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PubMed1977

Repair of DNA in human cells after treatment with activated aflatoxin B1.

Repair replication was examined in cultured human cells exposed to the hepatocarcinogen aflatoxin B1 using the combined bromodeoxyuridine density label and radioisotopic label method. Semiconservative DNA synthesis was strongly inhibited, and the repair replication mode was stimulated in diploid fibroblasts (W138) and in their SV40 transformants (VA13) only when exposure to aflatoxin B1 was in the presence of an activating system containing rat liver microsomal enzymes. The maximum amount of repair synthesis was about 20% of that obtained after saturating doses of ultraviolet light (UV). The time course of repair synthesis was similar to that seen after UV, and most of the synthesis was in 30- to 50-nucleotide "short patches." A line of SV40-transformed xeroderma pigmentosum cells (Group A) deficient in repair after exposure to UV was similarly deficient in repair replication after aflatoxin treatment. Treatment with aflatoxin resulted in a 25 to 45% inhibition of UV-induced repair replication, suggesting that in addition to producing lesions in DNA, which are substrates for the excision repair system, the toxin also inhibits excision repair. CsC1 gradients of DNA treated in vitro with activated aflatoxin demonstrated binding of the drug to DNA. Alkaline sucrose gradient sedimentation gave no indication that single-strand breaks or alkali labile bonds were introduced into DNA by treatment of cells with activated aflatoxin.

Aflatoxins↗
PubMed2004

Determination of aflatoxins B1, G1, B2 and G2 in medicinal herbs by liquid chromatography-tandem mass spectrometry.

An easy method for the determination of aflatoxins B1, G1, B2 and G2 in Rhammus purshiana by LC coupled to mass spectrometry has been developed. Aflatoxins were extracted with a mixture of methanol and water and then it was purified by solid-phase clean-up using a polymeric sorbent, not described previously, for the determination of these toxins. The eluted extract was injected into the chromatographic system using a reversed-phase C18 short column with an isocratic mobile phase composed of methanol-water (30:70). A single-quadruple mass spectrometry using an electrospray ionization source operating in the positive ion mode was used to detect aflatoxins due to derivatization presenting several disadvantages. Recoveries of the full analytical procedure were 110% for aflatoxin B1, 89% for aflatoxin B2, 81% for aflatoxin G1 and 77% for aflatoxin G2. Detection limit (S/N = 3) was 10 ng and quantification limit (S/N = 10) was 25 ng, calculated as amount in medicinal herb.

Aflatoxins↗
PubMed2004

Effect of gamma-irradiation on aflatoxin B1 production by Aspergillus flavus and chemical composition of three crop seeds.

The effect of gamma-irradiation on aflatoxin B1 production by Aspergillus flavus, and the chemical composition of some different crop seeds were investigated. A. flavus infected seeds behaved differently according to their principal constituents. A. flavus caused an increase in protein and decrease in lipids and carbohydrate contents of wheat, soyabean and fababean seeds. Growth of A. flavus and production of aflatoxin B1 was inhibited at a dose level of 5 kGy. A. flavus utilizes carbohydrates of seeds for its growth and aflatoxin production. Crops were arranged, in descending order, according to aflatoxin produced in seeds as wheat > soyabean > fababean. There were no changes in chemical constituents of irradiated seeds, such as protein, lipids, and carbohydrates.

Aflatoxin B1↗
PubMed2001

Selection and characterisation of recombinant single-chain antibodies to the hapten Aflatoxin-B1 from naive recombinant antibody libraries.

Selection of antibodies from large repertoire phage display libraries has become a common technique for isolation of specific antibodies to antigens. Many of these libraries are shown to contain antibodies specific to haptens, but only when these haptens are derivatised or conjugated to an immobilising molecule, such as bovine serum albumin (BSA). There has been little demonstration of the suitability of naive recombinant antibody libraries for isolating antibodies that bind low molecular weight haptens in the absence of a carrier molecule and few have addressed the problems associated with selecting antibodies that only recognize the combination of hapten and the carrier molecule. We have panned two-phage antibody libraries against AflatoxinB1-BSA and screened single-chain antibody fragments for binding to AflatoxinB1-BSA and Aflatoxin-B1. Many of the antibodies isolated specifically bound AflatoxinB1-BSA, but not soluble Aflatoxin-B1 or BSA. Modification of the protocol led to isolation of single-chain fragment variable antibody domain (scFv) antibodies that specifically bound soluble Aflatoxin-B1 with an affinity of 6x10(-9) M.

Aflatoxin B1↗
PubMed1983

Specificity of rat liver cytochrome P-450 isozymes in the mutagenic activation of benzo[a]pyrene, aromatic amines and aflatoxin B1.

The ability of three purified forms of rat liver cytochrome P-450 to metabolically activate benzo[a]pyrene, trans-benzo-[a]pyrene-7,8-dihydrodiol, 2-aminofluorene, aflatoxin B1, dimethylnitrosamine, and a pyrolysis product of tryptophan(3-amino-1-methyl-5H-pyrido(4,3-b)indole) (Trp-P-2) to mutagenic products was examined using Salmonella typhimurium strains TA98 and G46 in a reconstituted monooxygenase system. The isozymes examined were cytochrome P-450-PB (the major phenobarbital inducible form), and the two major 3-MC inducible forms (cytochromes P-448(52) and P-448(55)). Cytochromes P-448(52) and P-448(55) preferentially metabolize 2-aminofluorene and Trp-P-2 to mutagenic products. However, only cytochrome P-448(55) metabolizes benzo[a]pyrene and its 7,8-dihydrodiol derivative to mutagenic products. Both cytochrome P-448(52) and P-448(55) metabolize aflatoxin B1 to mutagenic products at a much faster rate than cytochrome P-450-PB. Dimethylnitrosamine was not activated by any of the isozymes tested.

Aflatoxin B1↗
PubMed1982

Determination and thin layer chromatographic confirmation of identity of aflatoxins B1 and M1 in artificially contaminated beef livers: collaborative study.

An international collaborative study involving 13 laboratories was conducted to test methods for the determination and thin layer chromatographic (TLC) confirmation of identity of aflatoxins B1 and M1 in beef liver. For the determination, each collaborator furnished fresh or frozen beef liver. Samples were artificially contaminated by adding solutions containing various concentrations of aflatoxins B1 and M1 (0.032-0.69 ng/g). Two TLC confirmation methods were tested with extracts obtained from the determination. Two measurement methods using 2-dimensional TLC were evaluated. In the first, sample extracts were compared directly with B1 and M1 standards on TLC plates; in the second, internal standards plus sample extracts were compared with B1 and M1 standards on the plates. Average within-laboratory coefficients of variation (CV) for the direct method were 26% for B1 and 26% for M1 compared with 24 and 26%, respectively, for the internal standard method. The average between-laboratory CV values were 39% for B1 and 41% for M1 by the direct method and 36% for B1 and 39% for M1 by the internal method and 36% for B1 and 39% for M1 by the internal standard method. Recoveries ranged from 64 to 90% for B1 and from 72 to 86% for M1. These data indicate that the more convenient direct method was sufficient, and internal standards were unnecessary. An analysis of variance was calculated from combined sample data to determine components of variance. The within-laboratory CV values were 27.0 and 32.3% for B1 and M1, respectively, and the between-laboratory CV values were 47.1 and 53.2%, respectively. Both TLC confirmation methods gave satisfactory results and have been adopted official first action, along with the determination method.

Aflatoxin B1↗
PubMed1976

Effect of sex difference on the in vitro and in vivo metabolism of aflatoxin B1 by the rat.

Hepatic microsome-catalyzed metabolism of aflatoxin B1 (AFB1) to aflatoxin M1 and aflatoxin Q1 and the "metabolic activation" of AFB1 to DNA-alylating metabolite(s) were studied in normal male and female Sprague-Dawley rats, in gonadectomized animals, and in castrated males and normal females treated with testosterone. Microsomes from male animals formed 2 to 5 times more aflatoxin M1, aflatoxin Q1, and DNA-alkylating metabolite(s) than those from females. Castration reduced the metabolism of AFB1 by the microsomes from males by about 50%, whereas ovariectomy had no significant effect on AFB1 metabolism by the microsomes from females. Testosterone treatment (4 mg/rat, 3 times/week for about 6 weeks) of castrated immature males and immature females enhanced the metabolism of AFB1 by their microsomes. A sex difference in the metabolism of AFB1 by liver microsomes was also seen in other strains of rats tested: Wistar, Long-Evans, and Fischer. The activity of kidney microsomes for metabolic activation was 1 to 4% that of the liver activity and was generally lower in microsomes from male rats as compared to those from female rats of Sprague-Dawley, Wistar, and Long-Evans strains. The in vitro results obtained with hepatic microsomes correlated well with the in vivo metabolism of AFB1, in that more AFB1 became bound in vivo to hepatic DNA isolated from male rats and from a female rat treated with testosterone than that isolated from control female rats. These data suggest that the differences in hepatic AFB1 metabolism may be the underlying cause of the sex difference in toxicity and carcinogenicity of AFB1 observed in rats.

Aflatoxins↗
PubMed1975

Aflatoxicol H1: a major metabolite of aflatoxin B1 produced by human and rhesus monkey livers in vitro.

Among the major metabolites of aflatoxin B1 produced by human and monkey livers in vitro is a derivative with the ketone carbonyl on the cyclopentane ring reduced to a secondary alcohol, and a hydroxyl introduced onto the carbon beta to the alcohol group. The metabolite was formed from aflatoxin B1 at a level similar to that of aflatoxin M1.Both the microsomal hydroxylase and the cytoplasmic reductase systems are required for its formation. Bioassay using chicken embryos and a mutant of Salmonella typhimurium revealed no toxicity. This newly identified metabolite was named aflatoxicol H1.

Aflatoxins↗
PubMed1990

Species susceptibility to aflatoxin B1 carcinogenesis: comparative kinetics of microsomal biotransformation.

The biotransformation of the potential human carcinogen aflatoxin B1 (AFB1) was studied using hepatic microsomes from the rat, mouse, monkey, and human. Initial rates of AFB1 oxidation to aflatoxins Q1, M1, and P1, as well as the reactive intermediate AFB1-8,9-epoxide, were determined using a high performance liquid chromatography assay. The rates of generation of these AFB1 metabolites were investigated at low substrate concentrations (more representative of environmental exposures) and also at high ("saturating") concentrations commonly utilized in studies in vitro. Striking differences in ratios of the metabolites were observed. At an AFB1 concentration of 124 microM, mouse and monkey microsomes had the highest rates of AFB1-8,9-epoxide formation. Primate liver microsomes formed aflatoxin Q1 in large amounts but failed to produce detectable aflatoxin P1. Determination of the rates of formation over initial AFB1 concentrations ranging from 15 to 475 microM revealed that the proportion converted to AFB1-8,9-epoxide increased at lower substrate concentrations in the case of the rat and human microsomes but not with mouse or monkey microsomes. The differences in patterns of metabolite formation with varying concentrations have implications for interspecies comparisons of carcinogenic potency of AFB1.

Aflatoxin B1↗
PubMedDate not supplied

Evaluation of enzyme-linked immunosorbent assay of cleanup for thin-layer chromatography of aflatoxin B1 in corn, peanuts, and peanut butter.

A simple, rapid enzyme-linked immunoassay (ELISA) was used to evaluate the performance of each step (extraction, filtration, solvent partition, and silica gel column chromatography) of a solvent-efficient thin-layer chromatographic (TLC) method which is undergoing interlaboratory collaborative study for the determination of aflatoxin B1 in corn, raw peanuts, and peanut butter. The apparent average recoveries using the ELISA method were about 30 to 50% higher than those using the TLC method if only the amount of B1 added to the samples was used in the calculations. After the cross-reaction of the antibody with other aflatoxins added to the samples was considered, the amounts recovered approached the levels of aflatoxins added in all 3 commodities tested. With no cleanup treatment, ELISA recoveries at aflatoxin B1 levels above 7.5 ng/g were 84, 79, and 103% for corn, raw peanuts, and peanut butter, respectively. The coefficients of variation were between 5.2 and 25.2%. With each cleanup step in the TLC method, ELISA detected a progressive decrease in recovery from 150.5 to 105.3% (before correction for the presence of other aflatoxins) or from 93.5 to 65.4% (after correction for other aflatoxins) of B1 added to the samples. The ELISA data support the conclusion obtained from previous studies that cleanup treatments were not necessary in the ELISA. When large amounts of other aflatoxins are present, an understanding of the cross-reactivity of antibody with other aflatoxins in the ELISA is essential for final interpretation of the data.

Aflatoxin B1↗
PubMed1988

Aflatoxin B1 carcinogenesis and its relation to DNA adduct formation and adduct persistence in sensitive and resistant salmonid fish.

Rainbow trout (Salmo gairdneri) and coho salmon (oncorhynchus kisutch) were exposed to aflatoxin B1 (AFB1) either by passive embryo uptake or by dietary treatment after hatching and feeding onset. Trout exposed as embryos to an aqueous solution of 0.5 p.p.m. AFB1 for 15 min showed a 62% tumor incidence 12 months later, whereas coho salmon exposed to a similar solution for 30 min showed only a 9% incidence. The difference between salmon and trout response was even greater by dietary AFB1 treatment. Trout exposed for 4 weeks to 20 p.p.b. dietary AFB1 had a 62% tumor response 12 months later, whereas salmon exposed to 40 p.p.b. dietary AFB1 for 4 weeks failed to develop tumors. A 5% tumor incidence was observed in salmon 12 months after 3 weeks exposure to 5000 p.p.b. dietary AFB1, a lethal dose for trout. In addition to a lower tumor incidence when compared to trout, the neoplastic response of salmon to AFB1 is to produce benign hepatic adenomas in contrast to the malignant hepatocellular carcinomas seen in trout. AFB1 metabolism, DNA adduct formation, adduct persistence in vivo and in vitro and cytochrome P-450 isozyme composition were compared in livers of trout and salmon to understand the role of metabolism and initiation in this species difference. AFB1-DNA binding was 7-56 times greater in trout than salmon liver at various times after AFB1 injection, 20 times greater in embryos or in freshly isolated trout hepatocyte preparations after a 1 h incubation with aflatoxin B1, and 18 times greater in trout liver after a three week dietary (80 p.p.b.) exposure. The major AFB1-DNA adduct was 8,9-dihydro-8-(N7-guanyl)-9-hydroxyaflatoxin B1 in both species. Persistence of AFB1-DNA adducts in vivo in liver was high compared to mammalian systems, implying that active enzymatic removal of bulky DNA adducts is low in both species and probably not a factor in their differential response to aflatoxin. Species differences in other phase I and phase II metabolism pathways and in AFB1 elimination were, overall, much less striking than those previously observed for trout fed inhibitors of aflatoxin carcinogenesis. Rates of bile elimination of AFB1 detoxication products, and total excretion of aflatoxins into water after AFB1 exposure, were not significantly different between trout and salmon. Since detoxication differences were not observed, the species difference in AFB1-DNA binding appears to reflect less efficient cytochrome P-450 metabolism of aflatoxin to the reactive 8,9-epoxide in salmon, compared to trout.(ABSTRACT TRUNCATED AT 400 WORDS)

Aflatoxin B1↗
PubMed1990

Involvement of singlet oxygen in photoactivation of aflatoxins B1 and B2 to DNA-binding forms in vitro.

UVA-activated aflatoxin B1 (AFB1) and AFB2 bound covalently to DNA. The rate of binding increased in D2O versus H2O and decreased by diazabicyclo-octane, azide, aniline, 2-naphthylamine and by efficient stripping of oxygen. Similarly to DNA-binding, singlet oxygen (1O2) formation increased in D2O and was inhibited by singlet scavengers, as judged by the formation of malonaldehyde from linolenic acid. The above argue for the involvement of 1O2 in aflatoxin photoactivation to DNA-binding species. A model for the mechanism is proposed.

2-Naphthylamine↗
PubMed2003

[Efficacy and stability of ammoniation process as aflatoxin B1 decontamination technology in rice].

Rice, a cereal widely used in Venezuela for human and animal nutrition, is susceptible to aflatoxin contamination in the field and during storage. Therefore, the goal of this research was the evaluation of the efficacy and permanence of the ammoniation process through high pressure/high temperature (HP/HT) and atmospheric pressure/moderate temperature (AP/MT) conditions applied to rice samples artificially contaminated with aflatoxin B1. For this purpose a 2k design was drawn up considering the temperature, the rice moisture and the process time as variables. Under both sets of conditions, aflatoxin B1 concentration was reduced in a range of 90% to 100%. After in vitro stomach digestion simulation, toxin reversion ranged from 0% to 19%. In conclusion, the process efficacy and permanence were achieved through the use of high temperature and long process time for both sets of conditions (HP/HT and AP/MT), respectively.

Aflatoxin B1↗
PubMed2004

Effects of prolonged administration of aflatoxin B1 and fumonisin B1 in laying Japanese quail.

In the present study, 288 8-wk-old Japanese quail were randomly distributed into 6 experimental groups (48 birds per group) and fed the following diets for 140 d: 1) 0 (control); 2) 10 mg of fumonisin B1 (FB1); 3) 50 microg of aflatoxin B1 (AFB1); 4) 50 microg of AFB1 + 10 mg of FB1; 5) 200 microg of AFB1; and 6) 200 microg of AFB1 + 10 mg of FB1/kg of feed. Each treatment consisted of 4 replicates of 12 quail. Egg production and individual egg weight were checked daily. Feed intake and feed conversion were determined weekly. Results showed that by the end of the fifth cycle, average egg weight was lower (P < 0.05) in groups fed 10 mg of FB1/kg, 50 microg of AFB1/kg, 200 microg of AFB1/kg, and 10 mg of FB1 + 50 microg of AFB1/kg of feed. Egg production decreased (P < 0.05) in birds fed 10 mg of FB1/kg by the third, fourth, and fifth cycles. Feed intake was lower (P < 0.05) in birds fed 10 mg of FB1/kg by the fourth and fifth cycles, and in birds fed 50 and 200 microg of AFB1/kg in the fifth cycle. Birds fed 10 mg of FB1 + 50 microg of AFB1/kg consumed less feed (P < 0.05) in the first, second, and fifth cycles. Results indicated that prolonged administration of FB1 and AFB1, singly or in combination at the levels evaluated, may cause economic losses to quail egg producers.

Aflatoxin B1↗
PubMed1991

Decrease of aflatoxin B1 in yoghurt and acidified milks.

Fermentation of yoghurt and acidified milks containing aflatoxin B1 (AB1) were studied. AB1 added to milk before fermentation at concentrations of 600, 1000 and 1400 micrograms/kg was reduced in yoghurts (pH 4.0) by 97, 91 and 90%, respectively. Coagulation time was approximately the same as in the controls. Streptococci had longer chains than those in the controls. The main decrease of AB1 occurred during the milk fermentation. A decrease of AB1 (conc. 1000 micrograms/kg) in milks acidified with citric, lactic and acetic acids (pH 4.0) was 90, 84 and 73%, respectively.

Acetates↗
PubMed1983

Photocarcinogenicity of 8-methoxypsoralen and aflatoxin B1 with longwave ultraviolet light.

The carcinogenicity of 8-methoxypsoralen (8-MOP) and aflatoxin B1 (AFB1) with longwave ultraviolet light (UVA) to hairless mouse skin was investigated. Skin tumors were induced efficiently by 8-MOP + UVA, and the time to 50% tumor incidence was about 24 weeks. Histopathologically, some tumors were squamous cell carcinomas. AFB1 did not show any phototoxic and photocarcinogenic effects on mouse skin in this study. Although the structure and the photoreactivity of AFB1 to DNA were similar to those of 8-MOP, the photocarcinogenic response of these compounds to mouse skin was quite different.

Aflatoxin B1↗
PubMed1990

Sequential monitoring of cytogenetic damage in rat lymphocytes following in vivo exposure to aflatoxin B1 and N-nitrosophenacetin.

Rats were treated intraperitoneally with different concentrations of aflatoxin B1 (AFB1) or N-nitrosophenacetin (NP). Blood was sequentially drawn by venous puncture at 6, 24, 72, 120 h and 14 days after a single injection of AFB1 or NP. After AFB1 the frequency of SCEs and chromosome aberrations increased progressively and reached a maximum level after 24 h and then decreased with time. By 2 weeks post treatment, the SCE and chromosome aberration values were within the control range. A small but significant SCE induction was observed when rats were treated with NP, but no chromosome breakage was induced even at the highest dose (20 mg/kg). We suggest that the elimination of DNA damage by repair mechanisms and lymphocyte turnover is responsible for the reduction of SCEs and chromosome aberrations with time. This assay seems promising for sequential monitoring of cytogenetic damage in rat lymphocytes following in vivo exposure to genotoxicants.

Aflatoxin B1↗
PubMed1991

Effect of allixin, a phytoalexin produced by garlic, on mutagenesis, DNA-binding and metabolism of aflatoxin B1.

Allixin, a phytoalexin isolated from garlic, was examined for its effects on aflatoxin B1(AFB1)-induced mutagenesis using Salmonella typhimurium TA100 as the bacterial tester strain and rat liver S9 fraction as the metabolic activation system. The effects of allixin on the binding of [3H]AFB1 to calf thymus DNA and on the formation of metabolites of [3H]AFB1 were also determined. Allixin showed a dose-related inhibition of Histidine+ revertants induced by AFB1. Allixin at 75 micrograms/ml inhibited [3H]AFB1 binding to calf thymus DNA and reduced formation of AFB1-DNA adducts. In addition, allixin exhibited a concentration-dependent inhibition of the formation of organosoluble metabolites and the glutathione conjugates of [3H]AFB1. The data indicate that the effect of allixin on AFB1-induced mutagenesis and binding of metabolites to DNA may be mediated through an inhibition of microsomal P-450 enzymes. Allixin may thus be useful in the chemoprevention of cancer.

Aflatoxin B1↗