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PubMed1996

Absence of mutations in the p53 tumor suppressor gene in woodchuck hepatocellular carcinomas associated with hepadnavirus infection and intake of aflatoxin B1.

Infection with hepadnaviruses and exposure to aflatoxin B1 (AFB1) are considered major risk factors in the development of hepatocellular carcinoma (HCC) in humans and in animals. A high rate of mutations in the p53 tumor suppressor gene in hepatocellular carcinomas of predominantly hepatitis B virus (HBV) carrier patients has been recently related to dietary aflatoxin. Another member of the hepadnavirus family, the woodchuck hepatitis virus (WHV), infects woodchucks in a manner similar to that of HBV in humans. Therefore, it was of particular interest to determine whether the p53 gene in woodchuck HCCs associated with hepadnavirus infection and with exposure to AFB1 is affected in the same manner as in human HCCs. By direct PCR-sequencing, we analyzed exons 4-9 of the p53 gene in 13 HCCs from 12 woodchucks (two uninfected, ten WHV carriers). Six WHV carrier and two uninfected woodchucks were treated with AFB1. None of the analyzed HCC samples exhibited mutations, either in p53 gene exons 4-9, or in splicing donor-acceptor sites. The present data are consistent with our previous study that indicated a low rate of p53 mutations in HCCs of AFB1-treated ground squirrels, either infected or not infected with ground squirrel hepatitis virus, and in WHV carrier woodchucks not exposed to AFB1. Overall, our findings indicate that in woodchucks and in ground squirrels exposure to aflatoxin may affect the development of p53 mutations less than in humans.

Aflatoxin B1↗

PubMed1997

Mechanism of action of dietary chemoprotective agents in rat liver: induction of phase I and II drug metabolizing enzymes and aflatoxin B1 metabolism.

A range of potential chemoprotective agents, most of them natural dietary constituents, has been examined for ability to modulate both phase I (cytochrome P450 1A1, 1A2, 2B1/2, 2C11, 2E1, 3A, 4A) and phase II drug metabolizing enzymes (glutathione S-transferases, in particular subunits Yc2 and P, aflatoxin B1-aldehyde reductase and quinone reductase) in rat liver. In addition to assays of total enzyme activity and Western blots for individual isozymes, the ability of microsomes to metabolize aflatoxin B1, and of cytosols to conjugate aflatoxin B1 (AFB1)-epoxide to GSH and to produce AFB1-dialcohol, were measured. Induction of gamma-glutamyl transpeptidase activity was examined by histochemistry. Differing patterns of induction were observed, reflecting differences in the control of expression of the individual enzymes studied. Of the compounds examined, butylated hydroxytoluene, ethoxyquin, indole-3-carbinol and phenethyl isothiocyanate were the most potent bifunctional agents (inducing both phase I and II activities). Oltipraz, while only weakly inducing CYP1A2 and 2B1/2, was a potent inducer of phase II enzymes. Caffeic acid, garlic oil, sinigrin and propyl gallate all showed some ability to induce phase II enzymes. 4-Methyl catechol, alpha-tocopherol and red wine decreased certain phase I enzyme activities, while inducing total GST activity. Butylated hydroxytoluene, ethoxyquin, garlic oil and indole-3-carbinol induced gamma glutamyltranspeptidase in periportal hepatocytes. Particularly because of their ability to induce the detoxifying activities of glutathione S-transferase Yc2 and aldehyde reductase, butylated hydroxytoluene, ethoxyquin, indole-3-carbinol, oltipraz, phenethyl isothiocyanate and sinigrin will be effective blocking agents in rodents, if administered prior to AFB1. While these studies indicate the relative contributions of phase I and II metabolism in the overall protective effect in rat, care should be taken that a similar balance is achieved in man, and that relevant enzymes or iso forms are induced.

Aflatoxin B1↗

PubMed2003

Application of immunoaffinity chromatography and enzyme immunoassay in rapid detection of aflatoxin B1 in chicken liver tissues.

Existing physicochemical analytical methods for the determination of aflatoxins in animal tissues are expensive, cumbersome, and hazardous. To offer an alternative to these methods, a novel and highly sensitive immunochemical method for the rapid detection of aflatoxin B1 (AFB1) in chicken liver tissues is described in this study. Liver tissues were homogenized with cold methanol-acetone (50:50), followed by AFB1 extraction with methanol-acetone-PBS (25:25:50). The tissue extracts were, with or without further purification by immunoaffinity chromatography (IAC), applied to a highly sensitive direct ELISA for determination of AFB1. The detection limits for this assay were 15 +/- 0.77 pg/mL when standards and samples were dissolved in methanol-PBS (10:90) and 17 +/- 2.0 pg/mL when methanol-acetone-PBS (5:5:90) solution was used. The average recoveries of AFB1 were 54.3 to 65.5% in artificially contaminated tissue samples at 1 to 5 ng/g. In samples spiked with AFB1 at 1 ng/g, the method had diagnostic sensitivity and specificity of 100% for samples processed with IAC and 91.7 and 100%, respectively, for samples without IAC purification. The test was successfully applied to the detection of AFB1 in liver tissues from chickens that were experimentally dosed with AFB1. It is hoped that this test will be applicable in rapid detection of aflatoxins in poultry meats and in diagnosis of aflatoxicosis in chicken.

Aflatoxin B1↗

PubMed1991

Case-control study of cigarette smoking and primary hepatoma in an aflatoxin-endemic region of China: a protective effect.

Aflatoxin is believed to be a major causative agent in the high incidence of primary liver cancer seen in certain regions of the world. In Fujian Province, an aflatoxin-endemic region of China, we compared the cigarette smoking habits of 200 primary hepatoma patients with those of 200 matched nonhepatoma controls. We excluded from our study all individuals with evidence of hepatitis B virus serum antigen and/or alcoholic cirrhosis. Interestingly, two groups of hepatoma patients could be discerned. In patients more than 50 years of age, a significantly higher number of cases of primary hepatoma was found among nonsmokers than smokers (odds ratio = 2.06; 95% confidence interval = 1.32-3.20). In patients less than 50 years of age, this difference was not seen. Previous studies in the rat, mouse and duck had suggested that agents present in cigarette smoke might induce a cytochrome P450-mediated detoxication pathway, leading to protection against aflatoxin-induced primary liver cancer. Our clinical data in the present study are therefore consistent with the previous laboratory animal experiments.

Adult↗

PubMed1975

Malonate as a precursor in the biosynthesis of aflatoxins.

Incorporation of [I-14C]acetate and [2-14C]malonate into aflatoxins by resting mycelia of Aspergillus parasiticus resuspended in different buffers was studied. A decrease in pH from 5-8 to 2-8, as well as addition of EDTA, markedly stimulated the incorporation of malonate but the effect on acetate incorporation was less pronounced. Mycelia took up comparatively more acetate than malonate, but more malonate (4-3%) entering mycelia was incorporated into aflatoxins than was acetate (1-6%). Furthermore, the addition of unlabelled acetate reduced the incorporation of label from [I-14C]acetate by 75% but from [2-14C]malonate by only 25%. These results suggest that malonate is an intermediate in aflatoxin synthesis and that is can be incorporated without prior conversion to acetate.

Acetates↗

PubMed1992

[Detection of aflatoxin B1 in tissues of free-living game animals (Lepus europaeus, Phasianus colchicus, Capreolus capreolus, Anas platyrhynchos)].

This contribution states concentrations of products of toxogenic mould fungus Aspergillus in livers, kidneys and testes of specific game animals. In hares (Lepus europaeus), there was determined an average concentration in livers of 0.407 microgram.kg-1 +/- 0.29, in kidneys 0.658 microgram.kg-1 +/- 0.60, in testes 0.523 microgram.kg-1 +/- 0.27 and in the ovaries 0.207 microgram.kg-1 +/- 0.19. Higher values were found in those animals with silage pits, hayricks and liquid manure pits nearby. In roe deer (Capreolus capreolus), average concentration of Aflatoxin showed the following results:livers--0.696 microgram.kg-1 +/- 0.59, kidneys--0.794 microgram.kg-1 +/- 0.48, testes--0.367 microgram.kg-1 +/- 0.22. The different values found in the organs are likely to be dependent upon the varying resistance of species when digesting, and also upon the wide-spread variance of intaken food. Average concentration of Aflatoxin B1 in pheasants (Phasianus colchicus) were recorded to be in livers 0.329 micrograms.kg-1 +/- 0.38, and in kidneys 0.676 micrograms.kg-1 +/- 0.59. Controlled contents of mycotoxin in livers of mallards (Anas platyrhynchos) was found to be 0.840 micrograms.kg-1, in kidneys 0.594 micrograms.kg-1 +/- 0.85. Animals living in ecologically strained localities showed maximum values of 3.605 micrograms.kg-1 in kidneys and 2.484 micrograms.kg-1 in livers. An alimentary and inhalatory path for mycotoxin or for solely mould fungus into the organism could be found in the rearing of chicken. Detection of Aflatoxin B1 was performed by the means of proved radioimmunological screening method (33) that had been accompanied by routine chromatographic methods.

Aflatoxin B1↗

PubMedDate not supplied

Primary liver cancer is of multifactorial origin: importance of hepatitis B virus infection and dietary aflatoxin.

Primary liver cancer has a variable incidence worldwide, occurring most frequently in South-East Asia and China, which indicates that environmental factors are important in its aetiology. Although hepatitis B virus and chemical agents are the major risk factors for primary liver cancer, current evidence strongly suggests that it is of multifactorial origin. Aflatoxins are thought to be important because they are common food contaminants and are potent liver carcinogens in a wide variety of animal species. Evidence for the possible interactions between aflatoxin and hepatitis B infection, and their effects on the prevalence of primary liver cancer, is obtained from animal data and epidemiological studies. The risk of developing primary liver cancer following exposure to hepatitis B infection and aflatoxin is shown to be increased and the possible molecular mechanisms involved are discussed.

Aflatoxins↗

PubMed1969

The effect of aflatoxin on blood clotting in the rat.

1. The action of aflatoxin on blood clotting of rats was investigated. Aflatoxin B(1) prolonged the blood clotting time of rats.2. Aflatoxin B(1) was effective as an anticoagulant in much smaller doses than 4-hydroxycoumarin.

Aflatoxins↗

PubMed1998

Transcript of a homolog of aflR, a regulatory gene for aflatoxin synthesis in Aspergillus parasiticus, was not detected in Aspergillus oryzae strains.

Some strains of Aspergillus oryzae were shown to have homologs of aflR, a regulatory gene for aflatoxin synthesis in Aspergillus parasiticus. Transcription of an aflR homolog was examined in six strains of A. oryzae having the homologs, using polymerase chain reaction (PCR) coupled with reverse transcription. No PCR product was obtained when the RNA prepared from the A. oryzae strains cultivated under aflatoxin-producing condition was used as template for amplification of the aflR cDNA. By contrast, a PCR product of the expected size was obtained with RNA from A. parasiticus NIAH-26 processed by the same procedure. From genomic DNA of these strains, PCR products of the same size as above were obtained. Possible degradation of the aflR mRNA in the RNA preparation of the A. oryzae strains was negligible, because the calmodulin transcript was detected by PCR from the same RNA samples. Thus, the aflR homologs in the non-aflatoxigenic A. oryzae strains examined are not expressed even under aflatoxin-producing condition.

Aflatoxins↗

PubMed1996

Effect of a lignan-enriched extract of Schisandra chinensis on aflatoxin B1 and cadmium chloride-induced hepatotoxicity in rats.

Treatment of rats with a lignan-enriched extract of the fruit of Schisandra chinensis could enhance hepatic antioxidant/detoxification system, as indicated by increases in hepatic reduced glutathione (GSH) level as well as hepatic glutathione reductase and glutathione S-transferase activities. The hepatoprotective action was evident after aflatoxin beta 1 or cadmium chloride (Cd) challenge. Schisandra chinensis pretreatment protected against aflatoxin B1-or Cd-induced hepatocellular damage in rats. However, pretreating rats with alpha-tocopherol acetate (vitamin E) did not protect against hepatic damage induced by both toxins. Results from the present as well as our previous studies demonstrate that the hepatoprotection afforded by Schisandra chinensis pretreatment is not hepatotoxin specific. Schisandra chinensis seems to be more effective than vitamin E in protecting against aflatoxin B1 and Cd toxicity. The mechanism of hepatoprotection afforded by Schisandra chinensis pretreatment may involve facilitation of both antioxidant and detoxification processes in the liver.

Aflatoxin B1↗

PubMed1977

Laser fluorimetry: subpicogram detection of aflatoxins using high-pressure liquid chromatography.

The use of high-pressure liquid chromatographic separation in conjunction with laser-induced fluorescence detection permits the analysis of trace fluorescent species at new limits of sensitivity. This technique was applied to the carcinogens aflatoxins B1, B2, G1, and G2, which were linearly quantitated to 7.5 x 10(-13) gram. The procedure consists of forming more fluorescent aflatoxin derivatives, eluting the aflatoxins from a reverse-phase column, focusing the 325-nanometer output of a helium-cadmium ion laser into a suspended droplet of the eluent, and measuring the resulting fluorescence using phase-sensitive detection.

Aflatoxins↗

PubMed1976

Field accumulation of aflatoxin in cottonseed as influenced by irrigation termination dates and pink bollworm infestation.

Aflatoxin accumulation in Deltapine 16 cottonseed, grown in Yuma, Ariz., in a 3-year study, was significantly influenced by the timing of irrigation terminations and by level of pink bollworm infestations. In 1971 and 1972, termination of irrigations by early August resulted in significantly less aflatoxin than in plots where two additional irrigations were applied. Significantly less aflatoxin also was found in the 1971 and 1973 plots where low levels of pink bollworm infestations were maintained.

Aflatoxins↗

PubMed1976

Enzymatic conversion of sterigmatocystin into aflatoxin B1 by cell-free extracts of Aspergillus parasiticus.

A cell-free extract, prepared from Aspergillus parasiticus ATCC 15517 grown in synthetic medium, was active in converting [14C]sterigmatocystin into aflatoxin B1 in the presence of reduced nicotinamide adenine dinucleotide phosphate. The activity was demonstrated by the time course of conversion and the linear dependence of the yield of product on enzyme concentrations. Optimum activity was obtained at pH 7.5 to 7.8 at 27 C. The results confirm sterigmatocystin as a biogenetic precursor of aflatoxin B1. Techniques were developed for enzymatic studies on aflatoxin biosynthesis.

Aflatoxins↗

PubMed1977

Aflatoxin in corn: ammonia inactivation and bioassay with rainbow trout.

Four samples of corn were compared with respect to their hepatocarcinogenicity in rainbow trout. One corn sample was found by chemical analysis to contain no detectable aflatoxin. A second sample was contaminated with aflatoxins at a level of 180 microgram/kg. Each of the above-mentioned samples was divided, and one-half of each was ammoniated. These four samples were added to a semipurified basal diet and fed to a sensitive strain of rainbow trout. It was found that ammoniation inactivated the aflatoxins and reduced the carcinogenicity of the contaminated corn to a level that was not significantly different from that with the basal control diet. It was also found that the ammoniation process did not reduce the nutritive value of the corn.

Aflatoxins↗

PubMed1979

Differentiation of aflatoxins from territrems.

Three methods were adopted for differentiation of aflatoxins B1 and B2 from territrems A and B. They were as follows. (i) Then-layer chromatography coupled with chemical confirmation. A significant decrease in the Rf value of trifluoroacetic acid-treated aflatoxin B1 developed in chloroform-acetone (85:15, vol/vol) was satisfactory in differentiating this toxin from the other three. (ii) High-pressure liquid chromatography monitored synchronously at two wavelengths, 365 and 335 nm. The ratio derived from this double-wavelengh detection could serve as an indicator of the presence of each toxin. (iii) Velasco's flurotoxin meter method, which is used for the determination of aflatoxins within the range of 0 to 50 ng/ml, was not significantly affected by territrems even when they were present in quantities at the microgram-per-milliliter level.

Aflatoxins↗

PubMed1980

Identification of averantin as an aflatoxin B1 precursor: placement in the biosynthetic pathway.

A new blocked mutant of Aspergillus parasiticus produces no detectable aflatoxin B1, but accumulates several polyhydroxyanthraquinones. One of these pigments was identified as averantin. This is the first report of its formation by A. parasiticus. Radiotracer studies with [14C]averantin showed that 15.3% of label from averantin was incorporated into aflatoxin B1. This incorporation was blocked by dichlorvos. With radiotracers and other mutants, averantin was placed after norsolorinic acid and before averufin in the biosynthetic pathway in which the general steps are norsolorinic acid leads to averantin leads to averufin leads to versiconal hemiacetal acetate leads to versicolorin A leads to sterigmatocystin leads to aflatoxin B1.

Aflatoxins↗

PubMed1980

Influence of inoculum size of Aspergillus parasiticus spores on aflatoxin production.

The influence of the inoculum size on growth and aflatoxin production was examined in Aspergillus parasiticus (NRRL 3145) by using a synthetic medium. The reduction in the number of spores by 4 to 5 log cycles either by serial dilution or by gamma irradiation caused a two fold increase in the toxin production. The decrease in the inoculum size induced a lag in growth of the culture, though the final yield of the mycelium over the 28-day experimental period was the same. The maximal accumulation of aflatoxin was observed on day 14 of incubation. A transition from the biphasic to monophasic pattern in aflatoxin production could be correlated with the size of the inoculum. The enhanced toxin production from dilute inocula was similar to that obtained with the surviving fraction of the spores after gamma irradiation (0 to 150 krads).

Aflatoxins↗

PubMed1981

Influence of white light on production of aflatoxins and anthraquinones in Aspergillus parasiticus.

The effect of continuous light and continuous darkness on the growth of Aspergillus parasiticus and on the production of aflatoxin, averufin, versicolorin A, and versicolorin C by Aspergillus parasiticus were determined at six different temperatures with six replicates for each experiment. No growth was observed at 15 degrees C in the light, although slight growth was observed at this temperature in the dark. No aflatoxins or anthraquinones were produced in the light or dark at 35 and 40 degrees C, although growth was good at these temperatures. Differences in aflatoxins and anthraquinones for cultures grown in light and in dark were consistent at each temperature. Higher mean quantities of these secondary metabolites were produced in the light at 20 and 25 degrees C; lower mean quantities were produced in the light at 30 degrees C. The ranges of values overlapped considerably, but in all cases the differences between temperatures were significant.

Aflatoxins↗