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PubMed1991

Efficacy of hydrated sodium calcium aluminosilicate and activated charcoal in reducing the toxicity of dietary aflatoxin to mink.

Mink were fed diets that contained 0, 34, or 102 ppb (micrograms/kg) aflatoxins with or without 0.5% hydrated sodium calcium aluminosilicate (HSCAS) and/or 1.0% activated charcoal (AC) for 77 days. Consumption of the diet that contained 34 ppb aflatoxins was lethal to 20% of the mink, while 102 ppb dietary aflatoxins resulted in 100% mortality within 53 days. The addition of AC to the diet containing 102 ppb aflatoxins reduced mortality and increased survival time of the mink while the addition of HSCAS, alone or in combination with AC, prevented mortality. Histologic examination of livers and kidneys from the mink demonstrated liver lesions ranging from extremely severe in mink fed 102 ppb aflatoxin to mild to moderate in those that received 34 ppb aflatoxins. The addition of HSCAS and/or AC to the diets that contained 102 ppb aflatoxins reduced or essentially eliminated histopathologic lesions in the livers. No histopathologic alterations associated with the dietary treatments were observed in the kidneys.

Aflatoxins↗

PubMed1994

Aspergillus flavus and aflatoxin B1 in flour production.

This paper discusses the results of investigations of contamination with aflatoxin-producing fungi and aflatoxin B1 affecting 545 samples of wheat grains, 475 samples of intermediate products of wheat grain being milled to flour (like middlings) and 238 samples of flour. A significant contamination with moulds was detected in analyzed samples. Although Aspergillus (34.87%) and Penicillium (32.37%) dominated, other types were also present, e.g., Cladosporium, Fusarium, Mucor, Alternaria, Rhizopus, Absidia and Trichoderma (listed in order of frequency). The presence of Aspergillus flavus, the known aflatoxin producer, was detected in 9.94% of analyzed samples. Isolates of A. Flavus were capable of producing aflatoxin B1 under favourable conditions. Aflatoxin B1 was found in 76.8% of samples contaminated with A. flavus. The highest contamination with aflatoxin B1 was detected in wheat grain samples (mean value of 16.3 micrograms/kg) and in intermediate products of wheat grain being milled to flour (mean value of 11.13 micrograms/kg). Contamination was lower in flour samples (mean value of 4.13 micrograms/kg). With regard to proposed standards given by the FAO and WHO, under which the content of aflatoxin should not exceed 30 micrograms/kg in food products, only two of 96 samples did not meet these criteria.

Aflatoxin B1↗

PubMed2004

Distribution and sub-cellular localization of the aflatoxin enzyme versicolorin B synthase in time-fractionated colonies of Aspergillus parasiticus.

Aflatoxins are highly toxic and carcinogenic fungal secondary metabolites. At least 18 enzyme activities are required for aflatoxin biosynthesis in the filamentous fungus Aspergillus parasiticus. One of these enzymes, versicolorin B synthase (VBS), catalyzes bisfuran ring closure in versiconal hemiacetal (a reaction near the middle of the pathway) to form versicolorin B. This reaction is required for the subsequent activation to aflatoxin B1-8,9 epoxide, a highly reactive and toxic aflatoxin metabolite, and is important for aflatoxin toxicity. We analyzed the localization of VBS in the aflatoxin-producing strain A. parasiticus SU-1 grown on solid media using a colony fractionation technique developed previously. A highly specific polyclonal antibody, raised against a maltose-binding protein-VBS fusion protein synthesized in Escherichia coli, was used to detect VBS in SU-1 grown on a rich solid medium via immunofluorescence confocal laser scanning microscopy (CLSM) and immunogold transmission electron microscopy (TEM). VBS was detected in both vegetative hyphae and in asexual developmental structures, called conidiophores. Western blot and CLSM analyses demonstrated the highest abundance of VBS in colony fraction S2 consisting of cells that had grown for 24-48 h; this fraction also contained the highest levels of newly developed conidiophores and the highest abundance of aflatoxin B1, consistent with VBS abundance. At the subcellular level, CLSM and TEM detected VBS distributed throughout the cytoplasm and concentrated in ring-like structures surrounding nuclei. It is uncertain whether enzymatically active VBS is present in either or both locations.

Aflatoxin B1↗

PubMed2001

Absence of aflatoxin biosynthesis in koji mold (Aspergillus sojae).

Ten strains isolated from industrial soy sauce producing koji mold were identified as Aspergillus sojae and distinguished from Aspergillus parasiticus morphologically and physiologically. There was no detectable aflatoxin in any culture extracts of A. sojae strains. Strain 477 was chosen as a representative strain of industrial A. sojae for further molecular analysis. All enzymatic activities associated with the aflatoxin biosynthesis were not detected or negligible in strain 477 compared with that of the A. parasiticus strain. Southern analysis suggested that the genomic DNA of strain 477 contained aflatoxin biosynthetic pathway genes. In contrast, all industrial strains lacked detectable transcripts of aflR, the main regulatory gene for aflatoxin biosynthesis, under the aflatoxin-inducing condition. Our data suggest that defects in aflR expression cause the lack of expression of aflatoxin-related genes which results in the absence of aflatoxin biosynthesis in A. sojae strains.

Aflatoxins↗

PubMed2006

Putative calmodulin-binding domains in aflatoxin biosynthesis-regulatory proteins.

The inhibition of aflatoxin production by trifluoperazine, an anticalmodulin (CaM) agent and the relevance of Ca(2+)/CaM-dependent phosphorylation and dephosphorylation during aflatoxin biosynthesis was previously reported. To identify proteins that may be regulated by CaM, an in silico analysis for putative CaM-binding domains (CaMBDs) in the aflatoxin-related proteins of Aspergillus parasiticus was performed using the CaM target database. Interestingly, the key regulators of aflatoxin biosynthesis such as AflR and AflJ contained predicted CaMBDs at their C-termini. Furthermore, potential phosphorylation sites for CaM-kinase II were present within these CaMBDs. In addition to other aflatoxin biosynthesis enzymes--such as Vbs, DmtA and OmtA, and the VeA protein (known to regulate the expression of AflJ and AflR)--also showed the presence of putative CaMBDs. Although the present report reaffirms earlier observations on CaM-mediated regulation of aflatoxin biosynthesis, it also opens new avenues for identifying the specific targets of CaM and elucidating the exact mechanism of initiation and regulation of aflatoxin biosynthesis.

Aflatoxins↗

PubMed2003

The Aspergillus parasiticus protein AFLJ interacts with the aflatoxin pathway-specific regulator AFLR.

The Aspergillus parasiticus aflJgene, which is located in the aflatoxin biosynthetic gene cluster and is transcribed divergently from the aflatoxin pathway regulatory gene aflR, encodes a 438-amino acid protein. Transformation with aflJplus aflR, but not aflJalone, increased the accumulation of aflatoxin precursors substantially in an O-methylsterigmatocystin-accumulating A. parasiticus strain. Disruption of aflJ resulted in non-pigmented mutants that lost the ability to synthesize aflatoxin intermediates. Transcript profiling by real time RT-PCR indicated that the lack of aflJtranscripts in the aflJ knockout mutants is associated with a significant decrease in the transcript levels of the genes for early (pksAand nor1), middle (ver1) and later (omtA) steps in the aflatoxin biosynthetic pathway, with the degree of reduction ranging from 5- to 20-fold. Deletion of aflJ, however, did not have any effect on the aflRtranscript level, and vice versa. Two-hybrid assays showed that AFLJ did not interact with aflatoxin biosynthetic enzymes, including NOR1, VER1, OMTA and ORDA. But AFLJ interacted with full-length AFLR, and the DNA-binding domain of AFLR was found not to be essential for this interaction. Simultaneous substitution of Arg427, Arg429, and Arg431 in the C-terminal region of AFLR with Leu residues abolished its ability to interact with AFLJ. Replacement of Asp436, which was previously shown to be crucial for AFLR's activation activity, with His, in contrast, had little effect on the interaction. On the other hand, deletions in most regions of AFLJ appeared to destroy its function, despite the fact that random amino acid substitution(s) in its C-terminal region did not drastically affect its capacity to interact with AFLR. The results show that aflJis involved in the expression of aflatoxin structural genes and support the hypothesis that aflJis a coactivator gene.

Aflatoxins↗

PubMed2006

Reduction of aflatoxin B1 in chicken feed by using Saccharomyces cerevisiae, Rhizopus oligosporus and their combination.

Aflatoxin B1 is a toxigenic and carcinogenic compound produced by Aspergillus flavus and Aspergillus parasiticus. An approach to prevent aflatoxin contamination in feed was carried out by using Saccharomyces cerevisiae (Sc) and Rhizopus oligosporus (Ro). Aspergillus flavus was cultured together with Sc, Ro and their combination (ScRo) in chicken feed. The aflatoxin B1 content was observed at day 0, 5, 10 and 15. The result showed that aflatoxin B1 contaminations in feed were reduced by Sc, Ro and ScRo addition. The highest reduction of aflatoxin B1 content was shown at day 5 for all treatments with Sc, Ro and ScRo. The best activity of reducing aflatoxin B1 was shown by Ro. Although the ability of reducing aflatoxin B1 of Sc, Ro or ScRo was not significantly different, Sc or Ro gave the better result than ScRo and they are better used individually.

Aflatoxin B1↗

PubMed1996

Aflatoxin exposure and cytogenetic alterations in individuals from the Gambia, West Africa.

Aflatoxin-albumin adducts in peripheral blood provide a measure of exposure to aflatoxin over the previous 2-3 months. In the present study, the levels of these adducts were determined in a group of individuals from The Gambia, West Africa and were compared in a cross-sectional study to the levels of various cytogenetic alterations (chromosomal aberrations, micronuclei, sister chromatid exchanges) in the same individuals to test whether an increase in genetic damage is associated with an increased exposure in this population. Of 35 subjects tested for aflatoxin-albumin adducts, all but 3 were positive. There were no correlations between the adduct level and the number of cytogenetic abnormalities at the individual level. A comparison of the cytogenetic alterations was made between Gambian individuals and a group of 22 healthy people from Italy where aflatoxin exposure is expected to be low. The levels of structural chromosomal aberrations, sister chromatid exchanges and micronuclei were all higher in the former group. Overall, these data are indicative of a higher exposure to genotoxins in Gambian subjects, one of which are aflatoxins, but suggest that more specific genetic markers of aflatoxin exposure are required to further examine the link between aflatoxin exposure and genetic alterations.

Adolescent↗

PubMed1994

Immunostimulating effects of protein A in immunosuppressed aflatoxin-intoxicated rats.

Aflatoxin B1, the potent carcinogenic compound produced by the Aspergillus flavus group of fungi on food and feed, induces immunosuppressive effects in rodents. In this communication, we report an immunomodulatory approach to abrogate aflatoxin B1-induced immunotoxicity in rats using protein A of Staphylococcus aureus Cowan 1. We have earlier demonstrated that protein A can protect the animals from toxicities induced by a number of drugs, chemicals and toxins. In the present study various combinations of aflatoxin B1 exposure and protein A treatment in animals were used. It was observed that protein A could provide protection to animals from aflatoxin B1-induced immunotoxicity, as measured by a battery of tests assessing cell-mediated immunity (CMI) profile of the host. Various parameters showing suppression of CMI following aflatoxin B1 exposure were reverted back towards normalcy in protein A-treated animals. It is concluded that protein A may prove to be a useful agent to protect the host from aflatoxin immunotoxicity, in view of its stimulatory effects on various immune functions even after their initial depression due to aflatoxin B1.

Adjuvants, Immunologic↗

PubMed2005

Sequence breakpoints in the aflatoxin biosynthesis gene cluster and flanking regions in nonaflatoxigenic Aspergillus flavus isolates.

Aspergillus flavus populations are genetically diverse. Isolates that produce either, neither, or both aflatoxins and cyclopiazonic acid (CPA) are present in the field. We investigated defects in the aflatoxin gene cluster in 38 nonaflatoxigenic A. flavus isolates collected from southern United States. PCR assays using aflatoxin-gene-specific primers grouped these isolates into eight (A-H) deletion patterns. Patterns C, E, G, and H, which contain 40 kb deletions, were examined for their sequence breakpoints. Pattern C has one breakpoint in the cypA 3' untranslated region (UTR) and another in the verA coding region. Pattern E has a breakpoint in the amdA coding region and another in the ver1 5'UTR. Pattern G contains a deletion identical to the one found in pattern C and has another deletion that extends from the cypA coding region to one end of the chromosome as suggested by the presence of telomeric sequence repeats, CCCTAATGTTGA. Pattern H has a deletion of the entire aflatoxin gene cluster from the hexA coding region in the sugar utilization gene cluster to the telomeric region. Thus, deletions in the aflatoxin gene cluster among A. flavus isolates are not rare, and the patterns appear to be diverse. Genetic drift may be a driving force that is responsible for the loss of the entire aflatoxin gene cluster in nonaflatoxigenic A. flavus isolates when aflatoxins have lost their adaptive value in nature.

5' Flanking Region↗

PubMed2005

Trametes versicolor: a possible tool for aflatoxin control.

The genotoxic, mutagenic and cancerogenic aflatoxins produced by Aspergillus parasiticus are not yet efficiently controlled besides the increasing researches on this topic. Aflatoxin production by A. parasiticus is related to oxidative stress and some antioxidants can inhibit their production. Some basidiomycetes as Trametes versicolor used as "healing mushrooms" present beta-glucans and glycoproteins which are responsible for the stimulation of the host immune response. In this work T. versicolor culture filtrates, from different isolates, have been tested on A. parasiticus cultures to assay their inhibiting effect on aflatoxin production. Filtrates from T. versicolor were lyophilised and exopolysaccharides and glycoproteins were extracted by subsequent steps and added (2% w/v) to liquid cultures of a toxigenic A. parasiticus strain. Fungal growth and aflatoxins production by A. parasiticus were analysed both in filtrates and in mycelia and no interference on the output of toxins from mycelia was evidenced. Furthermore antioxidant capacity (by crocin test) of the T. versicolor extracts was analysed. All the strains assayed are able to inhibit the toxin production from 40% to above 90% in liquid cultures as well as in maize and wheat seeds inoculated with A. parasiticus. Antioxidant activity and beta-glucans amount in T. versicolor extracts showed a close relationship with aflatoxin inhibition ability and demonstrated that beta-glucans could be involved in aflatoxin inhibition. Molecular data indicate the almost complete inhibition of norA mRNA expression and a delay of aflR mRNA transcription. Filtrates and fractions from T. versicolor could be promising agents in the challenge against aflatoxins.

Aflatoxins↗

PubMedDate not supplied

Chemoprevention with chlorophyllin in individuals exposed to dietary aflatoxin.

Because of the multiplicative interaction between dietary aflatoxins and hepatitis B virus infection in the etiology of liver cancer, efforts to reduce the consequences of either chemical or viral component are likely to have substantial public health benefit. Chlorophyllin (CHL), a water-soluble form of chlorophyll, was recently evaluated as a chemopreventive agent in a population at high risk for exposure to aflatoxin and subsequent development of hepatocellular carcinoma. CHL, which is used extensively as a food colorant and has numerous medicinal applications, is an effective anticarcinogen in experimental models including aflatoxin-induced hepatocarcinogenesis. CHL is thought to form molecular complexes with carcinogens, thereby blocking their bioavailability. In the clinical trial, administration of CHL three times a day led to a 50% reduction in the median level of urinary excretion of aflatoxin-N(7)-guanine compared to placebo. This excreted DNA adduct biomarker is derived from the ultimate carcinogenic metabolite of aflatoxin B(1), aflatoxin-8,9-epoxide, and is associated with increased risk of developing liver cancer in prospective epidemiologic studies. Compliance in the intervention was outstanding and no toxicities were observed. Thus, CHL has been found to be a safe and effective agent suitable for use in individuals unavoidably exposed to aflatoxins.

Aflatoxins↗

PubMed1998

Amaranth grain as substrate for aflatoxin and zearalenone production at different water activity levels.

The influence of water activity (a(w)) on the kinetics of aflatoxin and zearalenone production in amaranth grains at 25 degrees C was studied. Minimum a(w) for aflatoxin production in this substrate was 0.825. Accumulation of the four aflatoxins (B1, B2, G1 and G2) was similar at a(w) 0.825 (maximum 81.2 microg/kg after 42 days) and 0.868 (maximum 109.6 microg/kg after 49 days). Maximum accumulation of total aflatoxins at a(w) 0.902 (260.4 microg/kg) was detected after 21 days, with an appreciable increment in the concentration of aflatoxins B1 and G1. These quantities were lower than those reported for aflatoxin production on other cereals and legumes, indicating that amaranth is not a good substrate for aflatoxin production. Zearalenone was not detected at a(w) 0.902. Maximum accumulation of zearalenone was 1.5 microg/g after 35 days at a(w) 0.925 and 11.1 microg/g after 49 days at a(w) 0.950.

Aflatoxins↗

PubMed1983

High-performance liquid chromatography of aflatoxins in human urine.

A method was developed for the extraction and determination of unconjugated aflatoxins in human urine by high-performance liquid chromatography. The analysis is based on the elimination of lipid-soluble constituents other than unconjugated aflatoxins in urine by light petroleum extraction. The unconjugated aflatoxins were subsequently extracted from the aqueous phase with chloroform-acetone. Chromatography was performed isocratically with a silica column at 40 degrees C. The resolved aflatoxins were detected and identified by ultraviolet and fluorometric detectors. The recoveries of aflatoxins B1 and G1 added prior to the extraction were 72% and 83%, respectively. This procedure is simple, sensitive and practically useful for epidemiological survey of unconjugated aflatoxins in human urine from areas with a high risk of aflatoxin consumption.

Aflatoxins↗

PubMed1999

Mode of action of pesticides on aflatoxin biosynthesis and oxidase system activity.

The effects of nine pesticides on the biosynthesis of aflatoxin and oxidase activity in wild-type Aspergillus flavus and mutant strains of A. parasiticus avr-1 (w 49) and A. parasiticus ver-1 (wh 1) were investigated. In A. parasiticus, phosphonic acid derivative (lancer) reduced the formation of aflatoxin B2 but B1, G1 and G2 and anthraquinones (versicolorin A, versiconal hemiacetal acetat and averufin) accumulated. Phosphorothioic acid derivatives (pirimiphos-methyl and pyrazophos) reduced the formation of aflatoxin B2 and G2 but B1 and G1 and anthraquinones accumulated. Phosphorodithioic acid derivatives (dimethoate and malathion) blocked aflatoxin B2, reduced B1 and G2 but G1 and anthraquinones accumulated. Phosphoric acid derivative (profenfos) inhibited the formation of all aflatoxins, versicolorin A and versiconal hemiacetal acetate but averufin accumulated. The phenylurea derivatives (linuron and pencycuron) at concentrations of 500 and 1000 ppm inhibited all aflatoxin but anthraquinones accumulated. On the other hand, the dicarboximide derivative (iprodione) inhibited the whole pathway in the mutant strains of A. parasiticus. The oxidase system in wild-type A. flavus was active in the conversion of averufin and versicolorin A into aflatoxin B1. Most organophosphate and phenylurea derivatives may competitively increase or decrease the oxidase enzymes, however, profenfos and iprodione blocked the enzymes between averufin and versicolorin A.

Aflatoxins↗

PubMed1999

Interactions between hepatitis B virus infection and exposure to aflatoxins in the development of hepatocellular carcinoma: a molecular epidemiological approach.

Aflatoxins and hepatitis B virus (HBV) are major risk factors for hepatocellular carcinoma (HCC) in high incidence areas for this cancer, namely southeast Asia and parts of Africa. There is evidence from both epidemiological studies and animal models that the two factors can act synergistically to increase the risk of HCC. The cellular and molecular mechanism of the interaction between these two factors is as yet undefined. However, one possible mechanism attested to by studies in HBV transgenic mice is that chronic liver injury alters the expression of specific carcinogen metabolising enzymes thus modulating the binding of aflatoxin to DNA in hepatocytes. The high levels of aflatoxin exposure which occur in many areas of the world where chronic HBV infection is endemic indicate that measures to reduce aflatoxin exposure would contribute to reducing HCC incidence. In preliminary studies, Guinea-Conakry have established baseline data for the implementation of a community-based intervention study to evaluate the effectiveness of improved post-harvest processing and storage of the groundnut crop, a major source of aflatoxins. Aflatoxin-albumin adducts were measured in 423 sera from individuals living in the four natural geographic zones of Guinea. More than 95% of the serum samples were positive for this biomarker and highest exposures were found in Lower Guinea where groundnuts are consumed as a dietary staple. Variations in mean levels between villages within a geographic region did not vary greatly. HBV infection was endemic in all regions with an overall prevalence of 16.7% chronic carriers. Thus in this population both HBV vaccination and reduction in aflatoxin exposure would be beneficial in decreasing morbidity and mortality from liver disease.

Aflatoxins↗

PubMed2001

Inhibitory effects of naturally occurring compounds on aflatoxin B(1) biotransformation.

Effects of naturally occurring compounds from plants on biotransformation of a mycotoxin, aflatoxin B(1), were evaluated. Among 77 naturally occurring compounds tested, anthraquinones, coumarins, and flavone-type flavonoids were shown to be potent inhibitors of aflatoxin B(1)-8,9-epoxide formation. Addition of the flavonoids galangin, rhamnetin, and flavone strongly inhibited mouse liver microsomal conversion of aflatoxin B(1) to aflatoxin B(1)-8,9-epoxide, a metabolically activated mutagenic product. In contrast to these results, addition of isoflavonoids, catechins, terpenes, alkaloids, and quinones to mouse liver microsomes did not inhibit formation of aflatoxin B(1)-8,9-epoxide. Formation of the aflatoxin B(1) reductase product, aflatoxicol, by chicken liver cytosols was strongly inhibited by curcumin, the diferuloylmethane present in turmeric and other Curcuma species. Curcumin analogues also showed inhibitory effects, and a structure-activity study established that beta-diketone groups linked with two benzyl moieties were essential for inhibition of aflatoxicol formation. An additional 37 naturally occurring compounds tested did not inhibit formation of aflatoxicol. These results demonstrate that dietary constituents in certain fruits, vegetables, and spices may have significant inhibitory effects on metabolic transformation of aflatoxins to their hepatotoxic or carcinogenic derivatives or, alternatively, may promote their transformation into nontoxic products.

Aflatoxin B1↗

PubMed2005

Development of an immunoassay-based lateral flow dipstick for the rapid detection of aflatoxin B1 in pig feed.

The aim of this work was to develop an immunoassay-based lateral flow dipstick for the rapid detection of aflatoxin B(1) in pig feed. The test consisted of three main components: conjugate pad, membrane, and absorbent pad. The membrane was coated with two capture reagents, that is, aflatoxin B(1)-bovine serum albumin conjugate and rabbit anti-mouse antibodies. The detector reagent consisted of colloidal gold particles coated with affinity-purified monoclonal anti-aflatoxin B(1) antibodies, which saturated the conjugate pad. A comparison of several extraction methods for the pig feed matrix is presented. A mixture of methanol/water (80:20, v/v) gave the best recoveries. After sample extraction and dilution, the dipstick was put in the sample solution at the conjugate pad side and developed for 10 min. Analyte present in the sample competed with the aflatoxin B(1) immobilized on the membrane for binding to the limited amount of antibodies in the detector reagent. Thus, the line color intensity of an aflatoxin B(1)-positive dipstick is visually distinguishable from that of an aflatoxin B(1)-negative sample. The visual detection limit for aflatoxin B(1) is 5 microg/kg. The major advantages of this one-step striptest are that results can be obtained within 10 min and that all reagents are immobilized on the lateral flow dipstick.

Aflatoxin B1↗