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PubMed2005

[Recent advances in the determination methods of aflatoxins].

Aflatoxins are very harmful pollutants generally existing in peanuts, corns, farm products and so on. Many methods for the determination of aflatoxins have been developed in recent thirty years. The limits for aflatoxins have been set down for foods and farm products in different countries successively. In China, the methods for the determination of aflatoxins in foods cannot meet the need of new limit regulations. Aflatoxins were found in some traditional Chinese medicines according to some literatures. But the detective method and standard for the determination of aflatoxins is not established in active pharmacopoeia. The analytical methods for aflatoxins have been summarized in this paper, which can provide the references to the researchers who are engaged in the determination of aflatoxins in traditional Chinese medicines and foods. This paper mainly focuses on the liquid chromatography method with immunoaffinity column cleanup using post-column derivatization system for aflatoxins. Aflatoxins can be adsorbed in the immunoaffinity column peculiarly on the basis of this method, and then they can be eluted with organic solvent. It is the best way for cleanup using immunoaffinity column for the determination of aflatoxins in traditional Chinese medicines. This HPLC method with fluorescence detector using post-column derivatization system is a commonly used method in different countries, and it is more sensitive and accurate. Our studies have also proved that this method, that is: the liquid chromatography methods with immunoaffinity column cleanup using post-column derivatization system for aflatoxins, is the best method, which is suitable for the determination of aflatoxins in traditional Chinese medicines.

Aflatoxins↗

PubMedDate not supplied

A follow-up study of urinary markers of aflatoxin exposure and liver cancer risk in Shanghai, People's Republic of China.

A cohort of 18,244 mostly middle-aged (45-64 years) men residing in four small geographically defined areas of Shanghai was accrued between January 1986 and September 1989. In addition to an in-person interview regarding dietary and other past exposures, each subject donated a single void urine sample at recruitment so that the presence of aflatoxins in urine could be assessed. In addition, a 1-year survey of market foods in Shanghai was conducted to quantitatively estimate the extent of aflatoxin exposure in the study population. After close to 70,000 person-years of follow-up, 55 incident cases of hepatocellular carcinoma (HCC) had been identified. Levels of urinary aflatoxin B1 and the oxidative metabolites, including the major aflatoxin nucleic acid adduct, aflatoxin-N7-guanine, were determined for 50 of the 55 identified cases of HCC. Two hundred sixty-seven controls were chosen randomly from the cohort; they were matched to the 50 cases by age (within 1 year), time of specimen collection (within 1 month), and residence. After integrating the high-pressure liquid chromatography chromatograms to measure aflatoxin-N7-guanine, aflatoxin M1, aflatoxin P1, and aflatoxin B1, 49, 67, 53, and 71 of the urine samples had detectable levels of these compounds, respectively. The aflatoxin metabolite detected at the highest concentration was aflatoxin P1; the range was 0.59-16.0 ng/ml. The range of aflatoxin M1 in the urine was 0.17-5.2 ng/ml. The aflatoxin-N7-guanine adduct range was 0.3-1.81 ng/ml in the 49 positive samples.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗

PubMedDate not supplied

Comparison of three methods for determining aflatoxins in melon seeds.

The suitability of 3 methods for determining aflatoxins in melon seeds was examined. The first 2 are the Contaminants Branch (CB) method and the Best Foods (BF) method, both official methods for determining aflatoxins in peanuts and peanut products. The third method, the modified CB method-Rapid Modification of the Cottonseed (CB-RCS-Mod) method, devised in this work, was derived by combining steps from the CB method and the Rapid Modification of the Cottonseed method. The CB method was superior to the other 2 methods for quantitation of aflatoxins. It gave better recoveries and cleaner extracts that exhibit less fluorescent interference for thin-layer chromatography (TLC) than the BF method. Also, its solvent efficiency was better than that of the CB-RCS-Mod method. With the CB method, recoveries from spiked samples were 85.0% for aflatoxin B1 and 90.0% for aflatoxin B2. Recoveries of G aflatoxins were more variable, averaging 90.0% for aflatoxin G1 and 72.5% for aflatoxin G2. Total aflatoxin recovery was 86.5% for the CB method. At a low aflatoxin contamination level (8 micrograms B1/kg sample), aflatoxin B1 was detectable by the CB method but not by the BF method. Detection of aflatoxins in BF method sample extracts by TLC was not improved by the use of chloroform-acetone-water (88 + 12 + 1), benzene-ethanol-water, or ether-methanol-water (96 + 3 + 1) in place of the standard chloroform-acetone (88 + 12) developer. Use of ether-methanol-water (96 + 3 + 1) for detecting aflatoxins by TLC in the CB method extracts increased interference compared with the standard chloroform-acetone (88 + 12) developer.

Acetone↗

PubMedDate not supplied

Quantitation of aflatoxin B1-N7-guanine adduct in urine by enzyme-linked immunosorbent assay coupled with immunoaffinity chromatography.

A specific and sensitive method to quantitate aflatoxin B1-N7-guanine adduct in urine samples by immunoaffinity chromatography coupled with indirect competitive enzyme-linked immunosorbent assay (ELISA) is reported. A novel in vitro method to synthesize an antigen (bovine serum albumin-guanine-aflatoxin B1) and its use to produce polyclonal antibodies specific to the hapten aflatoxin B1-N7-guanine are discussed. An indirect competitive ELISA developed to quantitate aflatoxin adduct showed a 50% inhibition at 15.6 pmol aflatoxin B1-N7-guanine (y = 66.73 + (-19.8)chi; r = -0.997). Interference by aflatoxin B1 was less than 5%, and no interference by guanine, aflatoxin G1 and aflatoxin M1 was observed. An immunoaffinity column was also developed, by using these polyclonal antibodies, for single-step purification of aflatoxin B1-N7-guanine. The immunoaffinity column and the indirect competitive ELISA were evaluated and validated by quantitation of aflatoxin B1-N7-guanine in urine from rats dosed with aflatoxin B1 (1 mg/kg body weight). Spiking studies with standard aflatoxin B1-N7-guanine adduct at 2 and 4 micrograms/mL phosphate-buffered saline gave 96 and 100% recoveries, respectively, for immunoaffinity cleanup column. The method also was tested successfully for quantitating aflatoxin B1-N7-guanine adduct in spiked human urine. Recoveries of the adduct were 79-90%.

Aflatoxin B1↗

PubMed1997

Occurrence of Aspergillus flavus strains and aflatoxins in corn from Santa Fe, Argentina.

It has been demonstrated in several agricultural regions all around the world that Aspergillus flavus can infect corn grains and produce aflatoxins even before the harvest. It is also known that the incidence and levels of contamination of cereals factors. In the present work, the incidence of aflatoxins in corn grain from the central and northern areas of Santa Fe province in Argentina was studied. The relationship between the extent of kernel infection by the fungus and the presence of aflatoxins in the samples was examined. The isolation and identification of A.flavus were carried out by plating dilutions of the ground kernels on dichloran-rose bengal-chloramphenicol agar (DRBC). Simultaneously, kernels were superficially sterilized with 10% commercial CIONa and plated on potato-dextrose-chloramphenicol agar (PDA + C). The analysis of aflatoxins B1, B2, G1 and G2 was performed by thin layer chromatography (TLC) according with Norma IRAM 14803 (Argentina). A.flavus Link:Fr. was identified in 63.3% of the corn samples. Colonized kernels ranged from 2.5 to 25% and counts on DRBC were in the order of 10(3) CFU/g. Two samples colonized by A.flavus contained aflatoxins B1 and B2 (50 micrograms/kg of aflatoxin B1 and 30 micrograms/kg of aflatoxin B2, and 30 micrograms/kg of aflatoxin B1, and traces of aflatoxin B2, respectively). One sample contained only aflatoxin B1 (22 mu/kg). According to these results, it may be concluded that the incidence of A.flavus observed constitutes a call in attention with respect to the conditions required for storage and transportation of the grains, to minimize the proliferation of the fungus and the production of aflatoxins in these stages. Although the incidence of aflatoxins in the samples of grains was rather low, the levels of aflatoxin B1 recorded in the positive samples were higher than those recommended--or given as advisory levels for human foods, by most countries in the world.

Aflatoxins↗

PubMed1985

Biosynthetic relationship among aflatoxins B1, B2, M1, and M2.

Aflatoxins are a family of toxic, acetate-derived decaketides that arise biosynthetically through polyhydroxyanthraquinone intermediates. Most studies have assumed that aflatoxin B1 is the biosynthetic precursor of the other aflatoxins. We used a strain of Aspergillus flavus which accumulates aflatoxin B2 to investigate the later stages of aflatoxin biosynthesis. This strain produced aflatoxins B2 and M2 but no detectable aflatoxin B1 when grown over 12 days in a low-salt, defined growth medium containing asparagine. Addition of dichlorvos to this growth medium inhibited aflatoxin production with concomitant accumulation of versiconal hemiacetal acetate. When mycelial pellets were grown for 24, 48, and 72 h in growth medium and then transferred to a replacement medium, only aflatoxin B2 and M2 were recovered after 96 h of incubation. Addition of sterigmatocystin to the replacement medium led to the recovery of higher levels of aflatoxins B2 and M2 than were detected in control cultures, as well as to the formation of aflatoxins B1 and M1 and O-methylsterigmatocystin. These results support the hypothesis that aflatoxins B1 and B2 can arise independently via a branched pathway.

Aflatoxin B1↗

PubMed2000

Effect of climate and type of storage container on aflatoxin production in corn and its associated risks to wildlife species.

The effects of grain storage containers on aflatoxin production, and the relationship between the level of aflatoxin and the number and weight of fluorescing kernels were determined in corn (Zea maize) stored in controlled climate regimes. Two hundred and forty 100-g samples were held up to 3 mos using four types of storage containers placed in four climates. Storage containers included corn placed in metal cans, paper bags, plastic bags, and paper bags placed in plastic bags. Climates were constant during the duration of the project and included a combination of temperatures and humidities. Temperatures were 29-32 C and 14-18 C; relative humidities were 85-88% and 35-40%. In addition, corn was exposed to environmental conditions conductive for aflatoxin production and 100 g samples were randomly collected, examined under ultraviolet light for fluorescence, and then quantified for aflatoxin levels. Corn samples tested negative for aflatoxin at the beginning of the project. Main (i.e., container, climate, and month) and interactive effects were not observed. Mean levels of aflatoxin ranged from 0 to 151 microg/kg. Aflatoxin was produced regardless of type of storage container, time of storage, and climatic conditions; however, only 8% of the samples produced aflatoxin levels that exceeded 50 microg/kg. Fluorescing corn ranged from 0 to 19 kernels per sample, while aflatoxin levels ranged from 0 to 1,375 microg/kg for the same samples. No relationships were found between the number and weight of fluorescing kernels of corn and aflatoxin levels. The black light test yielded a false negative rate of 23% when in fact the aflatoxin concentrations exceeded 50 microg/kg. Therefore, quantifying fluorescing grain under UV light should not be considered a feasible alternative for aflatoxin testing of grain intended for wildlife.

Aflatoxins↗

PubMed1985

Quantitative and qualitative characterization of aflatoxin B1 adducts formed in vivo within the ribosomal RNA genes of rat liver DNA.

We have examined the time course and patterns of covalent aflatoxin B1:DNA adducts produced within the ribosomal RNA gene sequences isolated from the liver nuclear DNA of aflatoxin B1-treated animals. Liver nuclear DNA was initially enriched in ribosomal DNA by cesium salt density centrifugation, and incubated under alkaline conditions to stabilize bound aflatoxin B1-DNA moieties. Alkali-treated DNA was hybridized to 18S and 28S rRNA, and the RNA:DNA hybrids were recovered by cesium chloride centrifugation. Ribosomal DNA sequences within nuclear DNA were found to be preferential targets for aflatoxin B1 modification. Over a 12-h period after administration of 1-mg [3H]aflatoxin B1/kg dose ribosomal DNA contained 4 to 5 times more aflatoxin B1 residues per mg DNA than did total nuclear DNA. Aflatoxin B1 residues bound to ribosomal DNA were also found to be removed more rapidly than from total nuclear DNA by a factor of 5.7 over the 12-h period postdosing. Levels of the principal aflatoxin B1 adduct, 2,3-dihydro-3-hydroxy(N7-guanyl)aflatoxin B1, as well as the stable formamidopyrimidine derivatives of the parent adduct were also determined. Nuclear DNA isolates were heated to induce depurination of the principal N7-guanine adduct, and differences in adduct levels between alkali-treated (stabilized) and depurinated DNA samples were taken as an approximation of initial levels of this aflatoxin B1:DNA moiety in ribosomal isolates. No differences in the proportions of these aflatoxin B1:DNA adduct species were found in ribosomal as compared to total nuclear DNA, and we conclude that the preferential formation and removal of aflatoxin B1:DNA moieties within ribosomal DNA is not associated with a pattern of adducts qualitatively different from that in total nuclear DNA.

Aflatoxin B1↗

PubMed2000

Modulating role of Semecarpus anacardium L. nut milk extract on aflatoxin B(1) biotransformation.

As part of a substantial effort to curtail the adverse health effects posed by aflatoxin B(1), studies have been conducted to elucidate the possible mechanism for the anticarcinogenic action of Semecarpus anacardium nut extract against aflatoxin B(1)-induced hepatocellular carcinoma. Rats are monitored for levels of urinary, serum and liver biomarkers, namely, unmetabolised aflatoxin B(1), and its metabolites aflatoxin M(1), and aflatoxin Q(1), over the course of 2 weeks with nut extract therapy following a single-exposure to aflatoxin B(1). Due to the administration of nut extract, the excretion of unmetabolised aflatoxin B(1) was increased in day 1 urine when compared with rats without drug treatment. In serum and liver which were collected on day 16 and the rest of periodical urine samples showed aflatoxin B(1) and its metabolites in undetectable levels. The nut extract administration induced cytochrome P(450), glutathione, and glutathione-S-transferase levels in liver homogenates of aflatoxin B(1)-treated rats. These data seem to indicate that anticarcinogenic action by Semecarpus anacardium nut extract is possibly via suppression of aflatoxin B(1)activation and through interaction with microsomal-activating components. Previous evidence from this laboratory about the potency of Semecarpus anacardium nut extract against aflatoxin B(1)-induced hepatocellular carcinoma together with the present results suggest that extremely effective therapeutic protection can be achieved by this drug against aflatoxin B(1)-mediated ill effects.

Aflatoxin B1↗

PubMed1989

Aflatoxin is not a probably human carcinogen: the published evidence is sufficient.

Since the early 1960s, when aflatoxin, the mold-produced contaminant of a number of important food commodities, was found to be a potent hepatocarcinogen for laboratory rats, there has been a sustained search for evidence to support the regulatory presumption that aflatoxin is a probable human carcinogen. The developing laboratory evidence of differences between species in metabolism of aflatoxin and susceptibility to its oncogenic effects indicated that humans were probably refractory to aflatoxin carcinogenesis, but the early epidemiological evidence indicated otherwise. That epidemiological evidence, however, contained flaws so that Working Groups of the International Agency for Research on Cancer (IARC) meeting in 1970, 1976, and 1982, although ignoring the biochemical evidence, did consider the available epidemiological evidence insufficient for a conclusion of human carcinogenicity. During the 1970s and 1980s, studies on the connection between chronic infection with hepatitis B virus (HBV) and primary liver cell cancer (PLC), the expected lesion from aflatoxin exposure, had established a very strong etiological relationship between HBV and PLC. Since all the epidemiological studies of aflatoxin and PLC conducted prior to 1982 had been of populations with endemic HBV infection, and, in addition to other flaws, had not been controlled for this confounding factor, there was a solid basis for their rejection. Most epidemiological studies in the 1980s of aflatoxin and PLC were either in the United States, where HBV-infected groups could be excluded from the study, or, when in areas of chronic HBV infection, attempts were made to include that factor. The study of U.S. populations showed no difference in mortality rates from PLC that could be attributed to aflatoxin exposure. The studies of populations with endemic HBV infection produced no convincing evidence to support a primary role for aflatoxin in the induction of human PLC, although an accessory role to HBV infection for aflatoxin could not be ruled out. However, the epidemiological studies of the HBV/PLC relation indicate that an accessory factor is not an essential condition, a conclusion supported by animal models and a laboratory study that specifically found no interaction between aflatoxin and a hepatitis virus in the duck, a species in which liver cancer can be induced by either agent. It was surprising that an IARC Working Group meeting in 1987 concluded, on the basis of much of this evidence that was available at that time, and citing other studies that appear to be irrelevant to the issue, that there was sufficient evidence to consider aflatoxin a probable human carcinogen.

Aflatoxins↗

PubMed1984

Tissue deposition and clearance of aflatoxins from broiler chickens fed a contaminated diet.

A study was conducted to determine aflatoxin levels in the tissues of broiler chickens that had been fed a diet containing 2057 micrograms aflatoxin B1 and 1323 micrograms aflatoxin B2/kg for 35 days. Results showed that aflatoxins were deposited in all tissues. The highest levels of aflatoxins were present in the gizzards, livers and kidneys. There was evidence that the high levels of aflatoxins B1 and B2 in the gizzards might have been caused by contamination by the gizzard contents during the slaughtering process. After feeding the aflatoxin-contaminated diet for 35 days, mean values for the combined aflatoxins were less than 3 micrograms/kg of tissue. Four days after withdrawal of the aflatoxin-contaminated ration, there were no detectable amounts of aflatoxins in any of the tissues. The results indicate that broiler chickens rapidly clear aflatoxins from their tissues once they are transferred to an aflatoxin-free diet.

Aflatoxins↗

PubMed1997

Synthesis and characterization of aflatoxin B1 mercapturic acids and their identification in rat urine.

Biologic effects of the hepatocarcinogenic mycotoxin aflatoxin B1 are principally induced by one of its metabolites, the exo-aflatoxin B1 epoxide which produces both DNA and protein adducts in vivo. Detoxication of the exo-aflatoxin B1 epoxide can be mediated in part by glutathione S-transferases whose induction could be important in chemoprotection interventions. Thus, biomarkers of the enzymatic conjugation of exo-aflatoxin B1 epoxide with glutathione may be important indices of protection against the toxic effects of this agent. Since glutathione conjugates undergo further metabolic processing in vivo to yield mercapturic acids, increased urinary excretion of exo-aflatoxin B1 mercapturate could be expected during chemoprotection intervention. To determine if this mercapturic acid could be used as a biomarker, techniques for its specific measurement were developed using monoclonal antibody immunoaffinity chromatography and reverse phase high-performance liquid chromatography with ultraviolet absorbance and mass spectral detection. First, a synthetic exo-aflatoxin B1 mercapturate was characterized using mass spectrometry, ultraviolet absorbance, circular dichroism spectrometry, and chemical derivatization. In vivo metabolite characterization was then facilitated by comparison with the synthetically prepared exo-aflatoxin B1 mercapturate and both aflatoxin B1-glutathione conjugate diastereoisomers. In rats, 1% of the aflatoxin dose was excreted as exo-aflatoxin B1 mercapturate within 24 h. The finding that exo-aflatoxin B1 mercapturate was excreted in urine in a dose-dependent manner provides the basis for investigating its applicability as a biomarker of glutathione S-transferase status in aflatoxin chemoprotection studies.

Acetylcysteine↗

PubMed1997

Of sick turkeys, kwashiorkor, malaria, perinatal mortality, heroin addicts and food poisoning: research on the influence of aflatoxins on child health in the tropics.

Similarities between the geographical and climatic prevalences of kwashiorkor and of exposure to dietary aflatoxins, and between the biochemical, metabolic and immunological derangements in kwashiorkor and those in animals exposed to aflatoxins, prompted investigation of the associations between kwashiorkor and aflatoxins. Studies in Africa in the 1980s indicated a role for these toxins in the pathogenesis of the disease. Paediatric cases of kwashiorkor are less prone to severe Plasmodium falciparum malaria than normal children. In mice infected with P. berghei, aflatoxin exposure inhibits parasite growth and ameliorates morbidity. Aflatoxins occur in < or = 40% of samples of breast milk from tropical Africa, usually as low concentrations of the relatively non-toxic derivatives of aflatoxin B1 (AFB1) but sometimes as high concentrations of the very toxic AFB1. This could explain kwashiorkor in breast-fed babies. Aflatoxin exposure occurs in > or = 30% of pregnancies in tropical Africa and the toxins are often in cord blood, sometimes at extremely high concentrations. Aflatoxins are now incriminated in neonatal jaundice and there is circumstantial evidence that they cause perinatal death and reduced birthweight. Aflatoxin-induced immunosuppresion may explain the aggressive behaviour of HIV infection in Africa. There are similarities between observations on HIV cases in Africa and those on heroin addicts in Europe, where 'street' heroin is frequently contaminated with aflatoxin. Aflatoxins were found in 20% of random urine samples from heroin addicts in the U.K. and the Netherlands. Aflatoxins have also been incriminated in episodes of food poisoning which have been associated with serious morbidity and mortality, particularly among young children.

Adolescent↗

PubMed1976

Some interactions of light, riboflavin, and aflatoxin B1 in vivo and in vitro.

In previous studies, artificial sunlight and riboflavin synergistically increased acute aflatoxin toxicity in rats. Three new experiments were designed to provide information on the interaction of riboflavin, aflatoxin, and light. In a study of carcinogenesis, rats received low levels of aflatoxin 5 days/wk for 3 wk; 30 min after each dosing, half of them were irradiated for 2 hr. In some, levels of glucose-6-phosphatase and acid phosphatase were determined 5 days after completion of treatment. Remaining rats were killed at 30 or 53 wk. All underwent complete necropsies and histopathologic examination. In the second experiment, rats were dosed with riboflavin and divided into four groups: no further treatment; aflatoxin (LD50); irradiation (1-2 hr); or aflatoxin plus irradiation. Blood riboflavin levels were determined at intervals following these treatments. In the third experiment, the chemical reactions of irradated aflatoxin and/or riboflavin were studied by uv spectroscopy and TLC. The 53-wk study showed clearly that light decreased the incidence of aflatoxin-induced cancer. The other results may provide an explanation. Aflatoxin caused blood riboflavin levels to decrease-an effect enhanced by irradiation, suggesting that photosensitized riboflavin and aflatoxin form a complex. This interpretation gains support from studies in vitro that showed that riboflavin quenched aflatoxin photodegradation, perhaps by complexing with aflatoxin. Thus, low, carcinogenic doses of aflatoxin may complex with endogenous, photosensitized riboflavin, inhibiting its degradation into carcinogenic metabolites.

Aflatoxins↗

PubMed1995

Levels of aflatoxin-albumin biomarkers in rat plasma are modulated by both long-term and transient interventions with oltipraz.

The validation process for biomarkers to be used for monitoring the efficacy of preventive interventions in humans includes assessments of whether levels of the biomarker can be modulated in experimental models. From this perspective, the influence of two intervention protocols with the chemopreventive agent oltipraz on rates of formation and disappearance of aflatoxin-albumin adducts has been evaluated in rats chronically exposed to aflatoxin B1. Male F344 rats were treated daily with 20 micrograms aflatoxin B1, p.o. for 35 days. The first strategy employed a standard, long-term intervention in which basal AIN-76A diet was supplemented with 0.05% oltipraz beginning one week before AFB1 treatment and continuing throughout the period of carcinogen exposure. In this setting, treatment with oltipraz reduced the rate of formation of aflatoxin-albumin adducts such that steady-state levels were lowered by > 50% from control values of 400 pmol aflatoxin adducts/mg albumin. The time-course for reaching respective steady-state levels was unchanged, with or without oltipraz intervention. The second intervention strategy utilized a delayed, transient protocol in which oltipraz was fed for 2 weeks beginning 1 week after AFB1 dosing began and ending 2 weeks before AFB1 dosing was completed. This second strategy, which models clinical interventions in chronically exposed individuals, produced a steady decline in aflatoxin-albumin adduct levels that approached a 50% reduction by the end of the AFB1 exposure period. Development of smooth curve functions allowed for the estimation of the ratio of effects between the non-intervention and intervention groups as well as the simultaneous 90% confidence intervals for the aflatoxin-albumin adduct levels. These analyses indicated that long-term intervention with oltipraz produced a statistically significant reduction in levels of the aflatoxin-albumin biomarker at all times throughout aflatoxin exposure. By contrast, a statistically significant decrease in biomarker levels was not seen in the delayed, transient intervention protocol until the ninth day of the intervention. However, once achieved, significant differences from the control group were maintained for the remainder of the aflatoxin exposure period. These changes in aflatoxin biomarker levels are consistent with the cancer chemopreventive outcomes of these intervention protocols in rats. Collectively, these results support the utility of measuring this biomarker as a means for assessing the efficacy or chemopreventive interventions in individuals at high risk for aflatoxin exposure and development of hepatocellular carcinoma.

Aflatoxin B1↗

PubMed1985

Metabolism of aflatoxin B1 by rat hepatic microsomes induced by polyhalogenated biphenyl congeners.

The metabolism of aflatoxin B1 to aflatoxins M1 and Q1 by rat liver microsomes from animals pretreated with polychlorinated or polybrominated biphenyl congeners depended on the structure of the halogenated biphenyl inducers. Microsomes from rats treated with phenobarbital (PB) or halogenated biphenyls that exhibit PB-type activity preferentially enhanced the conversion of aflatoxin B1 to aflatoxin Q1. In contrast, microsomes from rats treated with 3-methylcholanthrene (MC) or halogenated biphenyls that exhibit MC-type induction activity increased the metabolism of aflatoxin B1 to aflatoxin M1. The coadministration of PB and MC produced microsomes that exhibited both types of induction activity (mixed type) in catalyzing the oxidative metabolism of diverse xenobiotic agents. However, PB-plus-MC-induced hepatic microsomes from immature male Wistar rats preferentially increased the metabolism of aflatoxin B1 to aflatoxin M1 but did not enhance the conversion of aflatoxin B1 to aflatoxin Q1. Comparable results were observed with microsomes from rats pretreated with halogenated biphenyls classified as mixed-type inducers; moreover, in some cases there was a significant decrease in the conversion of aflatoxin B1 to aflatoxin Q1 (compared with that of controls treated with corn oil).

Aflatoxins↗

PubMed1993

Cloning of the afl-2 gene involved in aflatoxin biosynthesis from Aspergillus flavus.

Aflatoxins are extremely potent carcinogens produced by Aspergillus flavus and Aspergillus parasiticus. Cloning of genes in the aflatoxin pathway provides a specific approach to understanding the regulation of aflatoxin biosynthesis and, subsequently, to the control of aflatoxin contamination of food and feed. This paper reports the isolation of a gene involved in aflatoxin biosynthesis by complementation of an aflatoxin-nonproducing mutant with a wild-type genomic cosmid library of A. flavus. Strain 650-33, blocked in aflatoxin biosynthesis at the afl-2 allele, was complemented by a 32-kb cosmid clone (B9), resulting in the production of aflatoxin. The onset and profile of aflatoxin accumulation was similar for the transformed strain and the wild-type strain (NRRL 3357) of the fungus, indicating that the integrated gene is under the same control as in wild-type strains. Complementation analyses with DNA fragments from B9 indicated that the gene resides within a 2.2-kb fragment. Because this gene complements the mutated afl-2 allele, it was designated afl-2. Genetic evidence obtained from a double mutant showed that afl-2 is involved in aflatoxin biosynthesis before the formation of norsolorinic acid, the first stable intermediate identified in the pathway. Further, metabolite feeding studies with the mutant, transformed, and wild-type cultures and enzymatic activity measurements in cell extracts of these cultures suggest that afl-2 regulates gene expression or the activity of other aflatoxin pathway enzymes. This is the first reported isolation of a gene for aflatoxin biosynthesis in A. flavus.

Aflatoxins↗

PubMed2002

Southwestern corn borer (Lepidoptera: Crambidae) damage and aflatoxin accumulation in maize.

Aflatoxin, a potent carcinogen, is produced by the fungus Aspergillus flavus Link: Fr. Drought, high temperatures, and insect damage contribute to increased levels of aflatoxin contamination in corn, Zea mays L. Plant resistance is widely considered a desirable method of reducing aflatoxin contamination. Germplasm lines with aflatoxin resistance have been developed. This investigation was undertaken to determine whether crosses among these lines exhibited resistance to southwestern corn borer, Diatraea grandiosella Dyar, and to assess the effects of southwestern corn borer feeding on aflatoxin accumulation. Differences in ear damage among southwestern corn borer infested hybrids were significant. Estimates of general combining ability effects indicated that the lines Mp80:04, Mp420, and Mp488 contributed to reduced ear damage, and SC213 and T165 contributed to greater damage when used in hybrids. Mean aflatoxin levels were 254 ng/g for hybrids infested with southwestern corn borer larvae and 164 ng/g for noninfested hybrids in 2000 when environmental conditions were conducive to aflatoxin production. In contrast, the overall mean aflatoxin level for southwestern corn borer infested hybrids was only 5 ng/g in 1999 when environmental conditions did not favor aflatoxin accumulation. Crosses that included lines selected for aflatoxin resistance as parents (Mp80:04 and Mp313E) exhibited lower levels of aflatoxin contamination both with and without southwestern corn borer infestation in 2000. Only the experimental line Mp80:04 contributed significantly to both reduced southwestern corn borer damage and reduced aflatoxin contamination.

Aflatoxins↗