neem leaf extract. At the time (96 h) when aflatoxin concentration reached to its maximum levels, the activity of GST in the toxigenic fungi was significantly higher (i.e., 7-11 folds) than that of non-toxigenic strains. The difference was highest in mycelial samples collected after 120 h. However unlike FAS and IDH, GST was readily inhibited (approximately 67%) in mycelia fed with 1.56% v/v of the neem extract. The inhibition reached to maximum of 80% in samples exposed to 6.25-12.5% of the extract. These results further substantiate previous finding that there is a positive correlation between GST activity and aflatoxin production in fungi.

Aflatoxins↗

PubMed1971

A comparative study on aflatoxin B 1 metabolism in mice and rats.

In vivo metabolic studies on rats and mice revealed a marked difference in the fluorescent compounds produced after ingestion of aflatoxin B(1). The mouse converted aflatoxin B(1) to three unknown fluorescent compounds, designated x(1), x(2) and x(3) and the known aflatoxin M(1), while the rat was only capable of producing aflatoxin M(1). The results suggested that metabolites x(1), x(2), x(3) and aflatoxin M(1) were not part of a major metabolic pathway, but produced independently. These unknown yellowish-green fluorescent compounds did not seem to be conjugated with sulphate or glucuronic acid.In vitro incubations of various mouse liver cell fractions with aflatoxin B(1) showed that metabolites x(1), x(2), x(3) and aflatoxin M(1), could only be produced by the microsomal fraction and that NADPH was needed as a co-factor. The differences in aflatoxin metabolism by mice and rats are discussed in relation to the apparent resistance of the mouse to the carcinogenic effects of this toxin.

Absorption↗

PubMed1988

Positive correlation exists between glutathione S-transferase activity and aflatoxin formation in Aspergillus flavus.

The presence of glutathione (GSH) S-transferase activity, using 1-chloro-2, 4-dinitrobenzene (CDNB) as a substrate, has been established in the cytosolic fraction of the toxigenic (aflatoxin producing) and nontoxigenic strains of Aspergillus flavus. Significant differences in the GSH S-transferase activity were observed between the toxigenic and non-toxigenic strains. A positive correlation has been demonstrated for the first time between aflatoxin formation and a biochemical parameter, namely GSH S-transferase activity. The evidence in support of A. flavus GSH S-transferase induction by endogenous aflatoxins is as follows: (i) the age-related production of aflatoxin follows the same pattern as the cytosolic GSH S-transferase activity profile; (ii) significantly higher enzyme activity was associated with mycelia of a toxigenic strain grown in medium supporting high aflatoxin production (sucrose-low-salts medium) while the enzyme activity was low in medium producing less aflatoxin (glucose-ammonium nitrate medium). The GSH S-transferase activity of the non-toxigenic strain was hardly affected by a change in the medium as it produces no aflatoxins; and (iii) the toxigenic strain demonstrated significantly higher apparent Vmax. with no change in Km as compared with the non-toxigenic strain. This indicates that the enzyme induction by endogenous aflatoxins is similar to the action of phenobarbitol and other inducing drugs (Kaplowitz et al., 1975).

Acetates↗

PubMed2000

Aflatoxin B1 residues in eggs of laying hens fed a diet containing different levels of the mycotoxin.

The present study was carried out to evaluate the excretion of aflatoxin B1 residues in eggs of young laying hens fed aflatoxin B1-contaminated rations for 8 weeks. To this end, 96 twenty-week-old hens were randomly distributed into four experimental groups (24 birds per group) and given rations containing either 0 (controls), 100 micrograms, 300 micrograms or 500 micrograms aflatoxin B1/kg feed. Egg aflatoxin B1 residues were determined by thin layer chromatography; two samples per treatment per week were used for analysis. Egg production and average egg weights were not affected (p < 0.05) in the groups receiving aflatoxin B1-contaminated rations. Residues of aflatoxin B1 were detected only in the eggs of hens given 500 micrograms/kg feed, at levels that ranged from 0.05 to 0.16 microgram/kg (average: 0.10 microgram/kg). The results indicate that the feed to eggs aflatoxin B1 transmission ratio was approximately 5000:1, emphasizing the importance of controlling aflatoxin levels in rations for laying hens.

Aflatoxin B1↗

PubMed2001

Distribution and stability of aflatoxin M1 during processing, ripening and storage of Telemes cheese.

Telemes cheeses were produced using milk that was artificially-contaminated with aflatoxin M1 at the levels of 0.050 and 0.100 microg/l. The cheeses produced in the two cheese-making trials were allowed to ripen for 2 months and stored for an additional 4 months to simulate commercial production of Telemes cheese. Concentrations of aflatoxin M1 in whey, curd, brine, and the produced cheeses were determined at intervals by liquid chromatography and fluorometric detection coupled with immunoaffinity column extraction. Concentrations of aflatoxin M1 in the produced curds were found to be 3.9 and 4.4 times higher than those in milk, whereas concentrations in whey were lower than those in curd and milk. Aflatoxin M1 was present in cheese at higher concentrations at the beginning than at the end of the ripening/storage period, and it declined to concentrations 2.7 and 3.4 times higher than those initially present in milk by the end of the sixth month of storage. Concentrations of aflatoxin M1 in brine started low and increased by the end of the ripening/storage period but only a portion of the amounts of aflatoxin M1 lost from cheese was found in the brine. Results showed that Telemes cheeses produced from milk containing aflatoxin M1 at a concentration close to either the maximum acceptable level of 0.05 microg/l set by the European union (EU) or at double this value, will contain the toxin at a level that is much lower or slightly higher, respectively, than the maximum acceptable level of 0.250 microg of aflatoxin M1/kg cheese set by some countries.

Aflatoxin M1↗

PubMed2002

Occurrence of aflatoxins and fumonisins in Incaparina from Guatemala.

The occurrence of aflatoxins and fumonisins in Incaparina was investigated. Incaparina is a mixture of corn and cottonseed flour with added vitamins, minerals and a preservative. It has been marketed as a high-protein food supplement, particularly for children on protein-deficient diets. According to estimates, 80% of Guatemalan children in their first year are given Incaparina to provide an adequate diet. Eight samples of Incaparina manufactured in Guatemala were collected. Five were from three different geographical locations in the USA and three were from Guatemala. Seven were examined for fungal contamination and analysed for aflatoxins and fumonisins. Aspergillus flavus was the predominant fungus in all samples purchased in the USA and in one sample purchased from Guatemala, whereas Fusarium verticillioides was present in only two samples (one from the USA and one from Guatemala). All samples contained aflatoxins, ranging from 3 to 214 ng g(-1) and <2 to 32ng g(-1) for aflatoxin B(1) and aflatoxin B(2), respectively; and one sample contained aflatoxin G(1) (7 ng g(-1)). Total aflatoxins present ranged from 3 to 244 ng g(1). All samples contained fumonisins, ranging from 0.2 to 1.7 microg g(-1), <0.1 to 0.6 microg g(-1), and <0.1 to 0.2 microg g(-1) for fumonisins B(1), fumonisin B(2), and fumonisin B(2), respectively. Total fumonisins present ranged from 0.2 to 2.2 microg g(-1). The identity of aflatoxin B(2) was confirmed using both the chemical derivatization method and liquid chromatographic (LC)/mass spectrometric (MS) analysis. Appropriate regulatory action was recommended for the import of Incaparina and has been in effect since 22 December 1998.

Aflatoxins↗