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PubMed1987

Aflatoxin exposure measured by urinary excretion of aflatoxin B1-guanine adduct and hepatitis B virus infection in areas with different liver cancer incidence in Kenya.

Two major etiological agents, hepatitis B virus and aflatoxin B1, are considered to be involved in the induction of liver cancer in Africa. In order to elucidate any synergistic effect of these two agents we conducted a study in various parts of Kenya with different liver cancer incidence in order to establish the rate of exposure to aflatoxin and the prevalence of hepatitis infections. Of all tested individuals 12.6% were positive for aflatoxin exposure as indicated by the urinary excretion of aflatoxin B1-guanine. Assuming no annual and seasonal variation, a regional variation in the exposure was observed. The highest rate of aflatoxin exposure was found in the Western Highlands and Central Province. The incidence of hepatitis infection nationwide as measured by the presence of the surface antigens was 10.6%, but a wide regional variation was observed. A multiplicative and additive regression analysis to investigate if hepatitis and aflatoxin exposure had a synergetic effect in the induction of liver cancer was negative. However, a moderate degree of correlation between the exposure to aflatoxin and liver cancer was observed when the study was limited to certain ethnic groups. The study gives additional support to the hypothesis that aflatoxin is a human liver carcinogen.

Aflatoxin B1↗

PubMed1983

Purified form of cytochrome P-450 from rainbow trout with high activity toward conversion of aflatoxin B1 to aflatoxin B1-2,3-epoxide.

Aflatoxin B1, the most potent hepatic chemical carcinogen known, is activated to the putative product aflatoxin B1-2,3-epoxide via a cytochrome P-450-dependent reaction. Mt. Shasta rainbow trout is the most sensitive species known to the hepatocarcinogenic effects of aflatoxin B1. We have previously isolated and purified a minor form of cytochrome P-450 from this strain of rainbow trout, with a lambda max in the carbon monoxide-reduced difference spectrum of 449.5 nm and a molecular weight of 54,000. In this study, we have compared in a reconstituted system this trout P-450 to trout cytochrome P-448 and rat cytochrome P-450 and P-448 for metabolism and activation of aflatoxin B1. Trout cytochrome P-450 had much higher activity towards aflatoxin B1 and a greater degree of regioselectivity in the formation of aflatoxin B1-2,3-dihydroxy-2,3-dihydrodiol and was much more efficient in producing aflatoxin B1 covalent adducts with DNA. The existence of such a form of cytochrome P-450 in Mt. Shasta rainbow trout may be responsible for the acute sensitivity of this strain to the carcinogenic effects of aflatoxin B1.

Aflatoxin B1↗

PubMed2005

Detection of transcripts of the aflatoxin genes aflD, aflO, and aflP by reverse transcription-polymerase chain reaction allows differentiation of aflatoxin-producing and non-producing isolates of Aspergillus flavus and Aspergillus parasiticus.

The aim of this study was to test the suitability of the RT-PCR (reverse transcription-polymerase chain reaction) technique to differentiate aflatoxin-producing from aflatoxin-non-producing strains of Aspergillus flavus and Aspergillus parasiticus. Total RNAs of 13 strains grown under inducing yeast extract-sucrose (YES) and non-inducing yeast extract-peptone (YEP) media, respectively, were analyzed by using specific primers based on the conserved regions of nine structural genes (aflD, aflG, aflH, aflI, aflK, aflM, aflO, aflP, and aflQ) and two regulatory genes aflS and aflR of the aflatoxin B1 biosynthetic pathway. Transcription was confirmed by the expression of the beta-tubulin gene. The expression of the majority aflatoxin biosynthetic genes including aflR and aflS of all strains varied with regard to the aflatoxin-producing ability and the growth conditions. Nonetheless, we found that the expression profile of the three genes aflD, aflO, and aflP was consistently correlated with a strain's ability to produce aflatoxins or not in YES as well as the inability to produce aflatoxins in YEP. The devised RT-PCR profiling method reflects aflatoxin concentrations ranging from 0.1 to 60 microg/ml of the culture filtrates as determined by fluorescence HPLC. The results are discussed in relation to the suitability of RT-PCR as well as cDNA-based array techniques in diagnostic laboratory settings where individual isolates are being tested for potential toxin production to identify toxigenic isolates of Aspergillus species.

Aflatoxins↗

PubMedDate not supplied

DNA conformation mediates aflatoxin B1-DNA binding and the formation of guanine N7 adducts by aflatoxin B1 8,9-exo-epoxide.

The binding of aflatoxin B1 to DNA and DNA adduction by aflatoxin B1 exo-8,9-epoxide were studied as a function of DNA conformation. Equilibrium binding of aflatoxin B1 to A-, B-, and Z-form helices was monitored by measurement of NMR linewidth for the methoxy protons of aflatoxin B1. The data revealed that as compared to B-form DNA, the association of aflatoxin with the A-form helix is significantly reduced. No binding to Z-DNA was observed. The yields obtained following reaction of the respective monomers with aflatoxin B1 exo-8,9-epoxide revealed that only dG forms an adduct. The reactivity of aflatoxin B1 exo-8,9-epoxide with single-strand DNA was determined via constant-temperature experiments in which the yield of adduct was measured for a family of oligonucleotides of increasing thermal stability. The results demonstrate that duplex structure favors adduct formation. Adduct yields were compared for A-, B-, and Z-form helices. About 12 times less adduct is produced from the A-form helix as compared to B-form, while no adduct is produced from a Z-form duplex. The results support the conclusion that reaction of aflatoxin B1 exo-8,9-epoxide with DNA proceeds via an intercalated transition-state complex only with the B-form double helix.

Aflatoxin B1↗

PubMed1999

Incidence of aflatoxin producing strains and aflatoxin contamination in dry fruit slices of quinces (Cydonia oblonga Mill.) from the Indian state of Jammu and Kashmir.

An investigation was undertaken to obtain data on the occurrence of aflatoxins and the aflatoxin producing potential of Aspergillus flavus strains isolated from dry fruit slices of quinces produced in jammu and Kashmir, India. A total of 147 A. flavus isolates recovered from dr fruit slices were grown in liquid rice flour medium and screened for the production of various aflatoxins by thin layer chromatography. The results showed that 23.14% of the tested isolates were aflatoxigenic, producing aflatoxins B1 and B2 in varying amounts. Aflatoxins G1 and G2 were not detected. All 25 of the investigated market samples were also found to be aflatoxin B1 positive and the level of contamination ranged from 96 to 8164 micrograms/kg of the dry fruit which is quite high in comparison to the permissible level of 30 ppb. As per these results biochemical composition of dry fruit slices of quinces, along with climatic conditions seem to be very favourable for aflatoxin production by the toxigenic A. flavus strains. Therefore, monitoring of aflatoxins in dry fruit slices of quinces is recommended for this region.

Aflatoxins↗

PubMed1990

Effects of dietary aflatoxin in aflatoxin-resistant and control lines of chickens.

The resistance to a single oral dose (12 mg of aflatoxin per kg of BW) and 4 wk of dietary aflatoxin (2.5 mg per kg of feed) were investigated in chicks selected for five generations for resistance to acute aflatoxicosis (AR) and unselected control (C) chicks. The AR chicks were more resistant to a single oral dose of aflatoxin and had significantly decreased sodium pentobarbital sleeping time compared to C chicks. Four-weeks exposure to dietary aflatoxin did not result in any significant change in BW or feed conversion ratios of chicks from either the C or AR line. However, more sensitive indicators of aflatoxicosis including plasma total protein, albumin, cholesterol concentrations, and gamma glutamyl transferase activity were significantly altered in C chicks but not in AR chicks fed aflatoxin. Percentages of liver lipid and liver hyperplasia score were also significantly altered as a result of dietary aflatoxin treatment in C but not AR chicks. These data indicate that selection-associated differences exist between the C and AR lines of chickens that convey resistance to not only a single oral dose of aflatoxin but also to a more chronic dietary exposure to aflatoxin.

Aflatoxins↗

PubMedDate not supplied

Two-dimensional chromatographic method for determination of aflatoxins in liver; occurrence of aflatoxins in animal liver.

A thin-layer chromatographic method is described for the analysis of aflatoxins in animal liver. Liver samples are extracted with chloroform and phosphoric acid. After filtration, an aliquot is evaporated and defatted by liquid-liquid partitioning. The extract is submitted to silica gel minicolumn cleanup and the final extract is concentrated and submitted to two-dimensional thin-layer chromatography (TLC). The identity of aflatoxins B1 and M1 is confirmed with trifluoroacetic acid (TFA) carried out on the thin-layer plate used for quantitation of these aflatoxins. The method permits the detection and confirmation of aflatoxins in liver in concentrations as low as 0.05 micrograms/kg. Average recoveries for aflatoxin M1 and aflatoxin B1 at spiking levels of 0.2 micrograms/kg were found to be 65% and 85%, respectively. With this method, 73 samples of bovine liver, 70 samples of porcine liver, and 56 samples of chicken liver taken from different slaughterhouses were investigated. In one sample of bovine liver, aflatoxins B1, B2, and M1 could be detected in concentrations of 0.10, 0.03, and 0.08 micrograms/kg, respectively.

Aflatoxin B1↗

PubMedDate not supplied

Occurrence of aflatoxins and aflatoxin-producing moulds in fresh and processed meat in Egypt.

A survey was carried out to detect aflatoxins and isolate aflatoxigenic moulds contaminating fresh and processed meat products. The fungal contamination was examined in 215 samples of fresh and processed meat products and 130 samples of spices used in the meat industry collected from different local companies in Cairo, Egypt. Processed meat products such as beefburger, hot-dog, kubeba, sausage, luncheon meat had the highest count of moulds as compared with fresh and canned meat. Out of 150 samples of meat products and 100 samples of spices, aflatoxin B1 was detected in five samples of beefburger, (8 micrograms/kg), four samples of black pepper (35 micrograms/kg), and four samples of white pepper (22 micrograms/kg). Aflatoxins B1 and B2 were detected in one sample of kubeba (150 micrograms B1/kg and 25 micrograms B2/kg); hot-dog (5 micrograms B1/kg and 2 micrograms B2/kg) sausage (7 micrograms B1/kg and 3 micrograms B2/kg) and luncheon meat (4 micrograms B1/kg and 2 micrograms B2/kg). Also, aflatoxins B1 and G1 were detected in two samples of turmeric (12 micrograms B1/kg and 8 micrograms G1/kg) and coriander (8 micrograms B1/kg and 2 micrograms G1/kg). Aspergillus flavus (24 isolates), and Aspergillus parasiticus (16 isolates) were the predominant aflatoxin-producing moulds isolated from both processed meat products and spices. Aflatoxins were absent in fresh meat, canned meat, salami, beefsteak and minced meat. The contamination of processed meat with aflatoxin was shown to correlate with the addition of spices to fresh meat.

Aflatoxin B1↗

PubMed1980

Quantitation of aflatoxin B1 and aflatoxin B1 antibody by an enzyme-linked immunosorbent microassay.

A specific microtest plate enzyme immunoassay has been developed for the rapid quantitation of aflatoxin B1 at levels as low as 25 pg per assay. Multiple-site injection of rabbits with an aflatoxin B1 carboxymethyloxime-bovine serum albumin conjugate was used for the production of hyperimmune sera. Dilutions of the purified antibody were air dried onto microplates previously treated with bovine serum albumin and glutaraldehyde and then incubated with an aflatoxin B1 carboxymethyloxime-horseradish peroxidase conjugate. The amount of enzyme bound to antibody was determined by monitoring the change in absorbance at 414 nm after the addition of a substrate solution consisting of hydrogen peroxide and 2,2'-azino-di-3-ethyl-benzthiazoline-6-sulfonate. Antibody titers determined in this manner closely correlated with those determined by radioimmunoassay. Competition assays as performed by incubation of different aflatoxin analogs with the peroxidase conjugate showed that aflatoxins B1 and B2 and aflatoxicol caused the most inhibition of conjugate binding to antibody. Aflatoxins G1 and G2 inhibited the conjugate binding to a lesser degree, whereas aflatoxins M1 and B2a had no effect of the assay.

Aflatoxins↗

PubMed1993

Dip-strip method for monitoring environmental contamination of aflatoxin in food and feed: use of a portable aflatoxin detection kit.

Aflatoxin contamination of food and feed have gained global significance due to its deleterious effect on human and animal health and its importance in the international trade. The potential of aflatoxin as a carcinogen, mutagen, teratogen, and immunosuppressive agent is well documented. The problem of aflatoxin contamination of food and feed has led to the enactment of various legislation. However, meaningful strategies for implementation of this legislation is limited by nonavailability of simple, cost-effective method for screening and detection of aflatoxin under field conditions. Keeping in mind the analytical constraints in developing countries, a simple-to-operate, rapid, reliable, and cost-effective portable aflatoxin detection kit has been developed. The important components of the kit include a hand-held UV lamp (365 nm, 4 W output), a solvent blender (12,000 rpm) for toxin extraction, and adsorbent-coated dip-strips (polyester film) for detecting and quantifying aflatoxin. Analysis of variance indicates that there were no significant differences between various batches of dip-strips (p > 0.05). The minimum detection limit for aflatoxin B1 was 10 ppb per spot. The kit may find wide application as a research tool in public health laboratories, environmental monitoring agencies, and in the poultry industry.

Aflatoxins↗

PubMed1991

Determination of exposure to aflatoxins among Danish workers in animal-feed production through the analysis of aflatoxin B1 adducts to serum albumin.

Aflatoxin B1 is suspected as an etiologic factor in the increased risk for primary liver cancer among workers in animal-feed processing plants in Denmark. Aflatoxin bound to serum albumin was therefore measured for feed-processing workers. Blood samples were collected immediately after vacation and after four weeks of work, and aflatoxin was quantified by competitive enzyme-linked immunosorbant assay. Seven of 45 individuals with an estimated exposure of 64 ng aflatoxin B1.d-1.kg-1 body weight were positive. Three positive workers had been unloading a cargo with an aflatoxin B1 level of 26 micrograms.kg-1 raw material. The exposure level correlated well with the job titles. Dust samples collected at different sites showed considerable variation in the amount of aflatoxin B1 (nondetectable to 8 micrograms.kg-1 dust). The exposure to aflatoxin B1 may only partially explain the increased risk of liver cancer.

Adult↗

PubMed1975

Screening method for the detection of aflatoxins in mixed feeds and other agricultural commodities with subsequent confirmation and quantitative measurement of aflatoxins in positive samples.

The method described will detect total aflatoxins (B1, B2, G1, and G2) in mixed feeds, grains nuts, and fruit products in samples containing as little as 5-15 mug/kg. In addition, the presence of aflatoxins in the positive samples can be confirmed and the toxins can be quantitatively measured, using the same extract as that used for the screening method. In the screening method, aflatoxins are extracted with acetone-water (85+15), and interferences are removed by adding cupric carbonate and ferric chloride gel. The aflatoxins are extracted from the aqueous phase with chloroform and the chloroform extract is washed with a basic aqueous solution. A Velasco-type minicolumn is used to further purify the extract and capture the aflatoxins in a tight band. The screening method has been successfully applied to 24 different agricultural commodities. Quantitative thin layer chromatography was also performed with extracts of each of these commodities. An average recovery of 94% B1, 108% B2, 130% G1, and 103% G2 was obtained compared to the official final action AOAC method for cottonseed products, 26.048-26.056. Within-laboratory coefficients of variation of 10-15% were obtained for each of the aflatoxins and total aflatoxins in a sample of peanut meal naturally contaminated with 11 mug B1+3 mug B2+11 mug G1+5 mug G2/kg.

Aflatoxins↗

PubMed1982

Kinetics of transformation of aflatoxin B1 into aflatoxin M1 in lactating mouse: an ELISA analysis.

A new enzyme-linked immunosorbent assay (ELISA) was used to study the kinetics of transformation of aflatoxin B1 into aflatoxin M1 in lactating mice. Aflatoxin M1 concentration in the milk samples reached a maximum 30 min after injection of aflatoxin B1 and decreased thereafter. At the maximum time, the levels of aflatoxin M1 in the samples were proportional to the dosages administered. Aflatoxin B1 was also detected in the milk samples but at a lower concentration.

Aflatoxin B1↗

PubMedDate not supplied

Distribution and clearance of aflatoxins B1 and M1 in turkeys fed diets containing 50 or 150 ppb aflatoxin from naturally contaminated corn.

Turkeys were fed a diet containing 50 or 150 ppb aflatoxin for 11 or 13 weeks or fed these diets for 11 weeks and then the control diet for 1 or 2 weeks. Aflatoxins B1 and M1 were found in liver, kidney, gizzard, and feces of poults fed the diets for 11 or 13 weeks. However, in turkeys fed the control diet for 1 or 2 weeks after the 11-week feeding trial, no residues of aflatoxin were found in the feces or tissues, except for some aflatoxin B1 remaining in detectable amounts in the gizzard. No mortality was attributable to aflatoxin, and there were no notable differences among groups in weight gains, feed conversion, or histopathologic changes in selected tissues. The response to a second inoculation with sheep erythrocytes was significantly lower in poults given dietary aflatoxin than in controls. This reduced antibody response was not observed when a Pasteurella multocida vaccine was administered.

Aflatoxin B1↗

PubMed1992

Aflatoxins in cosmetics containing substrates for aflatoxin-producing fungi.

29 random samples of eight different products of skin cleansing creams or powders and skin peeling products (including practically all products of this type available on the German market), containing substrates for aflatoxin-producing fungi or plant parts directly connected with such substrates, such as almond bran, peach bran, apricot seeds, wheat bran, horse chestnut and cob were analysed for aflatoxin B1, B2, G1 and G2. In 11 (38%) of the samples aflatoxins were not detectable ( < 0.1 micrograms/kg); 18 (62%) of the samples contained from 0.4 to 78.5 micrograms aflatoxin/kg. The majority of the positive samples contained all four types of aflatoxin. Aflatoxins can be absorbed through the skin. To what extent this happens with these products and the resulting toxicological significance is difficult to estimate. Nevertheless, potent carcinogens such as aflatoxins should be completely absent from cosmetics; this can be achieved by careful quality control of the raw materials.

Aflatoxins↗

PubMed1997

Direct synthesis of aflatoxin B1-N7 guanine adduct: a reference standard for biological monitoring of dietary aflatoxin exposure in molecular epidemiological studies.

Aflatoxin B1-N7-guanine and aflatoxin B1-human serum albumin adducts have been established as biomarkers of dietary aflatoxin exposure in epidemiological studies. Earlier chemical oxidants were used to synthesize aflatoxin B1-8,9-epoxide in vitro and its subsequent interaction with DNA or synthetic oligodeoxynucleotide was used as a source of authentic aflatoxin B1-N7-guanine adduct. In the present communication we report a simple single step procedure for the synthesis of aflatoxin B1-N7-guanine adduct using free guanine and m-chloroperbenzoic acid as the chemical oxidant for the production of AFB1-8,9-epoxide. At a molar ratio of 1:1 of AFB1-8,9-epoxide and guanine the recovery of the AFB1-N7-guanine adduct was found to be 60% while at higher molar ratios (1:2 and 1:4) of guanine the recovery of the AFB1-N7-guanine adduct was found to be low (30-40%). HPLC analysis of the AFB1-N7 guanine adduct showed a retention time identical with the retention time of the AFB1-N7-guanine adduct synthesized using calf thymus DNA. TLC-fluorodensitometric analysis indicated that the Rf of the AFB1-N7-guanine adduct was zero. Spectral analysis of the adduct synthesized showed an excitation wavelength of 360 nm and emission wavelength at 440 nm in phosphate buffer (100 mM, pH 7.4). Further, the formation of the AFB1-N7-guanine adduct was confirmed by perchloric acid treatment resulting in the destruction of the adduct. The AFB1-N7-guanine adduct thus synthesized was stable in both acidic as well as lyophilized conditions over a period of 2 weeks. The antibody capture assay showed that the antibodies produced against the antigen BSA-guanine-N7-AFB1 also cross-reacted with calf thymus DNA-AFB1 adduct, indicating specificity to the guanine-N7-AFB1 moiety. The method developed may find immediate application as a source of authentic reference standard in molecular epidemiological studies.

Aflatoxin B1↗

PubMed1990

Effects of phenobarbital and beta-naphthoflavone on the in vivo toxicity and in vitro metabolism of aflatoxin in an aflatoxin-resistant and control line of chickens.

The in vivo toxicity of aflatoxin and the in vitro microsomal metabolism of aflatoxin B1 (AFB1) were investigated in a population of chickens previously selected for resistance to aflatoxin (AR line) and a corresponding control population (NS line) after in vivo pretreatment with saline, sodium phenobarbital (PB), or beta-naphthoflavone (BNF) solutions. PB pretreatment increased survival and BNF pretreatment increased mortality in both the NS and AR lines when a single oral dose of aflatoxin was administered. The rate of in vitro metabolism of AFB1 was greater with microsomes from saline pretreated AR chicks than with microsomes from similarly treated NS chicks. In vivo pretreatment with PB increased AFB1 metabolism by NS and AR microsomes. After BNF pretreatment of vivo, AR microsomes metabolized more AFB1 than NS microsomes, and there was a dramatic decrease in AFB1 metabolism in NS microsomes. AFB1-dihydrodiol was the major metabolite produced by both lines, with aflatoxin M1 and aflatoxin Q1 recovered in small quantities from BNF-pretreated AR microsomal incubations only. These data indicate that increased in vivo resistance of the AR line to acute aflatoxicosis may be related to increased hepatic AFB1 metabolism and that genetic selection has resulted in altered in vitro quantitative and qualitative metabolism of AFB1 in the AR line.

Aflatoxins↗

PubMed1987

Regulation of aflatoxin biosynthesis: assessment of the role of cellular energy status as a regulator of the induction of aflatoxin production.

Possible relationships among cellular energy status and the induction and initiation of aflatoxin synthesis were studied by using replacement culture techniques in conjunction with aflatoxin-supporting and-nonsupporting media. Transcription and translation processes associated with the induction of aflatoxin synthesis occurred 3 to 6 and 6 to 10 h, respectively, after mycelia were transferred to glucose-containing media. From adenylate energy charge determinations and in situ 31P nuclear magnetic resonance analyses, a relationship between overall energy status and the induction or initiation of aflatoxin synthesis could not be identified; however, electron microscopic evaluations indicated that aflatoxin synthesis occurred in association with a glucose-mediated inactivation of mitochondria. The results suggest that aflatoxin synthesis is not regulated by the overall energy status of the fungal cell but may be controlled by the energy status of specific subcellular compartments.

Aflatoxins↗