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PubMed1984

Reduction of covalent binding of aflatoxin B1 to rabbit liver DNA after immunization against this carcinogen.

The covalent binding of [3H]aflatoxin B1 (AF) to liver DNA was determined, 6 h after oral administration to male rabbits. A Covalent Binding Index, CBI (mumol AF/mol DNA-P)/(mmol AF/kg b.w.) = 8,500 was found. Pretreatment of rabbits with AF coupled to bovine serum albumin in Freund's adjuvant led to the production of AF-directed antibodies. Administration of [3H]AF to such immunized rabbits resulted in a CBI of only 2,500, i.e., the immunization provided a protection by a factor of more than 3. Although this is encouraging evidence for the potential of active immunization against genotoxic carcinogens, a number of points will have to be clarified, such as the time course for the DNA binding and the question of a possible shift to other target cells.

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PubMed1983

DNA binding of aflatoxin B1 by co-oxygenation in mouse embryo fibroblasts C3H/10T1/2.

The mechanism of activation of aflatoxin B1 to ultimate metabolites capable of DNA binding was investigated in mouse embryo fibroblasts C3H/10T1/2. The contribution of co-oxygenation reactions which are coupled to arachidonic acid metabolism was assessed by the use of inhibitors of prostaglandin endoperoxide synthetase and lipoxygenase. Indomethacin and 5,8,11,14-icosatetraynoic acid inhibited AFB1-binding to maximally 60%. The antioxidant glutathione was also inhibitory while CuZn superoxide dismutase had no effect or slightly stimulated binding at high concentrations. These results indicate that co-oxygenation plays a major role in AFB1-metabolism in 10T1/2 cells. The observation that the phospholipase A2 inhibitor p-bromophenacylbromide diminished AFB1-DNA binding supports the notion that AFB1, because it is membrane-active, may enhance its own co-oxidative metabolism by stimulating the arachidonic acid cascade.

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PubMed1988

The lectin-binding characteristics of aflatoxin B1 induced lesions in the rat liver.

Hepatocellular carcinoma was induced in rats by administering aflatoxin B1 (AFB1) for 6 weeks. Malignant tumours were preceded by foci and nodules of altered hepatocytes of three histological types, composed of basophilic, eosinophilic, and vacuolated cells. In addition, there were areas of altered hepatocytes that were considered as hyperplastic. Lectins were used as histochemical markers to compare the expression of membrane glycoproteins in hepatocellular carcinomas and hepatic nodules with non-nodular or control hepatocytes. There were marked changes in the lectin-binding patterns of the hepatocellular carcinoma cells and the eosinophilic nodules. The lectin-binding patterns of basophilic nodules, vacuolated nodules, and hyperplastic areas were similar to non-nodular or untreated hepatocytes. The similarity in the lectin-binding changes of the eosinophilic nodules and hepatocellular carcinomas suggests that the eosinophilic nodules may be an early stage in the development of carcinoma.

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PubMed1985

Prophage induction and filamentation in Bacillus thuringiensis caused by the genotoxic mycotoxin aflatoxin B1.

Cultures of the lysogenic strain of Bacillus thuringiensis var. tolworthi were made in the presence of various drugs. The determination of bacterial size and plaque forming units (by using an indicator strain of B. thuringiensis var. galleriae) as well as colony forming units were then performed. Treatment of lysogenic cells by aflatoxin B1: provokes the formation of elongated cells (filamentation); induces a pathway that leads to the induction of prophage. Results of the present study indicated that filament formation and bacteriophage induction are two commonplace effects that occur in virtually every member of this cellular population exposed to low doses of certain drugs such as aflatoxin B1 (10 micrograms/ml); all of which have in common the ability to produce damaging changes in DNA. The following findings support the hypothesis that error-prone repair mechanisms seem to be present in B. thuringiensis as in Escherichia coli.

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PubMed1986

Potentiation of aflatoxin B1 induced hepatotoxicity in male Wistar rats with ethanol pretreatment.

The interaction of ethanol and aflatoxin B1 (AFB1)-induced hepatotoxicity was studied in male Wistar rats using the activity of plasma GOT and GPT, liver triglyceride and histopathologic changes of liver necrosis as indices. Pretreatment of four oral doses of ethanol (4.0 g/kg BW each) at 48, 45, 24 and 21 hrs prior to AFB1 (0.5 to 2.0 mg/kg BW) single i.p. administration caused a significant increase in the activity of PGOT (6 folds) and PGPT (5 folds), liver triglycerides (2 folds) and severity of liver necrosis at 48 hrs after AFB1 administration. Ethanol pretreatment potentiated AFB1-induced hepatotoxicity by increasing MFO enzymes, aniline hydroxylase and p-nitroanisole-O-demethylase activity and lipid peroxidation, and decreasing in cytochrome b5, epoxide hydrolase activity and hepatic glutathione content. However, it did not cause any significant change in the activity of NADPH-cytochrome c reductase and glutathione-S-transferase and cytochrome P-450. These results suggest that potentiation of ethanol pretreatment on AFB1-induced hepatotoxicity may be due to an increase in the metabolic formation of AFB1-2, 3-oxide and subsequent binding to DNA.

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PubMed1982

Liver DNA bound in vivo with aflatoxin B1 as a measure of hepatocarcinoma initiation in rainbow trout.

The in vivo binding of aflatoxin B1 (AFB1) to liver DNA was measured in rainbow trout subjected to various regimens and in coho salmon to determine if binding would correlate with tumor incidence and initiation of hepatocellular carcinoma. Establishment of time-course binding parameters showed no significant difference between 4, 12, 24, or 48 hours. Doses of 5, 25, 100, and 300 micrograms AFB1/kg body weight produced an almost linear increase in binding with increasing dose. Compared to that of controls, AFB1-DNA binding was twofold lower in beta-naphthoflavone-treated trout and twentyfold lower in coho salmon. These two comparisons reflected a decrease in the effective activation and binding of AFB1, correlated with tumor incidence, and are believed to correlate with a decrease in the initiation of hepatocellular carcinoma. AFB1 binding was not significantly altered by dietary protein or cyclopropenoid fatty acids, which are thought to increase hepatocellular carcinoma incidence through promotional effects. The data were consistent with the view that in vivo binding of AFB1 to liver DNA is a measure of cancer inititation by AFB1 and correlated with the incidence of hepatocellular carcinoma in salmonid fish.

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PubMed1988

Hepatic lipid peroxidation and intracellular calcium accumulation in ethanol potentiated aflatoxin B1 toxicity.

The possible role of hepatic lipid peroxidation and Ca2+ in enhanced hepatotoxicity of aflatoxin B1 (AFB1) by ethanol was examined along with changes in hepatic glutathione in male rats. Hepatic glutathione (GSH) was markedly decreased (43.9%) at 12 h after AFB1 administration in rats treated with ethanol (4.0 g/kg BW) and AFB1 (2.0 mg/kg BW) when compared to AFB1 alone. At 24 h after AFB1 administration, hepatic lipid peroxide levels in subcellular fractions, particularly in microsomes, were significantly increased (76.9%) in rats treated with ethanol and AFB1 following the decrease in hepatic GSH content. Hepatic lipid peroxide levels returned to normal values at about 48 h after AFB1 administration. Furthermore, Ca2+ in whole liver (60.9%), microsomes (83.8%) and mitochondria (51.2%) were significantly increased in the rats treated with ethanol and AFB1 as compared to those rats treated with AFB1 alone at 48 h after toxin administration. The increase in hepatic Ca2+ in rats treated with ethanol and AFB1 was a possible consequence of the increase in hepatic lipid peroxide. These findings suggest that there is a close relationship between hepatic GSH content, lipid peroxidation and intracellular accumulation of Ca2+. The pronounced effects on hepatic lipid peroxidation and intracellular accumulation of Ca2+ could play a role in ethanol-induced potentiation of AFB1 hepatotoxicity in rats.

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PubMed1990

NMR-studies of carcinogen reactions with DNA: ethylene dibromide and aflatoxin B1.

Two examples are described of the use of NMR spectroscopy to study the modification of DNA structure by carcinogens. The reaction of ethylene dibromide involves initial conjugation with glutathione, catalysed by glutathione S-transferase. Reaction of this adduct with DNA occurs at N7 of guanine. Through the use of stereospecifically 1,2-dideuteriated ethylene dibromide, the mechanism of reaction has been shown to involve an odd number, i.e. three, of SN2 inversions. Correlation spectra (COSY) were employed to analyse reaction stereochemistry. The relative configuration of the deuterium atoms in the products was initially assigned by 1H nuclear Overhauser effect (NOE) difference spectra and then confirmed by an independent synthesis of stereospecifically dideuteriated glutathione-guanine adducts. The second example involves reaction of the epoxide of aflatoxin B1 with DNA to form covalent adducts at N7 of guanine. Adduct formation was found to enhance duplex stability. Chemical shift changes for aflatoxin protons in the covalent adduct when compared with those for aflatoxin B1 non-covalently associated with DNA suggest that covalently linked aflatoxin is intercalated. NOEs confirm that the aflatoxin moiety is intercalated and show that it is on the 5' side of the guanine. This geometry leads to d(ATCGAT)2 forming an adduct in which only one chain has been modified by aflatoxin, while d(ATGCAT)2 forms a complex in which both chains have been modified.

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PubMed1975

Fluorescence changes of aflatoxins B1 and G1.

The effects of various factors, such as pH, buffer, sodiumchloride and ultra-violet radiation on the fluorescence of aflatoxins B1 and G1 have been studied. The fluorescence characteristics of aflatoxins B1 and G1 underwent a marked change at pH values above 7.2. Prolonged exposure to ultra-violet radiation lead to some degradation of aflatoxins and the extent of degradation was dependent upon the nature of the solvent. Sodium chloride partially protected the toxins from degradation by ultra-violet radiation or alkaline conditions.

Aflatoxins↗

PubMedDate not supplied

[Comparative immunochemical characteristics of polyclonal and monoclonal antibodies to aflatoxin B1].

Four hybrid clones (MM-(AB1)-1, MM-(AB1)-2, MM-(AB1)-3, and MM-(AB1)-4) were obtained by hybridoma technology with immunization of BALB/c mice with a BSA conjugate of aflatoxin B1 carboxymethyloxime derivative. Antibodies produced by these clones varied in the ability to recognize the aflatoxin B1 analogues. The sensitivity of enzyme immunoassay based on all monoclonal antibodies was higher compared to analysis based on polyclonal rabbit antibodies (0.1 and 0.4 ng/ml, respectively).

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PubMed1983

Sequence specificity in aflatoxin B1--DNA interactions.

The activated form of aflatoxin B1 (AFB1) causes covalent modification primarily of guanine residues, leading to alkali-labile sites in DNA. A simple extension of the Maxam-Gilbert procedure for sequence analysis permits the identification of alkali-labile sites induced by AFB1 and determination of the frequency of alkali-labile AFB1 modifications at particular sites on a DNA fragment of known sequence. Using this strategy, we have investigated the influence of flanking nucleotide sequences on AFB1 modification in a number of DNA fragments of known sequence. Our results show that certain guanine residues in double-stranded DNA are preferentially attacked by AFB1 over others in a manner predictable from a knowledge of vicinal nucleotide sequences. The observed in vitro sequence specificity is independent of a number of tested parameters and is likely to occur in vivo.

Aflatoxins↗

PubMed1981

Determining the kinetic behaviour for the secretion of milk toxin as related to dosage level of aflatoxin B1.

39 species which belong to 14 genera were isolated from 110 milk samples collected from different dairy sources at Assiut City. The most frequent fungi were A. niger, A flavus and Clasdosporium cladosporioides, followed by Curvularia spicifera and Penicillium corylophilum. The remaining species were of rare occurrence. The fluorescence-method for detecting aflatoxin-producing strains demonstrated the presence of two isolates namely A. flavus possesses this property. One of these toxic isolates was proved to produce high level of aflatoxin B1. It was used as a tool for determining the kinetic behaviour for the secretion of M1 toxin in milk of lactating animals which had received a toxic diet. The results revealed the following: 1. The milk toxin was detected in the milk of lactating animals next day after the toxin-containing ration was fed. 2. The level of milk toxin is gradually decreased when the feeding programme was interrupted. 3. When the animals supplied a ration containing the same concentration of aflatoxin for successive days, the milk toxin concentration was maintained at the same level. 4. The total amount of milk toxin secreted was less than one per cent of the amount of aflatoxin B1 received. 5. The concentration of milk toxin secreted by goats was higher than that of dairy cows. 6. Milk toxin failed to be detected five days after the feeding programme was discontinued.

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PubMed1982

Aflatoxin B1 metabolism and DNA binding in isolated hepatocytes from rainbow trout (Salmo gairdneri).

The metabolism of aflatoxin B1 (AFB1) was examined in freshly isolated hepatocytes from rainbow trout. Intracellular DNA adduct formation was linearly related to AFB1 dose, and qualitatively similar to adducts formed in vivo. The rate of adduct accumulation was constant during the first hour following completion of the preparation, after which an increase and gradual decrease in rate routinely occurred. The relative rates of production of the major unbound AFB1 metabolites aflatoxicol, aflatoxin M1, and polar conjugates, also remained constant over the first hour of preparation age, but subsequently changed in a manner consistent with the changes in DNA binding. The common solvent vehicles ethanol and dimethyl sulfoxide were shown to seriously perturb AFB1 metabolism and DNA binding even at levels less than 1%. A simple method is reported for removal of ethanol prior to introduction of hepatocytes for incubation with AFB1. The influence of cell concentration was also examined. DNA binding and relative distribution of AFB1 metabolites showed little or no dependence in the range 1-6 x 10(6) cell/ml, but were substantially altered above 10(7) cells/ml. Under defined conditions, studies in isolated hepatocytes appear to reflect in vivo cell capabilities for AFB1 metabolism.

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PubMed1975

New confirmatory test for aflatoxins B1 and B2.

A new confirmatory test for aflatoxins B1 and B2 is described. The test involves treatment of aflatoxins with excess sodium borohydride for 10 min at room temperature, to yield a fluorescent trihydroxy derivative of each aflatoxin. The test is sensitive and simple and gives no side reactions. The test is also applicable to aflatoxins G1 and G2.

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PubMed1990

[Changes in the mutagenic effect of a medium containing aflatoxin B1 as a result of the yeast activity].

Changes in the mutagenic activity of the nutrient medium containing aflatoxin Br as a result of living activity of the yeast Rhodotorula mucilaginosa I B has been studied. Reduction of mutagenic activity of the medium when tested on the strains Salmonella typhimurium TA98 (6.3 times fold), TA100 (2.2 times fold), AG262 (2 times fold) has been revealed. The data obtained leads to the conclusion that the technology, based on the use of the indicated strain of the yeast for the treatment of food and feed stuffs contaminated by aflatoxin B1, can be used.

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PubMed1984

Metabolism of food toxicants: saccharin and aflatoxin B1, a contrast in metabolism and toxicity.

The artificial sweetener, saccharin, and the secondary mold product, aflatoxin B1, are present in many foods consumed by humans. Both chemicals produce cancer in rats. For this reason, they have aroused concern among scientists and the public as to the carcinogenic risk that they pose to humans. A comparison of these two chemicals reveals striking contrasts in potency, metabolism, mechanism-of-action, and experimental approach to assessing metabolism. These contrasts are examined in detail to illustrate the importance of metabolism in safety evaluation.

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PubMed1983

Nucleotide sequence cleavage of guanine-modified DNA with aflatoxin B1, dimethyl sulfate, and mitomycin C by bleomycin and deoxyribonuclease I.

In guanine-modified DNA with aflatoxin B1, dimethyl sulfate, and mitomycin C, the nucleotide sequence cleavage of bleomycin or DNase I has been investigated using 32P-labeled DNA fragments. In contrast with cis-dichlorodiammine platinum (II) which induces intrastrand crosslinking of guanine N7 atoms, these mono-covalent modifiers did not give remarkable alteration of the DNA nucleotide cleavage mode by bleomycin and DNase I. From the viewpoint of combination drug, it is of interest that mitomycin C promoted the DNA cleavage activity of bleomycin.

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PubMed1991

Effect of aflatoxin B1 on the efficacy of turkey herpesvirus vaccine against Marek's disease.

The effect of feeding aflatoxin B1 (AFB1) (0.5 ppm) was studied in young chicks. The frequency and the severity of gross and microscopic lesions of Marek's disease were significantly higher in those birds which had been vaccinated with turkey herpesvirus (HVI) and birds challenged with Marek's disease virus which had been given AFB1 in the feed than in those given normal feed. The protective efficacy of HVT vaccine, as judged on the basis of gross and histopathological lesions, was 86.1 and 77.3 per cent in normally fed birds in comparison to 37.6 and 8 per cent in AFB1 fed birds.

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