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PubMedDate not supplied

The occurrence of aflatoxin in nuts and nut products imported to Finland for human consumption during the years 1974-1976.

An examination was made of 1050 lots of nuts and nut products, totalling 4.7 million kg, imported to Finland in the years 1974-1976. Of these, 44 lots (4.2%) were found to contain aflatoxin. The highest percentage of aflatoxin-containing lots, was observed in the case of sliced and crushed peanuts (29.4%). Of the positive samples, 20.5% contained 101-500 microgram aflatoxin per kg, 52.3% contained 6-100 microgram/kg and 20.5% contained less than or equal to 5 microgram/kg. Rest of the samples (6.7%) contained aflatoxin 501 microgram/kg or more. The most commonly detected toxin types were B1 and B2. The proportion of aflatoxin-containing lots showed a slight decrease during the 3-year research period. On the basis of the research results and the sampling plan used, and bearing in mind the acceptable quality level (AQL: 5 microgram/kg) employed in Finland, the reliability of approval and rejection decisions was discussed from the point of view of both the producer's and the consumer's risk.

Aflatoxins↗

PubMedDate not supplied

Analysis of aflatoxins in poultry and pig feeds and feedstuffs used in Colombia.

Feedstuffs and mixed feeds used for poultry and pig nutrition in Colombia were analyzed for aflatoxins by using a liquid chromatographic technique with a limit of detection of 1 microgram/kg for each aflatoxin (B1, B2, G1, and G2). Samples of grain sorghum, maize, processed soybean, rice meal, cottonseed meal, and poultry and pig feeds, representative of Colombian production for the 1995-1996 harvest, were taken from feed-manufacturing plants in various cities. Aflatoxins were detected in 11 of 45 samples of sorghum, 4 of 33 samples of maize, 8 of 22 samples of rice meal, 15 of 17 samples of cottonseed meal, 1 of 12 samples of other feedstuffs, 12 of 30 samples of poultry feed, and 7 of 16 samples of pig feed. Aflatoxins were not detected in soybean. Only 9 of 58 positive samples contained total aflatoxin levels exceeding maximum tolerable limits in Colombia.

Aflatoxins↗

PubMed1976

Distribution of aflatoxins in some samples of peanuts.

Naturally occurring G aflatoxins were found at approximately 20 times the level of B aflatoxins in one lot of roasted, blanched peanuts. Official methods, as well as high-pressure liquid chromatography, were used to confirm this finding. Additional routine sample analysis data of raw and roasted peanuts revealed that this finding is not so unusual formerly thought. It was found that 9.8% of the raw peanut samples contained higher levels of G than B aflatoxin; 4.9% containing 2-8 times more G than B aflatoxins. In a smaller sampling of roasted peanuts, 28% of the contaminated peanuts contained more G than B aflatoxins.

Aflatoxins↗

PubMed1976

Aflatoxin occurrence on raw and cooked york soybeans inoculated with three aspergillus isolates.

Raw and cooked soybean media were inoculated in separate experiments with Aspergillus flavus NRRL 3251, A. flavus ATCC 15548, and A. parasiticus NRRL 2999 isolates. The toatl quantity of aflatoxins produced and the percentage distribution of aflatoxins B1, B2, G1, and G2 varied with the state of the medium (raw or cooked) and with the fungal isolate used. Cooked soybean medium supported higher aflatoxin productions by A. flavus NRRL 3251 and A. parasiticus NRRL 2999 than did raw medium. Larger quantities of aflatoxins B1, B2, G1, and G2 were produced by A. flavus ATCC 15548 on raw soybean medium than were produced by any of the isolates on cooked medium. Application of these data is discussed briefly in relation to possible use of soybean media as a source of aflatoxin production.

Aflatoxins↗

PubMed1997

Individual and combined genotoxic response of boric acid and aflatoxin B1 in Escherichia coli PQ37.

The genotoxic potentials of boric acid in Escherichia coli PQ37 was assessed along in the presence of aflatoxin B1 using SOS chromotest. Boric acid induced beta-galactosidase synthesis on the tester bacteria both on the presence and absence of S9 activation mixture. Therefore, the inorganic acid may not require metabolic activation to be genotoxic for this bacteria. When present together with aflatoxin B1 in the assay medium, boric acid increased the degree of beta-galactosidase synthesis induced by the maximal inducing concentration of aflatoxin B1 before the toxin's activation. However, the degree of enzyme synthesis induced was significantly decreased when boric acid was present after aflatoxin activation. This suggests that boric acid may not interfere with nor block the expoxidation of aflatoxin B1. It may however interact with the expoxide thereby inhibiting its activity. Boric acid may be a genotoxin and could possibly act as a syngenotoxic and/or a cogenotoxic agent.

Aflatoxin B1↗

PubMed1998

Oltipraz chemoprevention trial in Qidong, People's Republic of China: modulation of serum aflatoxin albumin adduct biomarkers.

In 1995, 234 adults from Qidong, People's Republic of China, were enrolled and followed in a Phase IIa 4-methyl-5-(N-2-pyrazinyl)-1,2-dithiole-3-thione (oltipraz) chemoprevention trial. Residents of this area are at high risk for development of hepatocellular carcinoma, in part due to consumption of aflatoxin-contaminated foods. The intervention was a randomized, placebo-controlled, double-blind study. Elements of the study design and clinical outcomes have been recently published (Jacobson et al, Cancer Epidemiol. Biomark. Prev., 6: 257-265, 1997). The primary objective was to conduct a preliminary assessment of the ability of oltipraz to modulate levels of a validated biomarker of aflatoxin exposure and of the risk of hepatocellular carcinoma by determining levels of aflatoxin-albumin adducts in sera. Healthy eligible individuals were randomized into three arms to receive p.o. 125 mg of oltipraz daily, 500 mg of oltipraz weekly, or placebo for 8 weeks. There were no consistent changes in biomarker levels in the placebo arm over the 16-week observation period, nor was any apparent effect observed in the arm receiving 125 mg of oltipraz each day. However, individuals receiving 500 mg of oltipraz once a week for 8 weeks showed a triphasic response to oltipraz. No effect was observed during the 1st month of the intervention, whereas a significant (P = 0.001) diminution in adduct levels was observed during the 2nd month of active intervention and during the lst month of follow-up. A partial rebound in adduct levels toward baseline values was observed during the 2nd month postintervention. Linear regression models up to week 13 confirmed a significant (P = 0.008) weekly decline of biomarker levels in the group receiving 500 mg of oltipraz once a week. However, despite these effects relative to baseline values within the 500-mg weekly arm, there were no statistically significant differences in biomarker trajectories between treatment arms. The genotype for glutathione S-transferase M1, an oltipraz-inducible isoform involved in the detoxification of aflatoxin B1, did not appear to affect either baseline levels or rates of decline in the biomarker. A follow-up Phase IIb trial with a longer intervention period will be necessary to determine the full extent to which aflatoxin biomarker burden can be reduced and whether diminution of biomarkers can be sustained over the long term.

Adult↗

PubMedDate not supplied

Preliminary investigation on aflatoxin in cord blood of jaundiced neonates.

Cord blood was obtained from 164 neonates at birth and investigated for the presence of aflatoxins. 14 of the samples were neonates without jaundice and 150 from neonates with jaundice. There was significant reduction (P > 0.05) in birth weight of jaundiced neonates with aflatoxin. Neonates with jaundice have high mean concentration of aflatoxin B1 (32.3 ng/ml and 35.6 ng/ml). Aflatoxin G1 was not detected in any of the groups. The rate of detection was higher in wet (81.8%) than dry season (50.0%). These findings show that neonates are exposed to aflatoxin prenatally and that high incidence of jaundice occurred in the wet warm months.

Aflatoxin B1↗

PubMed1976

Mortality and some biochemical changes in mink (Mustela vison) given sublethal doses of aflatoxin each day.

Two feeding trials were done to study the susceptibility of mink (Mustela vison) to multiple sublethal doses of aflatoxins. In the 1st trial, twenty 3-month-old male mink were divided equally among groups. Each mink in groups 1, 2, 3, and 4 was given a meatball daily that contained 15, 30, 45, or 0 mug of aflatoxins (B1:G1, 40:60), respectively. All mink in group 3 died between the 25th and the 30th days of the feeding trial. Each mink had ingested 1,035 to 1,480 mug of aflatoxins. Four of the mink in group 2 died almost as soon as did mink in group 3. Four mink in group 1 died between 40 and 59 days after the start of the feeding trial. Generally, a marked increase in plasma cholesterol and alkaline phosphatase activity appeared before mink died. The liver from animals that died of aflatoxicosis showed prominent pathologic changes which included hemorrhages and appearance of pink yellow spots. Histopathologic examination of liver from dead mink revealed fatty infiltration, bile duct proliferation, bile stasis, pseudotubular formation, congestion, and fibrosis. The feeding trial was repeated with 20 mink (8 males and 12 females) that were 1.5 to 2 years old. In this instance, 0, 20, 40, and 60 mug of aflatoxins were administered each day. All treated animals, except 1, were dead within 37 days after the experiment started. The survivor was given the lowest dosage of toxins and died after 52 days by which time 960 mug of aflatoxins were consumed. Plasma cholesterol content and alkaline phosphatase activity generally were similar to those observed in younger mink of the 1st feeding trial.

Aflatoxins↗

PubMed1977

Regulation of aflatoxin biosynthesis. 2 Comparative study of tricarboxylic acid cycle in aflatoxigenic and non-aflatoxigenic strains of Aspergillus flavus.

The presence of a functional TCA cycle and its intermediates has been shown in Aspergillus parasiticus and Aspergillus flavus. The role of the TCA cycle in aflatoxin biosynthesis has been studied. In A. parasiticus the TCA cycle was activated on the second day of growth (exponential growth phase) resulting in the onset of aflatoxin biosynthesis. Pyruvate accumulation to toxic levels in A. parasiticus is suggested to shift the growth phase from exponential to stationary with the onset of aflatoxin biosynthesis. In A. flavus, a non-aflatoxigenic strain, no pyruvate accumulation was observed. Moreover, the onset of aflatoxin production in A. parasiticus was followed by a decline in the levels of TCA cycle intermediates indicating their possible utilization in secondary metabolite synthesis. Accumulation of TCA cycle intermediates in A. flavus is suggested to be due to non-diversion to aflatoxin biosynthesis.

Aflatoxins↗

PubMed2005

Fecal and urinary excretion of aflatoxin B1 metabolites (AFQ1, AFM1 and AFB-N7-guanine) in young Chinese males.

Our study was designed to assess the fecal and urinary excretion of 3 aflatoxin B1 (AFB1) metabolites, aflatoxins M1 (AFM1) and Q1 (AFQ1) and aflatoxin B1-N7-guanine (AFB-N7-guanine) that are produced by the predominant forms of cytochrome P450 enzymes responsible for the biotransformation of AFB1. Fecal and urinary AFM1, AFQ1 and urinary AFB-N7-guanine were assessed in 83 young Chinese males selected from a larger population (n = 300) based on detectable urinary AFM1. The concentration of fecal AFQ1 (median 137 ng/g fresh weight, IQR 9.1 to 450) was approximately 60 times higher than that of AFM1 (2.3 ng/g, IQR 0.0 to 7.3). In urine, the median AFQ1 was 10.4 ng/ml (IQR 3.4 to 23.3), and the median AFM1 and AFB-N7-guanine 0.04 ng/ml (IQR 0.01 to 0.33) and 0.38 ng/ml (IQR 0.0 to 2.15), respectively. A subgroup (n = 14) with hepatitis B virus (HBV) infection had significantly higher fecal concentrations of AFQ1 (p = 0.043) and AFM1 (p = 0.001) than those who were hepatitis B-virus antigen (HBsAg) negative, and the respective differences in urinary AFQ1 and AFM1 concentrations approached statistical significance (p = 0.054, p = 0.138). Our study demonstrates that AFQ1 is excreted in urine and feces at higher levels than AFM1, and feces are an important route of excretion of these AFB1 metabolites. AFQ1 should be further assessed for its predictive value as a marker for exposure and risk of dietary aflatoxins.

Aflatoxin B1↗

PubMed2007

Binding of aflatoxins to the 20S proteasome: effects on enzyme functionality and implications for oxidative stress and apoptosis.

Aflatoxins (AF) are contaminants of improperly stored foods; they are potent genotoxic and carcinogenic compounds, exerting their effects through damage to DNA. They can also induce mutations that increase oxidative damage. The goal of this study was to evaluate the possibility that a third mechanism could be involved in the carcinogenic action of aflatoxins, namely, direct binding to key enzymes involved in the regulatory pathways of the cell cycle, thereby modulating enzyme functionality. The 20S constitutive and immunoproteasome peptidase and proteolytic activities were assayed in the presence of aflatoxins B1, G1 and M1. All three toxins activated multiple peptidase activities of the proteasome. Aflatoxin (AF) M1 was the most potent activator of proteasome activity, while the constitutive 20S proteasome was specifically stimulated by AFG1. Furthermore, the effects of AFB1 on cultured hepatoma cells were investigated and the various proteasomal activities determined with cell lysates were differently affected. Taking into account the key role of the proteasome in cellular defense against oxidative stress, the carbonyl group content and the activities of antioxidant enzymes in cell lysates were analyzed. The proapoptotic effect of AFB1 was also investigated by measuring caspase-3 activity and cellular levels of p27 and IkappaBalpha.

Aflatoxin B1↗

PubMed1982

Effect of beta-naphthoflavone on calf liver metabolism of aflatoxin B1.

Eight male Holstein calves were raised to 6 wk of age on whole milk at 8% of body weight and calf starter ration (15% crude protein) free choice. For each of 2 days prior to sacrifice, four of the calves were selected at random and administered the mixed function oxidase inducer beta-napthoflavone by bolus in starch carrier at .005% of metabolic body weight. After sacrifice, 10,000 X g postmitochondrial supernatant preparations were made from the excised livers and incubated with a 50-micrograms challenge of aflatoxin B1. Although there was no significant difference in total percent of the challenge metabolized, there was a large increase in aflatoxin M1 production by liver preparations from calves administered the flavone inducer. If the flavone family of inducers could alter the metabolic profile for aflatoxin in the adult lactating bovine, aflatoxin M1 excretion rates could be increased and pathways for production of mutagenic metabolites could be enhanced.

Aflatoxin B1↗

PubMed1980

[Contamination of cow's milk during ingestion of small quantities of aflatoxin].

Sixteen cows, some in the early and the rest in the late lactation period, were given daily, during a eight day period a ration of peanut meal naturally contaminated by aflatoxin. The analysis for aflatoxin M1 of the milk obtained from these cows indicates the following points: --the level of aflatoxin M1 is not influenced by the volume of the daily milk secretion; --the quantity of this hydroxy-derivative expressed as a percentage of the parent toxin varies from 0.14 to 0.34 in the animals in the late lactation period, and from 0.66 to 0.95 in the cows producing some twenty litres of milk per day; --in order to achieve a tolerance limit of 20 ng/kg of aflatoxin M1, in the milk, the daily ingestion of the mycotoxin by cows should not exceed 90--100 micrograms per animal.

Aflatoxin B1↗

PubMed2006

A polyketide synthase gene required for biosynthesis of the aflatoxin-like toxin, dothistromin.

Dothistromin is a polyketide toxin, produced by a fungal forest pathogen, with structural similarity to the aflatoxin precursor versicolorin B. Biochemical and genetic studies suggested that there are common steps in the biosynthetic pathways for these metabolites and showed similarities between some of the genes. A polyketide synthase gene (pksA) was isolated from dothistromin-producing Dothistroma septosporum by hybridization with an aflatoxin ortholog from Aspergillus parasiticus. Inactivation of this gene in D. septosporum resulted in mutants that could not produce dothistromin but that could convert exogenous aflatoxin precursors, including norsolorinic acid, into dothistromin. The mutants also had reduced asexual sporulation compared to the wild type. So far four other genes are known to be clustered immediately alongside pksA. Three of these (cypA, moxA, avfA) are predicted to be orthologs of aflatoxin biosynthetic genes. The other gene (epoA), located between avfA and moxA, is predicted to encode an epoxide hydrolase, for which there is no homolog in either the aflatoxin or sterigmatocystin gene clusters. The pksA gene is located on a small chromosome of approximately 1.3 Mb in size, along with the dothistromin ketoreductase (dotA) gene.

Amino Acid Sequence↗

PubMed1984

Correlation of aflatoxin contamination with zinc content of chicken feed.

Feed samples from chicken houses in five commercial chicken operations were analyzed for Zn, Mn, Fe, Cu, Cd, and aflatoxin content. Mean aflatoxin content of these samples was 14 ppb (14 ng/g) as opposed to 1.2 ppb in samples taken when the feed was made. Aflatoxin content of the feed samples correlated (r = 0.325) significantly (P < 0.05) with Zn content but not with Mn, Fe, or Cu, all of which correlated significantly with Zn. Zn content of unamended feed (<20 ppm [20 mug/g]) is normally supplemented with a mineral premix containing Zn, Mn, Fe, and Cu to meet the nutrient requirements of chickens (40 ppm of Zn). The mean zinc concentration of the feed samples (117 ppm) was about threefold greater than the nutrient requirement and ranged from 58 to 162 ppm in individual samples. These field survey results parallel earlier reports of augmented production of aflatoxin in monocultures of aflatoxigenic fungi in corn and other ingredients supplemented with Zn. These results suggest that stricter control of Zn levels during manufacture could reduce aflatoxin contamination of feed consumed by chickens.

Journal Article↗

PubMed1999

Aflatoxin, Tobacco, Ammonia and the p53 Tumor-Suppressor Gene: Cancer's Missing Link?

Aflatoxin, the fungal carcinogen first identified in 1960, is now recognized as the prototypical laboratory carcinogen. It causes mutations in the p53 tumor-suppressor gene as well as ras mutations, which are involved in the majority of human cancers. Aflatoxin has been shown to contaminate tobacco products. Tobacco-related cancers, including those associated with ETS, often show the same p53 mutations associated with aflatoxin exposure. The role of ammonia in neutralizing aflatoxin contamination is examined, as well as the potential role of the FDA in regulating aflatoxin contamination of tobacco products.

Journal Article↗

PubMed2002

Aflatoxin biosynthesis.

Aflatoxins are toxic and extremely carcinogenic natural secondary metabolites produced primarily by the fungi Aspergillus flavus and Aspergillus parasiticus. The biosynthesis of aflatoxins is a complex process involving multi-enzymatic reactions. Genetic studies of the molecular mechanism of aflatoxin B1 biosynthesis have identified an aflatoxin pathway gene cluster of 70 kilobase pairs in length consisting of at least 24 identified structural genes including a positive regulatory gene as transcription activator. The structural genes encode cytochrome P450 monooxygenases, dehydrogenases, oxidases, methyltransferases, a polyketide synthase and two unique fatty acid synthases. The aflatoxin biosynthesis and its genetic regulation are discussed in this review. The current knowledge of the relationship between fungal development and secondary metabolism is also summarized.

Journal Article↗

PubMed2001

Aflatoxin synthesis in corn fields in Guanajuato, Mexico.

Aflatoxin contamination of corn is an important problem internationally, particularly in tropical and subtropical conditions that favor infection and synthesis by Aspergillus. Environmental conditions (drought) and agronomic practices i.e. N fertilization have been reported as favorable to aflatoxin synthesis in the field. This study was undertaken to investigate whether the contamination of corn commonly observed in stored conditions in this important corn producing region of Mexico known as "El Bajio" is related to infection by Aspergillus under field conditions. Results using three corn hybrids of recognized susceptibility to infection showed that corn ears artificially inoculated in the field with a toxigenic strain of Aspergillus parasiticus presented a low content of aflatoxin ranging from 13.6 to 24.7 microg Kg(-1). No significant differences were observed between the hybrids tested. Similarly, N fertilization practices, 260 Kg N ha(-1), applied at sowing did not have an effect on the extent of the contamination observed of 6.2 and 19.3 mg of aflatoxin kg(-1) in natural infected and inoculated samples with A. parasiticus NRRL 2999, respectively. Our data suggest that the cases of aflatoxin contamination of corn in this part of Mexico are not related to infection occurring during the crops growing period but most probably to poor storage conditions of corn.

Journal Article↗