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PubMed1991

Metabolism of aflatoxin B1 by Petroselinum crispum (parsley).

On administration of aflatoxin B1 to whole parsley (Petroselinum crispum) plants, a derivative was formed, which was shown to be aflatoxicol by its chromatographic properties and mass spectrometry. Optimum conditions for the production of the derivative was on the second day after administration of the toxin to the plants, which were 90 days old after germination. Cell-free preparations of parsley were found not to produce aflatoxicol A from added aflatoxin B1; instead they formed two new derivatives, which from chromatographic properties, were shown to be more polar than either aflatoxin B1 or aflatoxicol A.

Aflatoxin B1↗

PubMed1984

Failure of plant tissues to metabolize aflatoxin B1?

After exposure of peas and wheat kernels to aflatoxin B1 solutions the following aflatoxins could not be detected in seed extracts: aflatoxins M1, B2a, Q1, aflatoxicol and tetrahydrodeoxyaflatoxin B1.

Aflatoxin B1↗

PubMed1986

Production of aflatoxins by strains of the Aspergillus flavus group maintained in ATCC.

A total of 169 strains of the Aspergillus reference cultures in the Aspergillus flavus group maintained in the American Type Culture Collection (ATCC) were studied for their aflatoxin-producing abilities in rice, peanut and semisynthetic medium, utilizing high pressure liquid chromatography. Fifty-nine of the strains examined were positive for aflatoxin formation. No strains of the food fungi A. oryzae or A. sojae produced detectable levels of aflatoxins, while 33-85% of the strains of A. flavus and A. parasiticus were toxigenic.

Aflatoxin B1↗

PubMed1982

Detoxification of aflatoxin B1 by acidogenous yoghurt.

Serial concentrations of aflatoxin B1 ranged from 200 to 1000 p.p.b. were assayed for detoxification by acidogenous yoghurt. Thin-layered chromatography analysis revealed a complete transformation of 800 p.p.b. of aflatoxin B1 to a new fluorescing compound corresponding to aflatoxin B2a which is referred as hydroxydihydroaflatoxin B1. Partial conversion was present in yoghurt sample containing 1000 p.p.b. Toxicity test on chicken, confirmed Ciegler findings.

Aflatoxin B1↗

PubMed1989

Enzymes in aflatoxin B1 biosynthesis: strategies for identifying pertinent genes.

Recent work on the aflatoxin biosynthetic pathway is reviewed, with special emphasis on the enzymes of the late stages of the pathway involving conversion of sterigmatocystin (ST) to aflatoxin B1 (AFB1) through an O-methylsterigmatocystin intermediate. Two enzyme activities were discovered in subcellular fractions of cell-free extracts of a mutant strain of Aspergillus parasiticus (SRRC 163): 1) A post-microsomal methyltransferase (MT) catalyzed conversion of ST to OMST, and 2) a microsomal-associated activity (oxido-reductase) converted OMST to AFB1. The 168 KDa, anionic MT was purified to homogeneity and characterized (two subunits, 110 KDa and 58 KDa). Preliminary evidence indicated the presence of a cationic isozyme of the MT in mycelial extracts. The oxido-reductase has been partially purified and characterized. Polyclonal antibodies were prepared to the anionic MT and the enzyme's amino acid composition determined. A cDNA library has been constructed from mRNA isolated from Aspergillus parasiticus mycelia during the onset of AFB1 biosynthesis for the purpose of identifying the genes responsible for aflatoxin biosynthesis.

Aflatoxin B1↗

PubMed1989

Metabolic precursor regulation of aflatoxin formation in toxigenic and non-toxigenic strains of Aspergillus flavus.

Non-aflatoxin-producing isolates of Aspergillus flavus from nature and isolates of A. flavus that had lost their toxigenic trait following laboratory transfer were compared biochemically. After the addition of aflatoxin B1 precursors sterigmatocystin or O-methylsterigmatocystin to whole cell cultures, the non-toxin producing isolates from nature remained non-toxigenic while toxigenicity was restored in the non-toxigenic laboratory strains. Results imply a lack of enzymes needed for biochemical conversions of precursors to aflatoxin B1 in natural non-producers and suppression of these enzymes in the non-producing laboratory strains.

Aflatoxin B1↗

PubMed1987

[Culture of Aspergillus parasiticus in apple juice. II. The effect of butylhydroxyanisole (BHA) and butylhydroxytoluol (BHT) on fungal growth and aflatoxin biosynthesis].

Aspergillus parasiticus (NRRL 2999) was incubated in apple juice (from syrup), quiescently at 25 degrees C for up to 15 days in the presence of butylated hydroxyanisole (BHA) or butylated hydroxytoluene (BHT) at concentrations of 100, 200, 300, or 400 mg/l. Mycelial dry weight, pH and concentration of aflatoxin B1 and G1 were measured every 3 days with the initial pH of 2.5 remaining unchanged in all samples. BHA suppressed fungal growth and toxin accumulation during the observed incubation period. However, a concentration-dependent growth delay and earlier peaks of toxin accumulation suggested environmental adaptation of the mould. BHT (from 200 mg/l onwards), led to growth inhibition by about 25% (solubility limit of BHT lies between 200 and 300 mg/l), and at a concentration of 200 mg/l, it led to a reduction of toxin accumulation by approximately 45%. At 100 mg/l, however, BHT stimulated aflatoxin production (1.90 times more G1 and 6.65 times more B1 than in the controls). At all tested concentrations of BHA or BHT, as well as in the controls, the accumulation of aflatoxin G1, without exception, surpassed that of B1.

Aflatoxin B1↗

PubMed1980

[Aflatoxin M1 in milk and milk products. A comparison of some determination procedures].

Usual TLC-methods for the determination of Aflatoxin M1 in milk and milk products sometimes do not separate interfering substances with similar optical and chemical properties from Aflatoxin M1, thus leading to considerably incorrect results. Even after an additional clean-up on polystyrene column the solutions contain so many compounds that the identification of Aflatoxin M1 is difficult. The resolving power of HPLC yield pure frations, which may be determined by their MS and UV spectra.

Aflatoxin M1↗

PubMed1980

Growth and biosynthesis of aflatoxin by Aspergillus parasiticus in cultures containing nisin.

Nisin, 200 or 5000 Reading units/ml, was added to Aspergillus parasiticus cultures. The cultures were incubated at 28 degrees C for 3, 7 or 10 days and analyzed for mycelial dry weight, pH and accumulation of aflatoxin B1 and G1. During the first 3 days of incubation, dry weight, pH decrease and aflatoxin accumulation were suppressed by nisin, when compared with similar values for the nisin-free control. After longer incubation, differences in dry weight nd pH values decreased, whereas accumulation of aflatoxin in the nisin-containing cultures surpassed that of the control.

Aflatoxin B1↗

PubMed1986

Mechanism of counteraction of aflatoxin toxicity by thymine and folic acid in Bacillus megaterium.

Thymine and cytosine as well as the intermediates in pyrimidine biosynthetic pathway dihydroorotic acid, orotic acid, carbamyl aspartate and 5'-uridine monophosphate and folic acid, was synergistic. 2-14C-Thymine, 6-14C-orotic acid and 14C-formate but not 2-14C-uracil, were incorporated into DNA more in the presence of aflatoxin. These findings indicated that aflatoxin inhibited the pyrimidine base synthesis which could be overcome to a great extent by the addition of thymine and folic acid to aflatoxin-treated cells.

Aflatoxin B1↗

PubMed2005

Associated factors in modulating aflatoxin B1-albumin adduct level in three Chinese populations.

To elucidate the potential factors modulating exposure to aflatoxin B1 (AFB1) in three Chinese populations, an epidemiologic study was conducted in Fusui County and Nanning City of Guangxi Province and Chengdu City of Sichuan Province. The incidence rates of hepatocelluar carcinoma (HCC) for males in these three regions were 92-97 per 100,000, 32-47 per 100,000, and 21 per 100,000, respectively. Eighty-nine residents from Fusui, 196 residents from Nanning, and 118 residents from Chengdu were screened for AFB1-albumin adduct (AAA) levels and hepatitis virus (HBV, HCV, HDV, HEV, and HGV) infections, as well as liver biochemistry (alanine aminotransferase [ALT], aspartate aminotransferase [AST], alkaline phosphatase [ALP], y-glutamyl transpeptidase [GGT], 5'-nucleotidase, globulin [GLO], direct bilirubin, indirect bilirubin, and bile acid levels). At least one marker of hepatitis virus (HV) infection was present in 47.2% (42/89) of subjects from Fusui, while in Nanning and Chengdu the values were 15.8% (31/196) and 22.0% (26/118), respectively. In contrast to females, a higher level of AAA was observed in males; the difference was statistically significant in both the Nanning (P = 0.023) and the Chengdu (P = 0.026) subjects. In the Chengdu group, there was a significantly higher level of AAA in cases with HV infection (P = 0.041). There was a close association between AAA level and BMI in the adults without HV infection (r = 0.148, P = 0.044). Also, AAA was closely associated with DBIL and GGT in non-HV-infected minors (P < 0.05), closely associated with ALB, GLO, and GGT in HV-infected minors (P < 0.05), and closely associated with IBIL, GLO, TBA, and AST in non-HV-infected adults (P < 0.01). The co-effect of HV infection and AFB1 exposure may be responsible for the high risk of HCC in the Fusui region, whereas age, gender, BMI, and HV infection may modify individual aflatoxin levels. The relationship between AAA level and liver biochemistry indicates injury induced by aflatoxin to both hepatic parenchyma and biliary tract. But the associations vary with age and HV infection status.

Aflatoxin B1↗

PubMed1985

Aflatoxin B1 alters protein phosphorylation in rat livers.

A study was conducted on the effect of aflatoxin B1 on protein phosphorylation in rat livers by incubation of soluble and insoluble cell fractions with [gamma 32P] ATP. SDS-polyacrylamide gel electrophoresis indicated that a total of eight rat liver phosphoproteins were affected during a feeding period of 36 weeks on a carcinogenic aflatoxin B1-containing diet compared to the phosphoprotein patterns obtained from the livers of rats on a normal noncarcinogenic diet. The appearance of only two of these phosphoproteins were cAMP dependent. DEAE-cellulose chromatography employed to separate the different histone kinase activities in soluble rat liver cell fractions, showed that the specific activity of histone kinase I activity was increased but its total activity decreased while the histone kinase II activity stayed unchanged for rats submitted to the aflatoxin B1-containing diet compared to those on the normal noncarcinogenic diet.

Aflatoxin B1↗

PubMed1991

The in vivo disposition of aflatoxin B1 in rat liver.

The disposition of a non-toxic i.p. dose of [3H]-aflatoxin B1 (0.70 micrograms/kg) in the blood, plasma, and liver was studied in male Wistar rats. Uptake into the blood, plasma, and liver was biphasic; there was an initial rapid rise (0-2 hr) followed by a second phase (2-12 hr) of a gradual increase. Most of the radioactivity in the blood was bound noncovalently to albumin. Distribution of radioactivity in the subcellular fractions of liver showed that the microsomes exhibited the highest labeling which increased over the time course; labeling of the cytosol reached a maximum at 2 hr then decreased to a new steady state, whereas the mitochondria and nuclei reached a plateau. When the content of aflatoxin B1 in the nuclear subfractions was examined, greater than 92% of the total radioactivity was found in the deoxyribonucleoprotein fraction, and 84% of this was bound noncovalently. These results suggest that aflatoxin B1 is transported from the site of injection through the blood to the liver and its subcellular and subnuclear fractions primarily in a noncovalent form.

Aflatoxin B1↗

PubMed1982

Synthesis of transfer RNA in rat liver after acute and chronic aflatoxin B1 administration.

Synthesis of rat liver tRNA following acute and chronic administration of aflatoxin B1 was compared to protein synthesis. Twenty hours after acute administration of aflatoxin B1 total RNA synthesis was inhibited by 91% and tRNA synthesis by 77% while protein synthesis as assayed in vitro was inhibited by 75%. In the chronic (long-term) experiment at 7, 18 and 30 weeks after administration of aflatoxin B1 no inhibition of total RNA and tRNA synthesis was observed but protein synthesis in the cell-free system was inhibited by 16%. Thus, the inhibitory effects on protein synthesis observed in the long-term experiments are not correlated with the inhibition of tRNA synthesis.

Aflatoxin B1↗

PubMed1990

Chemical and physical properties of the major serum albumin adduct of aflatoxin B1 and their implications for the quantification in biological samples.

Aflatoxin B1 (AFB1) is a potent carcinogen. It reacts with liver DNA and serum albumin in a dose-dependent manner. Serum albumin adducts of aflatoxins have been used for exposure assessment. The immunological methods used so far do not differentiate between the different adducts of AFB1 and of AFG1. In order to establish an analytical method to measure one specific AFB1 adduct, we investigated the structure and the chemistry of the major serum albumin adduct of aflatoxin B1 (lysine-AFB1). 13C-NMR, 1H-NMR, UV, IR, fluorescence and MS spectra of lysine-AFB1 (8-[N-(2-amino-hexanoyl-6-yl)-5-oxo-3-pyrrolin-3-yl]-7-hydroxy-5- methoxycyclopentenone[2.3-c]coumarin) were recorded and discussed. The quantification of lysine-AFB1 was demonstrated in biological samples. Serum albumin was digested with pronase and analysed by HPLC with a fluorimeter as detector. The detection limit found for lysine-AFB1 was 20 fmol.

Aflatoxin B1↗

PubMed1987

Solvent effects on the spectroscopic properties of aflatoxin B1.

1. Solvent-induced changes in the spectral properties of aflatoxin B1 were investigated using protic and aprotic solvents. 2. The absorption data were less sensitive to solvent effects than the fluorescence emission data. 3. Stokes shifts in protic solvents were greater than those in aprotic solvents indicating hydrogen bond formation between solvent and the excited state of aflatoxin B1. 4. From the Stokes shift data for aprotic solvents, the dipole moment of aflatoxin B1 was estimated to increase by 15.7 Debye units upon excitation to the excited singlet state.

Aflatoxin B1↗

PubMed1991

Synergism between aflatoxins in covalent binding to DNA and in mutagenesis in the photoactivation system.

Aflatoxins (AFs) produce singlet oxygen upon their exposure to UV (365-nm) light. Singlet oxygen in turn activates them to mutagens and DNA-binding species. DNA binding and mutagenesis by AFs were enhanced in D2O as compared to reactions in H2O, and a singlet oxygen scavenger inhibited mutagenesis. DNA photobinding of 3H-AFB1 increased in the presence of unlabeled AFB2, and the addition of AFB2 enhanced mutagenesis by AFB1 in a synergistic manner. These results are compatible with the notion that singlet oxygen, formed by one aflatoxin molecule, can readily activate another aflatoxin molecule. This may bear an environmental implication in that the weakly carcinogenic AFB2, which is often produced in nature together with AFB1, may be important in enhancing the activation of AFB1 by sunlight.

Aflatoxin B1↗

PubMedDate not supplied

Enhanced depletion of glutathione and increased liver oxidative damage in aflatoxin-fed mice infected with Plasmodium berghei.

The effect of dietary aflatoxins B1 and G1 and Plasmodium berghei infection on glutathione (GSH) levels and liver status in mice was investigated. Three days after intraperitoneal injection of 0.1 x 10(6) parasitized red blood cells into the mice, there was a significant fall in blood glutathione levels accompanied by a significant increase in serum cholinesterase and liver malonic dialdehyde levels in the mice fed aflatoxin compared with those in the control group. The results suggested that malaria parasites can enhance depletion of host glutathione and oxidative damage of the liver in mice fed low levels of aflatoxins.

Aflatoxin B1↗