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PubMed1985

Differential sensitivity of Ah-responsive mice to beta-naphthoflavone-induced metabolism and mutagenesis of benzo[a]pyrene and aflatoxin B1.

Effects of the administration to C57BL/6ha (Ah-responsive) mice of a low (10 mg/kg) and a high dose (150 mg/kg) of beta-naphthoflavone (BNF) on the hepatic microsome-mediated mutagenesis and metabolism of benzo[a]pyrene (BP) and aflatoxin B1 (AFB1) were studied. Hepatic microsome-mediated mutagenesis of benzo[a]pyrene was not enhanced by the low dose (10 mg/kg) but at the high dose (150 mg/kg) the mutagenic activation was enhanced several fold relative to control (corn oil-treated). Mutagenic activity of aflatoxin B1 was however depressed by both the low and the high doses of beta NF. These results are consistent with the effects of beta NF administration on hepatic microsome-mediated metabolism of BP to its phenolic products and on the metabolism of aflatoxin B1 to aflatoxin M1 catalyzed by aflatoxin B1-4-hydroxylase. Relative to control, pretreatment of the mice with 10 mg/kg beta NF did not induce aryl hydrocarbon hydroxylase activity (a measure of BP metabolism), however, the same pretreatment induced the metabolism of AFB1 to AFM1 by 2.7 to 4.7-fold. Microsomal preparations from 150 mg/kg beta NF-pretreated mice showed a 3-fold induction of aryl hydrocarbon hydroxylase activity and a 6.8-fold induction of AFB1-4-hydroxylase activity. These results suggest that two different enzyme systems are involved in the metabolism of BP and the metabolism of AFB1 to AFM1.

Aflatoxin B1↗

PubMed1995

Functional impairment of rat Kupffer cells induced by aflatoxin B1 and its metabolites.

Contamination of food with mycotoxins is a major health problem. Impairment of several immune functions has been repeatedly reported in animals fed with contaminated fodder. Since the liver is a major target of toxicity by aflatoxins, the effects of aflatoxins B1, and its hepatic metabolites Q1 and M1 on Kupffer cell function was investigated in vitro. Aflatoxin B1 induced significant (P < 0.05) inhibition of phagocytosis, intracellular killing of Candida albicans, and intrinsic anti-Herpes virus activity at concentrations as low as 0.01 pg ml-1. Aflatoxin Q1 and M1 had similar effects on phagocytosis and microbicidal activity, but were two- to ten-fold less potent than aflatoxin B1.

Aflatoxin B1↗

PubMed1989

Preparation of protein conjugatable aflatoxin oxime derivative from significantly reduced starting quantities.

A modification of an existing technique for the preparation of aflatoxin B1-(0-carboxymethyl) oxime is presented which allows for a significantly reduced starting amount of aflatoxin. About 80% of the aflatoxin was converted to its oxime. The new technique will be particularly valuable when protein conjugatable oximes of more expensive aflatoxin metabolites, such as aflatoxin M1, are required for immunoassay production.

Aflatoxin B1↗

PubMedDate not supplied

Determination of aflatoxin M1 in milk and milk products contaminated at low levels.

A new method is described for the determination of aflatoxin M1 in milk and dairy products by thin layer chromatography. The main characteristic is the extraction system using an alkaline solution. Lipids are removed by centrifuging at low temperatures, and the aflatoxins are then extracted with CHCl3. The method has 2 options: Technique II (detection limit 0.02 ppb) requires cleanup on a chromatographic column; this is not necessary in Technique I (detection limit 0.1 ppb). The recovery rate in both techniques is over 92.8% in milk and yoghurt. This method may also be used for other aflatoxins. Because of the advantages of the method, Technique II is recommended for aflatoxin M1 control in milk, where a low detection limit is necessary. Technique I is proposed for experimental aflatoxin production studies in dairy products, which require analysis of a large number of samples but which do not require a very low detection limit.

Aflatoxin B1↗

PubMed1982

Metabolism and activation of aflatoxin B1 by reconstituted cytochrome P-450 system of rat liver.

Metabolism and activation of aflatoxin B1, a potent hepatocarcinogenic and mutagenic mycotoxin of Aspergillus flavus, were investigated in the reconstituted enzyme system composed of purified NADPH-cytochrome P-450 reductase and cytochrome P-450 or P-448 of rat liver. The aflatoxin M1 formation was strictly mediated by P-448 purified from the liver microsomes of polychlorobiphenyl- and 3-methylcholanthrene-treated rats, while the aflatoxin Q1 formation, as well as the binding of DNA, were catalyzed by both P-450 and P448. Differences between the kinetic data on metabolism and activation of aflatoxin B1 obtained with the reconstituted cytochrome systems and those obtained with the microsomal and nuclear systems were discussed, and the significance of these biochemical data in the in vivo carcinogenicity of aflatoxin B1 was evaluated.

Aflatoxin B1↗

PubMed1996

Fungal flora and aflatoxin contamination of feedstuff samples in Beida Governorate, Libya.

Fungi of 19 genera, 30 species, and one variety were isolated from 25 samples of sheep-, cattle- and camel feedstuffs collected from different farms in the Beida Governorate, Libya. Aspergillus, Penicillium and Fusarium were the most common genera in the three substrates tested. TLC was used to establish the identity of aflatoxins in the chloroform extract of all samples and the ability to produce aflatoxins by Aspergillus flavus in a synthetic liquid medium. Twenty samples out of 25 tested were naturally contaminated and 21 isolates of A. flavus out of 30 produced at least one of the following aflatoxins: B1; B1, G1; and B1, B2, G1, G2. This is the first report about the natural occurrence of aflatoxins and aflatoxins and aflatoxin-producers of the genus Aspergillus in Libya.

Animal Feed↗

PubMed2000

The influence of storage practices on aflatoxin contamination in maize in four agroecological zones of Benin, west Africa.

Aflatoxin level in 300 farmers' stores in four agro-ecological zones in Benin, a west African coastal country, were determined over a period of 2 years. At sampling a questionnaire was used to evaluate maize storage practices. Farmers were asked what storage structure they used, their storage form, storage period, pest problems in storage and what was done against them. Beninese farmers often changed their storage structures during the storage period, transfering the maize from a drying or temporary store to a more durable one. Most of the farmers complained about insects damaging stored maize. Often, storage or cotton insecticides were utilized against these pests. Regression analysis identified those factors that were associated with increased or reduced aflatoxin.Maize samples in the southern Guinea and Sudan savannas were associated with higher aflatoxin levels and the forest/savanna mosaic was related to lower toxin levels. Factors associated with higher aflatoxin were: storage for 3-5 months, insect damage and use of Khaya senegalensis-bark or other local plants as storage protectants. Depending on the agroecological zone, storage structures that had a higher risk of aflatoxin development were the "Ago", the "Secco", the "Zingo" or storing under or on top of the roof of the house. Lower aflatoxin levels were related to the use of storage or cotton insecticides, mechanical means or smoke to protect against pests or cleaning of stores before loading them with the new harvest. Fewer aflatoxins were found when maize was stored in the "Ago" made from bamboo or when bags were used as secondary storage containers.

Journal Article↗

PubMed1994

Inhibition of aflatoxin production by surfactants.

The effect of 12 surfactants on aflatoxin production, growth, and conidial germination by the fungus Aspergillus flavus is reported. Five nonionic surfactants, Triton X-100, Tergitol NP-7, Tergitol NP-10, polyoxyethylene (POE) 10 lauryl ether, and Latron AG-98, reduced aflatoxin production by 96 to 99% at 1% (wt/vol). Colony growth was restricted by the five nonionic surfactants at this concentration. Aflatoxin production was inhibited 31 to 53% by lower concentrations of Triton X-100 (0.001 to 0.0001%) at which colony growth was not affected. Triton X-301, a POE-derived anionic surfactant, had an effect on colony growth and aflatoxin production similar to that of the five POE-derived nonionic surfactants. Sodium dodecyl sulfate (SDS), an anionic surfactant, and dodecyltrimethylammonium bromide, a cationic surfactant, suppressed conidial germination at 1% (wt/vol). SDS had no effect on aflatoxin production or colony growth at 0.001%. The degree of aflatoxin inhibition by a surfactant appears to be a function of the length of the hydrophobic and hydrophilic chains of POE-derived surfactants.

Journal Article↗

PubMed1995

Prevalence of exposure to aflatoxin and hepatitis B and C viruses in Guinea, West Africa.

The prevalence of exposure to aflatoxin, hepatitis B virus (HBV), and hepatitis C virus (HCV), three important risk factors for hepatocellular carcinoma, was examined in Guinea, West Africa. A total of 75 sera were collected from men living in the Kindia region of lower Guinea. The sera were analysed by immunoassay for aflatoxin covalently bound to serum albumin as a marker of aflatoxin exposure. Over 90% of the sera contained detectable adduct levels, the highest level being 385 pg aflatoxin B1-lysine equivalent per mg albumin. Eleven subjects (14.7%) were positive for hepatitis B surface antigen in the serum and these subjects had a tendency to have higher aflatoxin-albumin adduct levels than the other subjects (mean level 70.4 pg/mg compared to 44.1 pg/mg), but the difference was not statistically significant (P = 0.23). Eight subjects were positive for antibodies to HCV antigens and, interestingly, seven of these were from one ethnic group, Mandinka (25% prevalence). These data demonstrate that all three exposures are prevalent in Guinea and that the prevalence of these risk factors is comparable to that observed in other countries in West Africa. It is now important to assess the public health impact of these exposures in this country.

Adolescent↗

PubMed1988

Comparative antimutagenicity of chlorophyllin and five other agents against aflatoxin B1-induced reversion in Salmonella typhimurium strain TA98.

Chlorophyllin was studied for its antimutagenic activity against aflatoxin B1 in Salmonella typhimurium strain TA98 using the plate-incorporation test in the presence of S9 activation. Comparative antimutagenicity between chlorophyllin and certain commonly studied antimutagens (i.e., vitamins A, C, and E, retinoic acid, and beta-carotene) was also examined. A dose-related inhibition of aflatoxin B1 mutagenicity by chlorophyllin was observed, with the mutagenicity being abolished by 860 nmole chlorophyllin per plate. The inhibitory activity of chlorophyllin occurred only when cells were treated concurrently with chlorophyllin and aflatoxin B1. The antimutagenic potency of chlorophyllin was comparable to that of vitamin A and higher than that of retinoic acid and beta-carotene. Vitamins C and E had no effect on aflatoxin B1 mutagenicity under the conditions used. The results of toxicity tests and a reconstruction experiment showed that inhibition of the mutagenicity of aflatoxin B1 by chlorophyllin and the other active agents was due to antimutagenicity.

Aflatoxin B1↗

PubMed1988

Immunoassay procedures to detect exposure to aflatoxin B1 and benzo(a)pyrene in animals and man at the DNA level.

Immunological methods were used to examine human liver for the presence of aflatoxin-DNA adducts and human lung for benzo(a)pyrene diol-epoxide DNA (BPDE-DNA) adducts. Eight liver samples obtained from Czechoslovakian patients with primary hepatocellular carcinoma were studied, seven of which had detectable anti-aflatoxin inhibitory material. Values ranged between 0.63 and 3.51 picomoles aflatoxin per mg DNA. In a separate, independent study performed in another laboratory the one sample with no aflatoxin bound to DNA also had no free aflatoxin present in the liver. In the case of the human lung DNA samples, 12 samples were examined, the samples having been removed during thoracic surgery, and five had detectable anti-BPDE-DNA antibody activity. The positive samples were all from smokers and had inhibitory values ranging from 4 to 12 femtomoles per mg DNA. Samples were prepared by immunoconcentration prior to analysis. These preliminary results support the view that immunological methods can be used to examine human tissue DNA for carcinogen adducts.

Aflatoxin B1↗

PubMed1990

Behaviour of Aspergillus flavus in presence of Aspergillus niger during biosynthesis of aflatoxin B.

Aspergillus niger or Aspergillus tamarii when grown as mixed cultures with toxigenic A. flavus inhibits biosynthesis of aflatoxin by A. flavus, owing primarily to its ability to produce inhibitors of aflatoxin biosynthesis and to their ability to degrade aflatoxin. Gluconic acid partly prevents aflatoxin production. The other factors such as changes in pH of the medium and the effect on the growth of a. flavus have no role in imparting capabilities to these cultures to inhibit aflatoxin production by A. flavus.

Aflatoxin B1↗

PubMed1986

Aflatoxin-producing potential of Aspergillus flavus strains isolated from Spanish poultry feeds.

A total of 126 fungal strains belonging to the Aspergillus flavus group isolated from commercial poultry mixed feeds were studied. One hundred and twenty-five were identified as A. flavus and one as A. parasiticus. Forty nine strains (39%) produced aflatoxins on a crushed moist wheat medium (28 degrees C/10 days), whereas only sixteen (13%) showed specific fluorescence on Aflatoxin-Producing Ability Medium. In both media, mainly aflatoxins B1 and B2 were detected, the average concentration of aflatoxins being 4 294 +/- 1 083 micrograms/kg in crushed moist wheat medium, and 877 +/- 257 micrograms/kg in Aflatoxin-Producing Ability Medium.

Aflatoxin B1↗

PubMed2003

A combinatorial approach to obtain affinity media with binding properties towards the aflatoxins.

In our work we performed a combinatorial solid-phase synthesis in aqueous medium to prepare peptide libraries from which to select an amino acid sequence with binding properties towards aflatoxins. We used polystyrene beads, functionalised with carboxylic groups as solid support and eight amino acids as monomers. During the first step 64 different sequences of two amino acids were prepared by exploiting the principles of combinatorial chemistry; then the binding properties of all sequences towards aflatoxin B(1 )were checked. We determined binding constants towards aflatoxin B(1) and towards aflatoxins B(2), G(1) and G(2). Results were promising, so we prepared a new library by using the selected dipeptide as the starting solid phase. After selecting the best tetrapeptide sequences, we determined binding constants towards the quoted aflatoxins. We obtained binding constants ( K>10(4) M(-1)) similar to those shown by human serum albumin for similar compounds. Preliminary studies on an extraction column were promising for the development of an SPE system and for its application in food matrices.

Aflatoxin B1↗

PubMed1981

A comparison of the effects of pretreatment with phenobarbitone and 3-methylcholanthrene on the metabolism of aflatoxin B1 by rat liver microsomes and isolated hepatocytes in vitro.

In agreement with previous reports (Neal and Colley, Biochem. J., 174 (1978) 839; Gurtoo and Dave, Cancer Res., 35 (1975) 382) the capacity of isolated hepatic microsomes to metabolise aflatoxin B1 (AFB1) is enhanced by pretreatment in vivo with phenobarbitone. Microsomes isolated from rats pretreated with 3-methylcholanthrene also exhibit increased metabolism of AFB1. The levels of metabolism are increased in proportion to the increased levels of cytochromes P-450 and P-448 indicating similar overall efficiencies of the two cytochromes to metabolise AFB1. However, the qualitative aspects of the metabolism induced by the two compounds are very different. In agreement with the previous data (Neal and Colley, Biochem J., 174 (1978) 839) the formation of aflatoxins Q1, M1 and B1-dihydrodiol are enhanced by pretreatment with phenobarbitone whereas pretreatment with 3-methylcholanthrene, while not affecting the production of aflatoxin Q1 and slightly lowering AFB1-dihydrodiol formation, increases the production of aflatoxin M1 greater than 10-fold. Covalent binding of AFB1 to microsomal protein in vitro is increased by pretreatment in vivo with phenobarbitone, but decreased by pretreatment with 3-methylcholanthrene. The changes in the level of protein binding in vitro brought about by these pretreatments are quantitatively similar to the relative changes in AFB1-dihydrodiol tris complex production induced by the two compounds indicating a role for this metabolite in protein binding. Covalent binding of AFB1 to DNA in vitro is also increased by pretreatment in vivo with phenobarbitone, but not by 3-methylcholanthrene and the total level of binding of AFB1 to DNA in the in vitro system is greater than binding to microsomal protein. The possible mechanisms for binding AFB1 to microsomal protein and DNA are discussed. In contrast to the microsomal incubations, only low levels of aflatoxins Q1 and M1 are present after 2 h incubation AFB1 with intact hepatocytes isolated from control, methylcholanthrene or phenobarbitone pretreated rats. Pretreatment with either phenobarbitone or 3-methylcholanthrene induces the formation of polar metabolites, presumably conjugates, emphasising the predominant role of phase 2 metabolism in intact cellular systems.

Aflatoxin B1↗

PubMed1983

The effect of aflatoxins on mammalian acid deoxyribonucleases.

1. Difference spectroscopy studies indicated that tetrahydrodeoxyaflatoxin B1 and aflatoxicol bind slightly to DNA, whereas aflatoxins B2a, G2a, G2 and aflatoxicol bind to bovine and porcine spleen DNAse II but aflatoxins B1, B2, G1 and tetrahydrodeoxyaflatoxin did not. 2. Kinetic studies showed that aflatoxins B1, G1 and B2 activated bovine and porcine spleen DNAse II while aflatoxins B2a, G2a and G2 had an inhibiting effect. 3. Dissociation constants for the enzyme: substrate-aflatoxin complexes (KAS) as well as the inhibition constants (Ki) were obtained from kinetic studies.

Aflatoxin B1↗

PubMed1985

Characterization of water-soluble glucuronide and sulphate conjugates of aflatoxin B1. 1. Urinary excretion in monkey, rat and mouse.

Water-soluble aflatoxin conjugates prepared from urine samples from rats, mice and rhesus monkeys dosed with [14C]aflatoxin B1 (AFB1) ip or iv were hydrolysed by enzymes (beta-glucuronidase and sulphatase), acid or a combination of both treatments. Different amounts of AFB1 and its metabolites were found in hydrolysates from different sources, indicating the presence of glucuronide, sulphate and possibly mercapturate conjugates of aflatoxins. In addition to aflatoxins M1, P1, Q1 and B2a, AFB1 was frequently identified in the products released from the hydrolysates. These water-soluble aflatoxin conjugates were not mutagenic to Salmonella typhimurium TA98 in the presence of rat-liver S-9 mix. However, chloroform extracts of the hydrolysates from beta-glucuronidase and sulphatase treatment showed mutagenic activity in these bacteria in the presence of S-9 mix. Although very low levels of AFB1 radioactivity were detected in the hydrolysates, the potent mutagenic activity of AFB1 contributed to the high numbers of revertant colonies. AFP1 was detected in urine samples from monkeys that were pretreated with phenobarbital before an iv dose of AFB1. No mutagenic activity was detected in the enzymatic hydrolysate of the sample from these monkeys. The results thus indicate that AFB1 can form glucuronide and/or sulphate conjugate(s) directly and be excreted in the urine.

Aflatoxin B1↗

PubMed1984

Toxicity of aflatoxin B1 in rat and mouse hepatocytes in vivo and in vitro.

The reported LD50 for the adult, male Fisher rat is 1.2 mg aflatoxin B1/kg body weight (i.p.); we have found that male C57BL/6 mice survive single doses of aflatoxin B1 as high as 60 mg/kg (i.p.). We have demonstrated a 1000-fold greater LC50 of aflatoxin B1 for primary mouse liver cell cultures from C57BL/6 male mice (3 X 10(-5) M) than for primary liver cells from F344 male rats (3 X 10(-8) M). In 4 h of exposure to a non-toxic dose (1 X 10(-9) M) of [3H]aflatoxin B1, cultured rat liver cells accumulated up to 5-fold higher concentrations of 3H label than did mouse liver cells. The difference in cell-associated counts was due largely to higher levels of aflatoxin B1 metabolites bound to macromolecules in the rat cells.

Aflatoxin B1↗