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PubMed1985

The effect of a single dose of aflatoxin B1 on the value of nucleolar index of blood lymphocytes and on histological changes in the liver, bursa Fabricii, suprarenal glands and spleen in ducklings.

The value of the nucleolar index of blood lymphocytes, as well as histopathological changes in liver, bursa Fabricii, suprarenal glands and spleen in ducklings administered per os a single dose of 1.5 micrograms aflatoxin B1 on the second day of their life, were observed for two weeks. There was a clear correlation observed between morphological changes in the lymphatic system organs and liver and the value of the nucleolar index of peripheral blood lymphocytes on the 13th and 14th day after administration of aflatoxin B1. The results obtained point to different susceptibility of the tested organs and lymphocytes to the action of aflatoxin B1.

Adrenal Glands↗
PubMed1986

[Fluctuation in the concentration of sex steroids and aflatoxin B1 in the seminal plasma of boars and its relation to sperm production].

The concentration of testosterone, 17-beta oestradiol and aflatoxin B1 were studied in the semen plasma of 21 boars of four breeds for the period of twelve months. The following spermiological parameters were investigated: semen volume, sperm concentration, percentage of abnormal spermatozoa, and survival of spermatozoa. The fertilizing capacity of ejaculates was evaluated according to the conception rate of sows and gilts after the first insemination, according to the average number of piglets per litter and average number of live-born piglets per litter. The highest aflatoxin B1 residues in sperm were recorded in March to May and were related with aflatoxin concentration in feed ration. The group of boars with fertility disorders had more aflatoxin in their sperm (up to 100 pmol . l-1), lower sperm concentration, lower survival of spermatozoa, and a larger proportion of abnormal spermatozoa. The year season had a significant influence on the concentration of the hormones. The highest average value of testosterone (10.2 +/- 1.28 nmol) was obtained in autumn and lower values were recorded in winter. The changes in 17-beta estradiol concentration were similar to the changes in testosterone content, with the maximum value in November (0.249 nmol X 1(-1]. The boars with reproduction disorders had a significantly lower concentration of 17-beta oestradiol. Significant correlations were found between the concentration of the hormones, semen volume, and sperm concentration. 17-beta oestradiol also had a significant positive correlation to abnormal spermatozoa and to the activity of aspartate aminotransferase.

Aflatoxin B1↗
PubMed1996

Bioactivation of aflatoxin B1 in the nasal and tracheal mucosa in swine.

Whole-body autoradiography of 3H-labeled aflatoxin B1 in young pigs showed a localization of bound label in the nasal olfactory and respiratory mucosa, in the tracheo-laryngeal mucosa, and in the conjunctiva, in addition to the liver. Whole-body and microautoradiography also showed a labeling of pigmented tissues, which can be ascribed to a melanin binding of AFB1. In vitro experiments with microsomal preparations of various tissues from sows revealed that the nasal respiratory and olfactory mucosa had the highest capacity to form DNA-bound aflatoxin B1-metabolites. The tracheal mucosa and the liver, in order, had lesser binding capacity. The lung was found to be devoid of aflatoxin B1-bioactivating capacity. In vitro microautoradiography revealed bound label in specific cell types in the nose and trachea and in some cells of the conjunctiva. A drastic decrease in the aflatoxin B1-DNA binding was observed when microsomal preparations of the nasal respiratory and olfactory mucosa were incubated in the presence of reduced glutathione, but without any addition of cytosolic glutathione-S-transferases. In incubations of liver microsomes under these conditions a somewhat lower inhibition of the aflatoxin B1-DNA binding was seen. Our results demonstrate that the nasal olfactory and respiratory mucosa and the tracheal mucosa have a higher capacity than the liver to bioactivate aflatoxin B1 in swine. Our data further show that microsomal-associated glutathione-S-transferases with a high capacity to catalyze the conjugation of the reactive aflatoxin B1-epoxide to reduced glutathione are present in the nasal olfactory and respiratory mucosa of swine.

Aflatoxin B1↗
PubMed1993

The effect of single administration of aflatoxin B1 and ACTH on the intensity of acid phosphatase reaction in bursa Fabricii and in periellipsoidal lymphatic tissue of the spleen of ducklings.

The experiments were carried out with Peking breed female ducklings which on their second day of life were administered into the crop a single dose of 1.5 micrograms of aflatoxin B1. On the 14th and 15th day from administration of aflatoxin B1 the ducklings were intravenously injected a single dose of ACTH at 1 i.u. per 100 g bodyweight. Disturbances in the ducklings, initiated by aflatoxin and then increased by ACTH, manifested themselves by a change in the intensity of acid phosphatase reaction in the lymphatic organs tested. The occurrence of differentiated APh reaction (but intensified differently as compared to that in control ducklings) within bursa Fabricii and in periellipsoidal lymphatic tissue of the spleen was the expression of unevenly changed reactivity of respective tissues in those organs due to the action of aflatoxin B1. These results seem to present an interesting starting point for further multidirectional experiments, first of all in the range of immunological reactivity in birds.

Acid Phosphatase↗
PubMed1976

The relationship between the turnover of UTP and RNA synthesis in cultured cells treated with aflatoxin B1.

Methods have been adapted to measure the specific activity of UTP in cells in monolayer culture. In HeLa cells labelled with [3H]uridine and treated with aflatoxin B1 there was reduced radioactivity in crude acid extracts, but the toxin did not affect the radioactive incorporation into UTP. Using cells in which the UTP was pre-labelled, the subsequent addition of aflatoxin B1 inhibited UTP incorporation into RNA. Accordingly aflatoxin B1 did not inhibit the uptake of uridine or the latter's conversion to UTP but inhibited the incorporation of UTP into RNA.

Aflatoxins↗
PubMed1986

Purification and characterization of a form of cytochrome P-450 with high specificity for aflatoxin B1 from 3-methylcholanthrene-treated hamster liver.

A form of cytochrome P-450 highly active in inducing mutagenicity of aflatoxin B1 was purified to a specific content of 15.1 nmol/mg of protein from 3-methylcholanthrene-treated hamster liver. This species of cytochrome P-450, having its absorption maximum at 448.5 nm in carbon monoxide-complex of reduced form and low spin ferric ion, is of molecular weight of 56,000 and distinctly different in physicochemical and catalytic properties from major forms of cytochrome P-450 purified from phenobarbital- or 3-methylcholanthrene-treated rat liver. In the induction of aflatoxin B1 mutagenicity, this hamster cytochrome P-450 is 50 times more potent than those from rat liver.

Aflatoxin B1↗
PubMed1992

Kinds of mutations induced by aflatoxin B1 in a shuttle vector replicating in human cells transiently expressing cytochrome P4501A2 cDNA.

Transient expression of rat liver cytochrome P450lA2 cDNA was combined with the use of a shuttle vector as a mutational target to determine the frequency and types of mutation caused by the conversion of aflatoxin B1 into genotoxic metabolites within human cells. Ad293 cells were first transfected with p91-lA2, a rat liver P450lA2 cDNA expression vector, or with p91-lA2(i) (a control vector that has the P450 cDNA in the inverted orientation) and incubated for 24 h to permit P450lA2 accumulation. Cells were then transfected with the pS189 shuttle-vector plasmid, which carries the Escherichia coli supF gene as a mutational target, and incubated for a further 24 h in the presence of aflatoxin B1 to permit promutagen activation and pS189 replication. In shuttle vectors replicated in p91-lA2-transfected cells, the supF point-mutation frequency increased with increasing concentration of aflatoxin B1. This frequency was nine to 23 times greater than the background point-mutation frequency obtained with aflatoxin B1-treated control (p91-lA2(i)-transfected) cells. The large majority of the aflatoxin B1-induced supF point mutations were base substitutions, mostly G:C----T:A transversions. This mutagenesis system permits the molecular analysis of mutations induced by specific P450/promutagen pairs in a shuttle vector replicating in human cells and will permit the investigation of host cell mechanisms involved in the generation of these mutations.

Aflatoxins↗
PubMedDate not supplied

Aflatoxin B1 in compound-feed reference materials: an intercomparison of methods.

The BCR has undertaken a project to prepare compound-feed reference materials to provide a basis for analytical quality control for this assay. The first phase of the project, an intercomparison of methods for aflatoxin B1 in compounded feedstuffs at a level of ca 15 micrograms/kg is now described. The study involved 24 European laboratories who analysed two pairs of compounded feedstuffs. Each pair of feeds consisted of a contaminated and an almost uncontaminated sample (a near-blank) of otherwise identical composition. The feed pairs differed essentially only in their citrus-pulp and barley contents. The participants used a variety of methods of analysis, including chloroform, methanol-water and acetonitrile-water for extraction, TLC, reversed phase disposable cartridges and immunoaffinity columns for extract clean-up and TLC, HPLC and ELISA in the determinative step. Several performance characteristics were checked and the aflatoxin B1 contents were determined. Recoveries were found to range from approximately 70 to 110%. Coefficients of variation calculated from all the results obtained with the two pairs of contaminated samples were 16 and 19%. The study showed that, when properly applied, a number of methods employing variations in extraction, clean-up and end-method gave results which were in close agreement. It is concluded that there exists a sound basis for the establishment of reference values for the aflatoxin B1 content of compound feed reference materials which have been prepared in this project.

Acetonitriles↗
PubMed1988

Effect of aflatoxin B1 on the delayed type hypersensitivity and phagocytic activity of reticuloendothelial system in chickens.

Efforts were made to see the effect of feeding aflatoxin B1 at 0.3 ppm level on various aspects of the immune system in chickens. The birds were fed aflatoxin B1 (AFB1) mixed ration from 0 to 6 weeks of age and thereafter normal feed was given up to 12 weeks of age. The delayed type hypersensitivity reaction of these birds was assessed by contact sensitivity to Dinitrofluorobenzene. The dietary AFB1 significantly suppressed the cell mediated immune response at all the three periods tested (30, 45 and 60 days of age). The toxin showed residual effect on immunity as the suppression of cell mediated immunity was maximum three days after the withdrawal of toxin from the feed. The effect of AFB1 on the phagocytic status of reticulo endothelial system (RES) was assessed by colloidal carbon clearance test at various intervals. The residual effect of toxin was observed on RES too as phagocytic index of AFB1 fed birds was significantly lowered up to 45 days of age.

Aflatoxin B1↗
PubMed1984

Factors modulating the formation of DNA adduct by aflatoxin B1 in vitro.

Forty-two compounds belonging to various chemical groups have been tested for their ability to suppress formation of aflatoxin B1--DNA adduct mediated by microsome in vitro. While many of these compounds have either marginal or no modulating effect, some have been identified as effective inhibitors. The strong inhibition of DNA adduct formation by retinoids (retinol, retinal, retinoic acid and retinyl acetate), riboflavin, riboflavin 5'-phosphate, flavin adenine dinucleotide, Cu2+, 7,8-benzoflavone, disulfiram, butylated hydroxyanisole, butylated hydroxytoluene and phenothiazine suggests that these agents may have potential anticarcinogenic activity against aflatoxin B1.

Aflatoxin B1↗
PubMed1981

Activation and inhibition of benzo(a)pyrene and aflatoxin B1 metabolism in human liver microsomes by naturally occurring flavonoids.

The effects of several naturally occurring and synthetic flavonoids on the metabolism of benzo(a)pyrene and aflatoxin B1 were evaluated. Addition of apigenin, chrysin, fisetin, flavonone, galangin, hesperitin, kaempferol, morin, myricetin, haringenin, or quercetin to human liver microsomes inhibited the hydroxylation of benzo(a)pyrene. In contrast to these results, the addition of flavone, nobiletin, tangeretin, or 7,8-benzoflavone to human liver microsomes caused a many-fold stimulation in the hydroxylation of benzo(a)pyrene, the metabolism of aflatoxin B1 to 2,3-dihydro-2,3-dihydroxyaflatoxin B1, and the metabolic activation of aflatoxin B1 to mutagenic products. Quercetin, morin, and kaempferol inhibited cytochrome c (P-450) reductase in human liver microsomes whereas flavone and 7,8-benzoflavone had no effect. These results suggest that the inhibitory effects of quercetin, morin, and kaempferol on monooxygenase activity may be caused at least in part by an inhibition in the reduction of cytochrome P-450. An examination of the structural features required for the inhibition and stimulation of benzo(a)pyrene hydroxylation indicated that all of the 12 flavonoid inhibitors that were studied possessed hydroxyl groups whereas the flavonoid activators were less polar molecules that lacked hydroxyl groups.

Aflatoxins↗
PubMed1993

A review of the dose-response induction of DNA adducts by aflatoxin B1 and its implications to quantitative cancer-risk assessment.

The induction of DNA adducts by aflatoxin B1 in the liver has been extensively reviewed in a quantitative cancer-risk assessment of aflatoxins (CDHS, 1990). Rat is the most sensitive species for aflatoxin tumorigenesis and liver is the most sensitive site. In vitro DNA-adduct studies were mostly on adduct identification and specificity of binding. In vivo studies provided dose-response relationship of aflatoxin B1, binding to DNA and DNA-adduct formation. Most in vivo studies were conducted in rats. The dose-response curves of DNA-adduct induction after ingestion or injection treatments in this species were reviewed. A linear dose-response relationship was observed in both injection and ingestion studies at low doses. For cancer-risk assessment, this observation is consistent with the assumption of the linear dose-response risk-assessment model for genotoxic agents, and justifies the use of this model for quantitative cancer-risk assessment for aflatoxins.

Aflatoxin B1↗
PubMed1985

Genotoxicity of fungal metabolites related to aflatoxin B1 biosynthesis.

The genotoxicity of several anthraquinone compounds metabolically related to aflatoxin B1 was examined by means of the hepatocyte primary culture (HPC)/DNA repair test and the Salmonella microsome mutagenesis test, and compared to versicolorins A and B which are potent mutagenic and genotoxic intermediates of the aflatoxin biosynthetic pathway. 6,8-O-Dimethyl-versicolorins A, B and 6-deoxyversicolorin A were found to be strongly mutagenic and genotoxic. Genotoxicity of versicolorin A and 6,8-O-dimethylversicolorin A was stronger than that of versicolorin B and 6,8-O-dimethylversicolorin B, respectively, in the HPC/DNA repair test. Nidurufin and norsolorinic acid, which do not possess a bisfuran ring, exhibited questionable activities for mutagenicity and no genotoxicity. It is suspected that 6,8-O-dimethylversicolorins A, B and 6-deoxyversicolorin A as well as versicolorins A and B are genotoxic carcinogens.

Aflatoxin B1↗
PubMed1997

Bioactivation and inactivation of aflatoxin B1 by human, mouse and rat liver preparations: effect on SCE in human mononuclear leucocytes.

The purpose of this study was to investigate the use of human and animal subcellular liver fractions in an in vitro evaluation of carcinogenic risk. The bioactivation and bioinactivation of the known genotoxic carcinogen aflatoxin B1 by human, mouse and rat liver preparations was investigated using the SCE assay in human lymphocytes as a genotoxic endpoint. There was a 10-fold variation in SCE response (1.1-11.6 SCE/Cell) in human mononuclear leucocytes (MNLs) after aflatoxin B1 was activated by human liver microsomes (n = 6). Activation correlated with the CYP1A2 phenotype of livers (r = 0.8; p < 0.05), but there was no correlation with either GST M1 genotype or epoxide hydrolase phenotype. Mouse liver microsomes activated aflatoxin B1 to a greater extent [(1 micro M) 12.8 +/- 2.51 SCE/Cell] than either rat [(10 micro M) 12.0 +/- 3.84 SCE/Cell or human (L25) [(10 micro M) 8.8 +/- 2.00 SCE/Cell liver microsomes. The addition of mouse liver cytosol and reduced glutathione (GSH) significantly (p < 0.001) reduced aflatoxin B1-dependent genotoxicity, whereas the addition of either human or rat cytosol (+GSH) was without effect. These data indicate that species variation in both bioactivation and bioinactivation can exist. Therefore there is a necessity for careful selection of activation systems from species whose biochemical profile reflects that of man.

Aflatoxin B1↗
PubMed1981

Role of lactone ring of aflatoxin B1 in toxicity and mutagenicity.

Cleavage of the lactone ring of aflatoxin B1 results in a nonfluorescent compound that has greatly reduced biological activity. Mutagenicity, as measured by the Ames test, is reduced 450-fold compared to that of B1, and toxicity, as measured by the chick embryo test, is reduced 18-fold.

Aflatoxin B1↗
PubMed1984

Stimulation of aflatoxin B1 and T-2 toxin production by sorbic acid.

Aspergillus flavus grown on yeast extract-sucrose medium produced higher amounts of aflatoxin B1 in the presence of 0.025% sorbic acid than without this chemical with a maximum at 17 days of incubation. Addition of 0.05 to 0.0125% sorbic acid stimulated T-2 toxin production of Fusarium acuminatum cultures grown on maize meal. The highest amounts of the mycotoxin were detected in 14-day-old cultures containing 0.025% sorbic acid. It is assumed that certain amounts of sorbic acid near the minimal inhibitory concentration reduce the activity of the tricarboxylic acid cycle; this may lead to an accumulation of acetyl coenzyme A, which is an essential intermediate in the biosynthesis of aflatoxin B1 and T-2 toxin.

Aflatoxin B1↗
PubMed2006

Co-occurrence of aflatoxin B1, fumonisin B1, ochratoxin A and zearalenone in cereals and peanuts from Côte d'Ivoire.

This survey examined 30 samples of rice (n = 10), maize (n = 10) and peanuts (n = 10) from Côte d'Ivoire for aflatoxin B1, fumonisin B1 and zearalenone using immunoassays, and ochratoxin A using a validated HPLC method with fluorescence detection. In Côte d'Ivoire, as in other countries, several mycotoxins are present in the same commodities. These mycotoxins are from different structural families: aflatoxin B1, fumonisin B1, zearalenone and ochratoxin A, normally produced by fungal species from Aspergillus, Penicillium and Fusarium genera. Some samples contained four mycotoxins (86%). Four peanuts samples did not show ochratoxin A (14%), whereas they contained aflatoxin B1 concentrations above the EU regulatory limits. Concentrations of ochratoxin A, zearalenone and fumonisin B1 were low and may not cause problems per se; however, fears remain that the tolerable daily intake may be exceeded due to eating habits and synergistic effects could be important with the combination of several mycotoxins. Investigations in this direction are underway, together with isolation and characterization of the fungal species involved.

Aflatoxin B1↗