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PubMed1981

Effects of dietary aflatoxin on existing bacterial intramammary infections of dairy cows.

Aflatoxin, a naturally occurring mycotoxin with immunosuppressive properties, was given to 4 lactating dairy cows that had experimentally induced or naturally occurring mammary infections in 2 of their 4 mammary quarters. Aflatoxin was given orally in daily doses approximating 0.3 mg of B1 activity/kg of body weight for periods of 12 to 14 days. Infecting organisms were Streptococcus agalactiae, Staphylococcus aureus, and Staphylococcus hyicus. The 4 cows were monitored for clinical signs of disease and signs of mastitis for periods before, during, and after aflatoxin consumption. The cows developed inappetence, lost body weight, and had variable reductions in daily milk yield. Serum ornithine-carbamoyl transferase and sorbitol dehydrogenase activities were elevated during and 1 to 3 weeks after aflatoxin consumption. Exacerbations of acute clinical mastitis did not occur in any of the infected quarters; however, bacterial populations in the milk increased in 3 of the 4 cows during aflatoxin consumption. Mean California mastitis test scores were generally highest in the infected quarters in the period after the last dose of aflatoxin was given. Aflatoxin M1 appeared in milk 3 to 6 hours after aflatoxin consumption began, and persisted for 72 hours or longer after the last dose of aflatoxin was given. Aflatoxin B1 and M1 were present in urine samples taken at 6 hours after aflatoxin consumption began and persisted for 72 through 120 hours after the last dose of aflatoxin was given.

Aflatoxins↗

PubMed1977

Toxic effects of aflatoxin B1 in male Holstein calves with prior infection by flukes (Fasciola hepatica).

This experiment was designed to compare 3 dose levels of aflatoxin B1 (0.0, 0.5, and 1.0 mg/kg of body weight) and 2 infection levels of Fasciola hepatica metacercariae (0 and 220) to determine whether an additive effect from aflatoxin B1 occurs when fascioliasis is present in dairy calves. Twenty-four male, Holstein calves, 4 weeks old, and averaging 45.8 kg each, were assigned at random to 6 treatment groups, 4 calves per group: group 1--negative control; group 2--0.5 mg of aflatoxin B1/kg; group 3--1.0 mg of aflatoxin B1/kg group 4--220 metacercariae; group 5--220 metacercariae plus 0.5 mg of aflatoxin B1/kg; and group 6-220 metacercariae plus 1.0 mg of aflatoxin B1/kg. The single oral dose of 220 metacercariae was given (groups 4, 5, and 6) at the start of the 10-week experiment, and 5 weeks later, the single oral dose of aflatoxin B1 was given (groups 2, 3, 5, 6). Results from the principals, as compared with that from the controls (group 1), included significant decreases of dry matter intake (P less than 0.006), body weight (P less than 0.024), and serum albumin (P less than 0.04), and in groups 4, 5, and 6 infected with 220 flukes, there were significantly increased values of prothrombin time (P less than 0.014), serum alkaline phosphatase (P less than 0.04), and serum sorbitol dehydrogenase (P less than 0.007). Significant differences in number of flukes recovered from liver were seen in groups 4 to 6 given 0, 0.5, and 1.0 mg of aflatoxin B1/kg (P less than 0.046). The single oral dose of 22* fluke metacercariae in groups 4, 5, and 6 resulted in significantly increased concentrations of serum total protein (P less than 0.003) and globulins (P less than 0.01). Results from the development of the flukes from metacercariae to the mature state with sizes, numbers, feeding habits, and pathologic lesions were described. Differences in numbers of flukes recovered from liver of groups 4 to 6 and the presence of pneumonia in calves of group 6 indicated aflatoxin B1 produced persisting, lowered resistance. In all animals necropsied, the liver was the organ most affected by aflatoxin B1 as well as with flukes. Periportal fibrosis, monocytic infiltration, fatty infiltration, and bile duct proliferation were the usual lesions induced by aflatoxin B1. Additive toxic effects were observed in the groups 5 and 6 dosed with flukes and aflatoxin B1, with significant variations of serum and plasma values, as well as increased severity of histopathologic changes.

Aflatoxins↗

PubMed2005

Survey of aflatoxins in beer sold in Canada.

Between March 1998 and March 2002, 304 samples of domestic (Canadian) and imported beers from 36 countries were picked up for the determination of aflatoxins B1, B2, G1 and G2. Twelve samples were positive with aflatoxins greater than the limit of quantitation (LOQ) (aflatoxin B1, 4.4 ng l(-1); aflatoxin B2, 3.4 ng l(-1); aflatoxin G1, 11.2 ng l(-1); and aflatoxin G2, 6.2 ng l(-1)). Five samples from Mexico, two samples from Spain and one from Portugal contained aflatoxin B1. Four samples from India contained aflatoxins B1 and B2. The remaining samples contained less than the LOQ for aflatoxins B1, B2, G1 and G2. The analytical method for this survey was based on that of Scott and Lawrence (Scott PM, Lawrence GA. 1997. Determination of aflatoxins in beer. Journal of AOAC International 80:1229-1234.). Aflatoxins B1, B2, G1 and G2 were determined at parts per trillion (ng l(-1)) levels in beer by immunoaffinity column cleanup followed by derivatization with trifluoroacetic acid and reversed-phase liquid chromatography with fluorescence detection.

Aflatoxin B1↗

PubMed1988

Carcinogen-nucleic acid interactions: equilibrium binding studies of aflatoxins B1 and B2 with DNA and the oligodeoxynucleotide d(ATGCAT)2.

Equilibrium binding is believed to play an important role in directing the subsequent covalent attachment of many carcinogens to DNA. We have utilized UV spectroscopy to examine the non-covalent interactions of aflatoxin B1 and B2 with calf thymus DNA, poly(dAdT):poly(dAdT), and poly(dGdC):poly(dGdC), and have utilized NMR spectroscopy to examine non-covalent interactions of aflatoxin B2 with the oligodeoxynucleotide d(ATGCAT)2. UV-VIS binding isotherms suggest a greater binding affinity for calf thymus DNA and poly(dAdT):poly(dAdT) than for poly(dGdC):poly(dGdC). Scatchard analysis of aflatoxin B1 binding to calf thymus DNA in 0.1 M NaCl buffer indicates that binding of the carcinogen at levels of bound aflatoxin less than 1 carcinogen per 200 base pairs occurs with positive cooperativity. The cooperative binding effect is dependent on the ionic strength of the medium; when the NaCl concentration is reduced to 0.01 M, positive cooperativity is observed at carcinogen levels less than 1 carcinogen per 500 base pairs. The Scatchard data may be fit using a "two-site" binding model [L.S. Rosenberg, M.J. Carvlin, and T.R. Krugh, Biochemistry 25, 1002-1008 (1986)]. This model assumes two independent sets of binding sites on the DNA lattice, one a high affinity site which binds the carcinogen with positive cooperativity, the second consisting of lower affinity binding sites to which non-specific binding occurs. NMR analysis of aflatoxin B2 binding to d(ATGCAT)2 indicates that the aflatoxin B2/oligodeoxynucleotide complex is in fast exchange on the NMR time scale. Upfield chemical shifts of 0.1-0.5 ppm are observed for the aflatoxin B2 4-OCH3, H5, and H6a protons. Much smaller chemical shift changes (less than or equal to 0.06 ppm) are observed for the oligodeoxynucleotide protons. The greatest effect for the oligodeoxynucleotide protons is observed for the adenine H2 protons, located in the minor groove. Nonselective T1 experiments demonstrate a 15-25% decrease in the relaxation time for the adenine H2 protons when aflatoxin B2 is added to the solution. This result suggests that aflatoxin B2 protons in the bound state may be in close proximity to these protons, providing a source of dipolar relaxation. Further experiments are in progress to probe the nature of the aflatoxin B1 and B2 complexes with polymeric DNA and oligodeoxynucleotides, and to establish the relationship between the non-covalent DNA-carcinogen complexes observed in these experiments, and covalent aflatoxin B1-guanine N7 DNA adducts.

Aflatoxin B1↗

PubMedDate not supplied

Sampling almonds for aflatoxin, part I: estimation of uncertainty associated with sampling, sample preparation, and analysis.

Domestic and international regulatory limits have been established for aflatoxin in almonds and other tree nuts. It is difficult to obtain an accurate and precise estimate of the true aflatoxin concentration in a bulk lot because of the uncertainty associated with the sampling, sample preparation, and analytical steps of the aflatoxin test procedure. To evaluate the performance of aflatoxin sampling plans, the uncertainty associated with sampling lots of shelled almonds for aflatoxin was investigated. Twenty lots of shelled almonds were sampled for aflatoxin contamination. The total variance associated with measuring B1 and total aflatoxins in bulk almond lots was estimated and partitioned into sampling, sample preparation, and analytical variance components. All variances were found to increase with an increase in aflatoxin concentration (both B1 and total). By using regression analysis, mathematical expressions were developed to predict the relationship between each variance component (total, sampling, sample preparation, and analysis variances) and aflatoxin concentration. Variance estimates were the same for B1 and total aflatoxins. The mathematical relationships can be used to estimate each variance for a given sample size, subsample size, and number of analyses other than that measured in the study. When a lot with total aflatoxins at 15 ng/g was tested by using a 10 kg sample, a vertical cutter mixer type of mill, a 100 g subsample, and high-performance liquid chromatography analysis, the sampling, sample preparation, analytical, and total variances (coefficient of variation, CV) were 394.7 (CV, 132.4%), 14.7 (CV, 25.5%), 0.8 (CV, 6.1%), and 410.2 (CV, 135.0%), respectively. The percentages of the total variance associated with sampling, sample preparation, and analytical steps were 96.2, 3.6, and 0.2, respectively.

Aflatoxin B1↗

PubMedDate not supplied

Visual and semiquantitative spectrophotometric ELISA screening method for aflatoxin B1 in corn and peanut products: follow-up collaborative study.

A joint AOAC/IUPAC (International Union of Pure and Applied Chemistry) interlaboratory study of an enzyme-linked immunosorbent screening assay (ELISA) for aflatoxins was conducted in laboratories in Canada, France, Japan, The Netherlands, Switzerland, Tunisia, and the United States. Twelve raw and roasted peanut and corn portions containing various concentrations of natural aflatoxins and supplemented when appropriate with aflatoxin B1 were distributed to participating laboratories for testing. The assay is based on competition between an enzyme-conjugated aflatoxin B1 and (free) aflatoxins in the test sample for aflatoxin-specific antibodies coated onto interior surfaces of microtiter wells. After a wash step to remove all unbound aflatoxins, a substrate added to each well is catalyzed from a colorless to a blue solution by any bound enzyme-conjugated aflatoxin B1 present. The intensity of the color decreases as the amount of free aflatoxin B1 in the test portion increases. Final determination of aflatoxin concentrations can be made by either visual comparison with standard solutions or spectrophotometric comparisons (at 650 nm) to knowns. Overall correlation was good between ELISA and thin-layer chromatographic results for corn and roasted peanut products, with 93 and 98% correct responses for visual and instrumental determinations, respectively. For instrumental determinations of aflatoxin in corn and roasted peanuts in the less than or equal to 20 ng/g range, the relative standard deviations for repeatability (RSDr) were 14.9 and 41.4%, respectively, and the relative standard deviations for reproducibility (RSDR) were 45.7 and 43.5%, respectively. For instrumental determination of greater than 20 ng/g, the respective RSDr and RSDR values were 19.4 and 52.7% for corn and 23.3 and 23.3% for roasted peanuts.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxin B1↗

PubMed1996

Aflatoxin exposure and risk of hepatocellular carcinoma in Taiwan.

To investigate the carcinogenic effect of environmental aflatoxin exposure, 56 cases of hepatocellular carcinoma (HCC) diagnosed between 1991 and 1995 were identified and individually matched by age, sex, residence and date of recruitment to 220 healthy controls from the same large cohort in Taiwan. Blood samples were analyzed for hepatitis B and C viral markers and for aflatoxin-albumin adducts; urine was tested for aflatoxin metabolites. We obtained information about sociodemographic characteristics, habitual alcohol drinking, cigarette smoking and diet in a structured interview. Hepatitis B virus surface antigen (HBsAg) carriers had a significantly increased risk for HCC. After adjustment for HBsAg serostatus, the matched odds ratio (ORm) was significantly elevated for subjects with high levels of urinary aflatoxin metabolites. When stratified into tertiles, a dose-response relationship with HCC was observed. The ORm for detectable aflatoxin-albumin adducts was not significant after adjustment for HBsAg serostatus. HBsAg-seropositive subjects with high aflatoxin exposure had a higher risk than subjects with high aflatoxin exposure only or HBsAg seropositivity only. In male HBsAg-seropositive subjects, adjusted ORs were 2.8 (95% confidence interval [CI] = 0.9-9.1) for detectable compared with non-detectable aflatoxin-albumin adducts and 5.5 (CI = 1.3-23.4) for high compared with low urinary aflatoxin metabolite levels. Our results suggest that environmental aflatoxin exposure may enhance the hepatic carcinogenic potential of hepatitis B virus. A large-scale study will be needed to evaluate the effect of aflatoxin exposure on HBsAg non-carriers.

Aflatoxins↗

PubMed2004

Identification and reduction of urinary aflatoxin metabolites in dogs.

Hydrated sodium calcium aluminosilicate (HSCAS) is a phyllosilicate clay commonly used as an anticaking agent in animal feeds. HSCAS tightly and selectively adsorbs aflatoxin. In 1998, 55 dogs died in Texas after eating dog food containing aflatoxin (150-300 ppb). The corn in the diets was contaminated with aflatoxin. Six dogs were given a low-level, sub-clinical dose of aflatoxin B(1). On average, 71.5% of aflatoxin M(1) cleared within 6 h after dosing, increasing to 90.4% after 12 h. Aflatoxin M(1) was no longer detectable in urine after 48 h. Aflatoxin P(1) was not found in urine compared to large amounts of M(1) and trace amounts of Q(1). In a crossover study, six dogs randomly fed a commercial dog food (no-clay control) or coated with HSCAS (0.5% by weight) were subsequently administered a sub-clinical dose of aflatoxin B(1). Diets were switched and the process repeated. The HSCAS-coated diet significantly reduced urinary aflatoxin M(1) by 48.4%+/-16.6 SD versus the control diet. In conclusion, HSCAS protects dogs fed diets with even minimal aflatoxin contamination. Despite regular and careful ingredient screening for aflatoxin, low concentrations may reach the final product undetected. Therefore, HSCAS may provide the pet food industry further assurance of canine diet safety.

Adsorption↗

PubMed1989

Chromatographic and spectroscopic properties of hemiacetals of aflatoxin and sterigmatocystin metabolites.

Improved fluorescence detection of aflatoxin B1 by chromatographic analysis is accomplished by conversion to the corresponding hemiacetal, aflatoxin B2a. Because the metabolites aflatoxin M1, aflatoxin P1, aflatoxin Q1, sterigmatocystin, and O-methylsterigmatocystin have the same molecular conversion site, we investigated the chromatographic and spectroscopic properties of hemiacetals of these compounds to assist in confirming aflatoxins and sterigmatocystins in human urine. Nuclear magnetic resonance and infrared absorbance were used to confirm the hemiacetal structure for aflatoxin B1 and sterigmatocystin. The ultraviolet absorbance, fluorescence, and chromatographic properties of the metabolites were investigated. Using these data, we optimized the detection and solvent conditions for high-performance liquid chromatography. We determined that, of the conditions studied, maximum sensitivity and resolution for the native aflatoxins were achieved with a mobile phase of methanol, tetrahydrofuran, and water, a C8 column in series with a C18 column, and fluorescence detection with 365 nm excitation and 430 nm emission wavelengths for aflatoxins B1 and M1 and with 500 nm emission wavelength for aflatoxins P1 and Q1. For the analysis of the hemiacetals, a mobile phase of methanol, acetonitrile, and water provided better chromatography and fluorescence detection. Sterigmatocystin and O-methylsterigmatocystin were readily converted to the hemiacetal forms, which, like the aflatoxins, were more polar and, therefore, earlier eluting by reversed-phase HPLC (methanol, acetonitrile, and water, 236 nm absorbance). These data are important to maximize the sensitivity and confidence for detecting the mycotoxin metabolites in biological specimens.

Acetals↗

PubMed1998

Molecular dosimetry in fish: quantitative target organ DNA adduction and hepatocarcinogenicity for four aflatoxins by two exposure routes in rainbow trout.

Rainbow trout, a species highly sensitive to aflatoxins, was used to investigate the relative carcinogenicities of four structurally related aflatoxins in terms of their target organ DNA binding characteristics. Tritiated syntheses were carried out, DNA binding dose-response curves were established, and liver DNA binding indices were calculated for the four aflatoxins following a 2-week dietary fry exposure protocol. The results indicated that adduct levels increased linearly with dietary dose concentration, with relative DNA binding indices of 20.7, 20.3, 2.35, and 2.22 x 10(3) (pmoles aflatoxin mg-1 DNA)/(pmoles aflatoxin g-1 diet) for aflatoxin B1 (AFB1), aflatoxicol (AFL), aflatoxin M1 (AFM1), and aflatoxicol M1 (AFLM1), respectively. A similar protocol used over 7200 trout fry averaging 1.2 g initial body weight to establish full carcinogen dose-response curves for each aflatoxin, along with a single-dose estimate of DNA binding index within the tumor study animals. Owing to trout sensitivity a total of 180 micrograms or less of each aflatoxin was required. Data analyzed on logit incidence vs. Ln dose coordinates generated four curves which were modeled as parallel in slope over most or all dose ranges studied. By this analysis, relative tumorigenic potencies were: AFB1 1.00; AFL 0.936; AFM1 0.086; and AFLM1 0.041. When data were plotted as logit incidence vs. Ln adducts (effective dose received), all aflatoxin adducts described the same dose-response curve; that is, they were equally tumorigenic, except those from AFLM1, which were 2-3 fold less potent. Therefore, by these molecular dose studies, differences in tumorigenicity among the four dietary aflatoxins are largely or entirely accounted for by differences in uptake and metabolism leading to DNA adduction, rather than any inherent differences in tumor initiating potency per DNA adduct.

Aflatoxins↗

PubMed1982

A case-control dietary study of primary liver cancer risk from aflatoxin exposure.

UNLABELLED: The dietary intakes of 90 confirmed primary liver cancer cases were compared against 90 age-sex matched controls. Dietary recall, obtained by the same nutritionist, was taken for each change of residence lasting one year or more. The frequency and amounts of food items consumed were calculated into units of aflatoxin load per day using a Philippine table of aflatoxin values of these items. Of the total subjects' aflatoxin load, 51.2% came from cassava, 20.3% from corn, 6.8% from peanuts and 5.8% from sweet potato. The mean aflatoxin load per day of the cases as found to be 440% that of the controls. Upon grouping dietary aflatoxin loads (and alcohol intakes) into Heavy and Light, and upon comparing cases versus controls, the relative risk (RR) of developing primary liver cancer was found to be statistically significant in the following order of rank: cassava, peanuts, sweet potato, corn and alcohol. Boiled rice which had negligible aflatoxin content gave no difference in risk. Combining aflatoxin load and alcohol intake gave a synergistic and a statistically significant effect on RR with Light Aflatoxin, Light Alcohol as RR = 1. RESULTS: Light Aflatoxin, Heavy Alcohol RR = 3.9; Heavy Aflatoxin, Light Alcohol RR = 17.5; Heavy Aflatoxin, Heavy Alcohol RR = 35.0.

Adolescent↗

PubMedDate not supplied

Effect of aflatoxin ingestion in feed on body weight gain and tissue residues in rabbits.

The effect of a subclinical dose of aflatoxin on body weight gain and risk assessment of aflatoxin in muscle tissue for food safety were the focus of the study. Thirty New Zealand rabbits, 2 months old, were used. A group of 24 rabbits was fed aflatoxin 2 p.p.m. day-1 for a period of 4 months. The weights of the individual aflatoxin-fed rabbits and those of the control group were recorded weekly. Aflatoxin was withdrawn from a group of six rabbits chosen at random for a period of 4 weeks before the termination of the experiment. All rabbits were necropsied at the end of the study for gross and microscopic changes of the internal organs. Samples of muscle tissue were also collected and analysed chemically for aflatoxin using thin-layer chromatography. Significant weight loss equivalent to 13% mortality was found in the aflatoxin-fed rabbits. Characteristic pathological changes were found. Aflatoxins B1 and G2 were detected in muscle tissue at alarming concentrations far exceeding the permissible levels in food for human consumption in the aflatoxin-fed group. No detectable aflatoxins were found in the aflatoxin-withdrawal group.

Aflatoxins↗

PubMed1980

Ammoniation of corn contaminated with aflatoxin and its effects on growing rats.

Corn naturally contaminated with 2,000 ppb total aflatoxin was adjusted to 17% moisture and ammoniated (Am) with 1.5% (w/w) anhydrous ammonia in an attempt at detoxification. The ammonia treatment reduced the detectable concentration to 510 ppb total aflatoxins. Ninety-six male Sprague-Dawley rats (75 g avg) were randomly divided into eight treatment groups with 12 rats per treatment. A fortified 12%-protein corn-soybean meal diet served as the control (C) diet. The corn used in the C diet contained no detectable aflatoxin. Treatment 2 contained 1,670 ppb aflatoxin; treatments 3 and 4 were similar to treatments 1 and 2, respectively, except the corn used was ammoniated. Treatments 5 through 8 contained 830, 420, 210 and 100 ppb total aflatoxin, respectively. Liver weights expressed as a percentage of final live weight were increased (P less than .05) in rats consuming diets containing 1,670 ppb aflatoxin compared to the other treatments. Serum albumin, IgG and IgM concentrations were not affected by ammoniation or by concentration of aflatoxin in the corn. At the end of 4 weeks, total serum protein was increased (P less than .05) in rats consuming diets containing aflatoxin-contaminated (AfC) corn and Am corn compared to those consuming the C diet. Average daily gain and average daily feed consumption were reduced (P less than .01) in rats consuming the diet containing 1,670 ppb aflatoxin. The growth of rats consuming AfC corn that was Am was equal to that of rats consuming a similar concentration of aflatoxin by dilution. From these results and the results of others, it appears that ammoniation of corn contaminated with aflatoxin may be a practical and economical method for detoxification.

Aflatoxins↗

PubMed1996

Resistance to aflatoxin contamination in corn as influenced by relative humidity and kernel germination.

Kernels of corn population GT-MAS:gk, resistant to aflatoxin B1 production by Aspergillus flavus, and susceptible Pioneer hybrid 3154 were tested for aflatoxin when incubated under different relative humidities (RH). High aflatoxin levels were not detected in either genotype at RH < 91%. Resistance in GT-MAS:gk was consistent across all RH levels (91 to 100%) at which significant aflatoxin accumulation was detected. Aflatoxin levels in GT-MAS:gk averaged about 98% less than those in susceptible Pioneer 3154, which suggests that storage of this or other genotypes with similar resistance mechanisms may be possible under moisture conditions less exacting than are required with susceptible hybrids. Results for fungus growth and sporulation ratings on kernel surfaces were similar to those for aflatoxin levels. When kernels of both genotypes were preincubated 3 days at 100% RH prior to inoculation with A. flavus, germination percentages increased to very high levels compared to those of kernels that were not preincubated. In preincubated kernels aflatoxin levels remained consistently low in GT-MAS:gk but decreased markedly (61%) in Pioneer 3154. When eight susceptible hybrids were evaluated for aflatoxin accumulation in preincubated kernels, seven of these supported significantly lower toxin levels than kernels not subjected to preincubation. Average reduction across hybrids was 83%, and reductions within hybrids ranged from 68 to 96%. Preincubated kernels of one susceptible hybrid (Deltapine G-4666) supported aflatoxin levels comparable to those in resistant GT-MAS: gk. Data suggest that an inhibitor of aflatoxin biosynthesis may be induced during kernel germination. Possible mechanisms for embryo effects on resistance to aflatoxin accumulation are discussed.

Aflatoxins↗

PubMedDate not supplied

Predicting aflatoxin and fumonisin in shelled corn lots using poor-quality grade components.

A study was conducted to determine if aflatoxin and fumonisin are concentrated in the poor-quality grade components of shelled corn. Four 1.0 kg test samples were each taken from 23 lots of shelled corn marketed in North Carolina. Inspectors from the Federal Grain Inspection Service divided each test sample into 3 grade components: (1) damaged kernels (DM), (2) broken corn and foreign material (BCFM), and )3) whole kernels (WH). The aflatoxin and fumonisin concentration was measured in each component and a mass balance equation was used to calculate the total concentration of each mycotoxin in each test sample. Averaged across all test samples, the aflatoxin concentrations in the DM, BCFM, and WH components were 1300.3, 455.2, and 37.3 ppb, respectively. Averaged across all test samples, the fumonisin concentrations in the DM, BCFM, and WH components were 148.3, 51.3, and 1.8 ppm, respectively. The DM and BCFM components combined accounted for only 5.0% of the test sample mass, but accounted for 59.8 and 77.5% of the total aflatoxin and fumonisin mass in the test sample, respectively. Both aflatoxin mass (ng) and aflatoxin concentration (ng/g) in the combined DM and BCFM components had high correlations with aflatoxin concentration in the lot. The highest correlation occurred when aflatoxin mass (ng) in the combined DM and BCFM components was related to aflatoxin concentration in the lot (0.964). Similar results were obtained for fumonisin. This study indicated that measuring either aflatoxin or fumonisin in the combined DM and BCFM grade components could be used as a screening method to predict either aflatoxin or fumonisin in a bulk lot of shelled corn.

Aflatoxins↗

PubMed1993

Transient intervention with oltipraz protects against aflatoxin-induced hepatic tumorigenesis.

Oltipraz [5-(2-pyrazinyl)-4-methyl-1,2-dithiole-3-thione] protects against aflatoxin B1-induced hepatocarcinogenesis in rats when fed before and during carcinogen exposure; however, such an exposure-chemoprotection intervention paradigm is not directly relevant to most human populations. To model and assess the possible efficacy of short term interventions targeted at individuals at risk for sustained exposure to aflatoxins, 175-g male F344 rats were treated daily with 25 micrograms of aflatoxin B1, p.o., for 28 days. One week after the start of aflatoxin B1 exposure, half of the animals were fed a diet supplemented with 0.075% oltipraz for 10 days; these rats were then restored to the unsupplemented AIN-76A diet for the remainder of the experimental period. Livers were analyzed 2 or 3 months after the last aflatoxin B1 dose for burden of glutathione S-transferase P (GST-P)-positive foci, as an index of presumptive preneoplastic tumors. The transient intervention with oltipraz reduced the volume percent of hepatic GST-P-positive foci by 54% (P = 0.047) and 72% (P = 0.004) at 2 and 3 months, respectively. A strong positive correlation was also observed between the extent of fibrosis in the livers of these animals and the hepatic burden of GST-P-positive foci, implying that cytotoxicity is associated with the tumorigenic process. This protection may reflect alterations in the metabolism and disposition of aflatoxin B1 induced by oltipraz. Glutathione S-transferase catalyze the detoxication of aflatoxin-8,9-oxide and were found to be rapidly induced in the livers of animals after the beginning of the oltipraz intervention. Glutathione S-transferase activity remained significantly (P < 0.05) higher until 9 days after the end of the oltipraz intervention. In contrast, levels of hepatic aflatoxin-DNA adducts were not significantly reduced until 4 days after the beginning of the intervention but remained significantly (P < 0.05) lower up to 11 days after the end of the intervention. The cumulative reduction in levels of hepatic aflatoxin-DNA adducts (approximately 25%) by the oltipraz intervention underestimated the reduction in the hepatic burden of GST-P-positive foci. The significant protection against presumptive preneoplastic tumors, despite the delay of intervention, suggests that oltipraz may exert substantial activity against the cytotoxic and autopromoting action of repeated exposures to aflatoxin B1 and supports the utility of intervention trials with oltipraz in individuals chronically consuming aflatoxin B1-contaminated foods, particularly in regions with high incidences of liver cancer.

Aflatoxin B1↗

PubMed1967

Aflatoxin Production by Aspergillus flavus as Related to Various Temperatures.

Two aflatoxin-producing isolates of Aspergillus flavus were grown for 5 days on Wort media at 2, 7, 13, 18, 24, 29, 35, 41, 46, and 52 C. Maximal production of aflatoxins occurred at 24 C. Maximal growth of A. flavus isolates occurred at 29 and 35 C. The ratio of the production of aflatoxin B(1) to aflatoxin G(1) varied with temperature. Aflatoxin production was not related to growth rate of A. flavus; one isolate at 41 C, at almost maximal growth of A. flavus, produced no aflatoxins. At 5 days, no aflatoxins were produced at temperatures lower than 18 C or higher than 35 C. Color of CHCl(3) extracts appeared to be directly correlated with aflatoxin concentrations. A. flavus isolates grown at 2, 7, and 41 C for 12 weeks produced no aflatoxins. At 13 C, both isolates produced aflatoxins in 3 weeks, and one isolate produced increasing amounts with time. The second isolate produced increasing amounts through 6 weeks, but at 12 weeks smaller amounts of aflatoxins were recovered than at 6 weeks.

Journal Article↗

PubMed1988

Hepatocellular uptake of aflatoxin B1 by non-ionic diffusion. Inhibition of bile acid transport by interference with membrane lipids.

Aflatoxin B1 permeates isolated rat hepatocytes by non-ionic diffusion. Its uptake is neither saturable nor influenced by metabolic energy and not inhibited by treatment of cells with proteases. The initial rate of aflatoxin B1 uptake measured at 7 degrees C is between 40 and 50% compared to that at 37 degrees C. However, after an incubation period of 7 minutes identical equilibrium uptake is reached at both temperatures. The apparent activation energies, calculated for aflatoxin B1 uptake by Arrhenius diagrams ranged between 1.69 and 4.5 kcal/mol. A Q10 value of 1.34 was calculated for a temperature interval of 7-17 degrees C but decreased to 1.05 for the interval of 27-37 degrees C. Liposomes or lipoproteins added to the cell suspension inhibited the aflatoxin B1 uptake into hepatocytes. Liposomes mainly composed of unsaturated fatty acids bind twice as much aflatoxin B1 as those composed of saturated ones, indicating that the lipophilicity of the mycotoxin is crucial in the determination of its uptake into liver cells. At concentrations above 5 micrograms/ml, aflatoxin B1 inhibited the carrier-mediated uptake of cholic acid and of phalloidin into hepatocytes. This effect was reversible and abolished by washing the cells after preincubation with aflatoxin. In concentrations below 5 micrograms/ml the uptake of phallotoxin and cholic acid was however stimulated by 15-25%. These results indicate, that a carrier-mediated uptake into hepatocytes via the multispecific bile salt transporter is not responsible for the organoselective clearance of aflatoxins by the liver. On the other hand, the cholestatic effect of aflatoxin B1 results at least partially from the inhibition of the multispecific bile acid transport system. This inhibition may arise from affinity of aflatoxins to lipid domains of the cell membrane.

Aflatoxin B1↗