SEARCH · PubMed Health

Results for “Aflatoxin”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources

PubMed2004

Aflatoxin biosynthesis cluster gene cypA is required for G aflatoxin formation.

Aspergillus flavus isolates produce only aflatoxins B1 and B2, while Aspergillus parasiticus and Aspergillus nomius produce aflatoxins B1, B2, G1, and G2. Sequence comparison of the aflatoxin biosynthesis pathway gene cluster upstream from the polyketide synthase gene, pksA, revealed that A. flavus isolates are missing portions of genes (cypA and norB) predicted to encode, respectively, a cytochrome P450 monooxygenase and an aryl alcohol dehydrogenase. Insertional disruption of cypA in A. parasiticus yielded transformants that lack the ability to produce G aflatoxins but not B aflatoxins. The enzyme encoded by cypA has highest amino acid identity to Gibberella zeae Tri4 (38%), a P450 monooxygenase previously shown to be involved in trichodiene epoxidation. The substrate for CypA may be an intermediate formed by oxidative cleavage of the A ring of O-methylsterigmatocystin by OrdA, the P450 monooxygenase required for formation of aflatoxins B1 and B2.

Aflatoxins↗

PubMedDate not supplied

Binding reaction of aflatoxin B1 with immunoglobulin G against aflatoxin B1-bovine serum albumin complex.

Polyclonal immunoglobulin G antibodies were raised against aflatoxin B1-bovine serum albumin complex and characterised. Antibodies against the complex were obtained after a single intradermal multiple site injection of water in oil emulsion of the complex into adult female albino rabbits. Equilibrium dialysis and Scatchard plot analysis of the interaction of the antibodies with aflatoxin B1 showed that the antibodies have high affinity for binding aflatoxin B1. The average number of binding sites on the antibody molecules for aflatoxin B1 is 1.74 +/- 0.20 with mean standard free energy change (delta F1(0) of -23.10 KJ/mol, while the average association constant is 2.35 +/- 0.73 x 10(-4)M-1. Male wistar strain albino rats after immunization with the complex showed lower mortality when challenged with a single dose of aflatoxin B1. The results suggest that such antibodies with high affinity for aflatoxin B1 could be used in the immunointerception of the toxin.

Aflatoxin B1↗

PubMed1979

Metabolism of aflatoxin B1 and identification of the major aflatoxin B1-DNA adducts formed in cultured human bronchus and colon.

Aflatoxin B1 and benzo(a)pyrene were activated by both cultured human bronchus and human colon as measured by binding to cellular DNA and protein. The binding of aflatoxin B1 to DNA was dose dependent, and the level of binding was higher in cultured human bronchus than it was in the colon. When compared to aflatoxin B1, the binding level of benzo(a)pyrene to both bronchial and colonic DNA was generally higher. The major adducts formed in both tissues by the interaction of aflatoxin B1 and DNA were chromatographically identical to 2,3-dihydro-2-(N7-guanyl)-3-hydroxyaflatoxin B1 (Structure 1) with the guanyl group and hydroxy group in trans-position and an adduct which has been tentatively identified by other investigators as 2,3-dihydro-2-(N5-formyl-2',5',6'-triamino-4'-oxo-N5-pyrimidyl)-3-hydroxyaflatoxin B1 (Structure 11). Seventy % of the radioactivity associated with bronchial DNA was found in these two peaks, and the ratio of radioactivity between the peaks was nearly 1. In colonic DNA, the ratio between Structures 1 and 11 was approximately 2. These observations add aflatoxin B1 to the list of chemical procarcinogens metabolized by cultured human tissues and in which the carcinogen-DNA adducts are similar to the adducts formed in animal tissue susceptible to the carcinogenic action of aflatoxin B1.

Aflatoxins↗

PubMed1985

Aflatoxin and aflatoxicosis: V. The kinetic behaviour of dietary aflatoxins in colostrum drawn from cows postpartum.

This work was conducted in order to study the kinetic behaviour of dietary aflatoxins in the colostrum of a pregnant cow exposed to contaminated feeds for a short period. In this study, two pregnant cows received a single dose of dietary aflatoxins in the form of rice powder contained 31.20 ppm aflatoxin B and 19.68 ppm aflatoxin G during the last stage of pregnancy, at about two weeks before parturition. Samples of colostrum were collected from dams and assayed for the presence of toxic metabolites as well as its conjugations by electrophoretic analysis. The results revealed that the intake of aflatoxins appeared in the colostrum postpartum as AFM1 and also AFB2a which is a non toxic metabolite. Moreover, it was found that the excreted metabolites including AFB2a were conjugated to the immunoglobulin protein fraction of the colostrum. The significance of the obtained results to the newborn calf are discussed.

Aflatoxins↗

PubMedDate not supplied

Effect of antiserum against aflatoxin B1-bovine serum albumin complex on aflatoxin B1-induced lysogenesis.

Escherichia coli K12 bacteria lysogenic for the lambda phage were used to study the effect of antiserum against aflatoxin B1-induced lysogenesis. The antiserum was obtained from rabbits immunized with water in oil emulsion of aflatoxin B1-bovine serum albumin complex (AFB1-BSA). A marked reduction in the degree of lysogenesis was observed when the antiserum was added to the reaction medium prior to microsomal enzyme activation of aflatoxin B1. There was no detectable effect when the antiserum was added after aflatoxin B1 activation. The result presented suggests that the antibodies in the AFB1-BSA antiserum can interact with aflatoxin B1 prior to its activation. This implies that an immune-protective effect can only be exerted if the antibodies intervene before activation.

Aflatoxin B1↗

PubMed2006

Determinants of aflatoxin levels in Ghanaians: sociodemographic factors, knowledge of aflatoxin and food handling and consumption practices.

Aflatoxins are among the most potent of carcinogens found in staple foods such as groundnuts, maize and other oil seeds. This study was conducted to measure the levels of aflatoxin B(1) (AFB(1)) albumin adducts in blood and aflatoxin M(1) (AFM(1)) metabolite in urine of people in a heavy peanut and maize consuming region of Ghana and to examine the association between aflatoxin levels and several socio-demographic factors and food handling and consumption practices. A cross-sectional study was conducted in four villages in the Ejura Sekyedumase district of Ghana. A socio-demographic survey was administered to 162 participants. Blood samples were collected from 140 and urine samples from 91 of the participants and AFB(1) albumin-adduct levels in blood and AFM(1) levels in urine were measured. High AFB(1) albumin-adduct levels were found in the plasma (mean+/-SD=0.89+/-0.46pmol/mg albumin; range=0.12-3.00pmol/mg; median=0.80pmol/mg) and high AFM(1) levels in the urine (mean+/-SD=1,800.14+/-2602.01pg/mg creatinine; range=non-detectable to 11,562.36pg/mg; median=472.67pg/mg) of most of the participants. There was a statistically significant correlation (r=0.35; p=0.007) between AFB(1)-albumin adduct levels in plasma and AFM(1) levels in urine. Several socio-demographic factors, namely, educational level, ethnic group, the village in which participants lived, number of individuals in the household, and number of children in the household attending secondary school, were found to be significantly associated with AFB(1) albumin-adduct levels by bivariate analysis. By multivariate analyses, ethnic group (p=0.04), the village in which participants live (p=0.02), and the number of individuals in the household (p=0.01), were significant predictors of high AFB(1) albumin-adducts. These findings indicate strongly that there is need for specifically targeted post-harvest and food handling and preparation interventions designed to reduce aflatoxin exposure among the different ethnic groups in this region of Ghana.

Aflatoxin B1↗

PubMed1993

Molecular epidemiology of aflatoxin exposures: validation of aflatoxin-N7-guanine levels in urine as a biomarker in experimental rat models and humans.

Human epidemiology and experimental animal data have provided the statistical association and biological information necessary to propose that aflatoxins are risk factors for human liver cancer. As liver cancer causes at least 200,000 deaths per year, prevention measures must be developed to ameliorate this nearly always fatal disease. Preventive strategies will be facilitated by the identification of individuals at high risk. It is the goal of the molecular dosimetry field to provide facile and accurate biomarkers to identify people at high risk for carcinogen exposure and consequent adverse health effects. We have developed methods to defect the major aflatoxin DNA adduct, aflatoxin N7-guanine (AFB-N7-guanine), in urine, examined the dose-response characteristics in people living in China and The Gambia, and have found an excellent association of this biomarker with exposure. In addition to exposure studies in people, our laboratories have monitored AFB-N7-guanine excretion in the urine of rats whose risk for developing cancer has been modulated with dietary chemoprotective agents such that independent groups of animals receiving the same dosage of aflatoxin B1 were at either high or low risk for tumorigenesis. The production of DNA damage by aflatoxins is not the exclusive mechanism for liver cancer. Many other factors, including hepatitis B virus, cell proliferation, and nutritional status, can exert strong modification effects in human disease. Thus, molecular epidemiological investigations that examine only one biomarker may greatly underestimate or overestimate the risk for an individual.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1984

Synthesis and degradation of aflatoxins by Aspergillus parasiticus. I. Synthesis of aflatoxin B1 by young mycelium and its subsequent degradation in aging mycelium.

Aflatoxin production and degradation were examined in three isolates of A. parasiticus. Maximum yields were present after incubation for 14 days and these declined gradually as the culture aged. Young mycelia (4 days old) synthesized the greatest amounts of aflatoxin, but aging mycelia (14 days old) were mainly responsible for degradation. Addition of cycloheximide to young cultures and removal of mycelia from aging cultures both prevented further aflatoxin degradation. Intramycelial substances released from fragmented or homogenized mycelium were capable of degrading aflatoxins, and their concentration increased as the mycelium aged. When 14C-labelled aflatoxin was added to a 2-day-old culture and further incubated, 75% of the radioactivity at 12 days was intramycelial, but at 20 days, most radioactivity was in the filtrate.

Aflatoxin B1↗

PubMed1989

Aflatoxins in sunflower seeds: influence of Alternaria alternata on aflatoxin production by Aspergillus parasiticus.

The aim of the present work was to determine the influence of Alternaria alternata upon aflatoxin production by Aspergillus parasiticus. A mixture of spores of both strains was inoculated in sunflower seeds at 0.90 aw and incubated for 42 days at 28 degrees C +/- 1. The cultures were observed and analyzed every 7 days to determine the infection level of the seeds and the production of aflatoxins. Results showed that when the seeds were inoculated only with Aspergillus parasiticus, 100% were infected from the 7th day. When Aspergillus parasiticus and Alternaria alternata were simultaneously inoculated the infection level of the seeds was 100% for Aspergillus parasiticus following 7 days of inoculation and 0% for Alternaria alternata. After the 14th day of inoculation there was no significant difference in the infection percentage of both strains (approximately 80% of each one). As far as toxin production is concerned a remarkable decrease was observed when seeds were inoculated with both strains simultaneously. In accordance to the results, Alternaria alternata would not compete with Aspergillus parasiticus in colonization of seeds but would either degrade the aflatoxins by Aspergillus parasiticus or compete for aflatoxin biosynthesis precursors. Alternaria alternata could also secrete some substance that specifically inhibits aflatoxin synthesis.

Aflatoxins↗

PubMed1982

Aflatoxin and aflatoxicosis. II. Effects of aflatoxin on ovaries and testicles in mature domestic fowls.

The present study aimed at: 1. Examination of commercial chicken and duck eggs for the possible presence of aflatoxins. 2. Study of the sex susceptibility of mature chickens when fed on ration containing aflatoxins. 3. Study of clinicopathological effects on their ovaries and testicles. In this investigation, 100 chicken and 50 duck eggs collected from markets in the vicinity of Assiut Governorate, were examined individually for the presence of aflatoxins in the whites and yolks. The study revealed that the examined eggs contained no aflatoxins. Experimentally, aflatoxin BV(8.1 ppm) and G. (1.6 ppm) were incorporated into the feed of five laying hens and five mature cooks for three weeks duration. The layers showed cessation of egg production during the whole feeding period. Histopathological examinations revealed that, the ovaries showed follicular atresia while testicles were normal. It was shown that, aflatoxicosis cause pathological changes in the chicken ovaries, which has a detrimental effect on egg production.

Aflatoxins↗

PubMed1982

Aflatoxin and aflatoxicosis. III. Effect of dietary aflatoxin on the morphology of buffalo bull spermatozoa.

The main aim of this study was to determine the effect of aflatoxin on male reproduction by exposure to fodders contaminated by moulds producing toxins as a natural environmental contaminants. Semen was collected from three normal healthy buffalo bulls every ten days for one month before adding the toxin and examined for livability percentages. Moldy rice containing aflatoxin B and G was incorporated into the ration of the studied bulls in a daily amount of 2.0, 3.0 and 4.0 gm respectively for each bull for two weeks. Each gramme of the rice powder contained 15.6 ppm aflatoxin B and 9.84 ppm aflatoxin G as determined spectrophotometrically. Semen was collected in the middle of the two weeks experimental period. Moreover, one week, one month and two months later, semen was collected again and examined for the same parameters. The results showed marked decrease in the alive percentage of spermatozoa from 91.11% to 80.8% after the addition of aflatoxin. Moreover, a very high increase in the sperm abnormalities up to 54% was recorded.

Aflatoxins↗

PubMed2004

aflT, a MFS transporter-encoding gene located in the aflatoxin gene cluster, does not have a significant role in aflatoxin secretion.

The aflT gene resides between the polyketide synthase gene pksA and the P450-encoding cypA gene in the aflatoxin gene cluster of Aspergillus parasiticus. It is a single copy gene in the genome of A. parasiticus SRRC 2043 and SU-1 and was also found at the same relative position in the genome of Aspergillus flavus isolates. The predicted AFLT protein contained 14 transmembrane domains and had various degrees of the amino acid identity (34-56%) to fungal transporters belonging to the major facilitator superfamily. Targeted deletion of aflT in A. parasiticus SU-1 yielded transformants that were morphologically similar to SU-1. These aflT-deleted mutants produced and secreted aflatoxins comparable to the parental strain although they lost the production of the aflT transcript. Real-time RT-PCR analysis showed that the expression of aflT was controlled neither by the aflatoxin pathway-specific activator AFLR nor by the co-activator AFLJ, which differed from the regulation of the aflatoxin biosynthetic genes pksA, nor1, ver1, and omtA. The FadA-dependent G-protein signaling pathway previously shown to govern aflatoxin biosynthesis and sporulation plays a role in the regulation of aflT expression.

Aflatoxins↗

PubMed1990

Risk assessment for aflatoxin: I. Metabolism of aflatoxin B1 by different species.

A comparison of the generation and detoxification of reactive aflatoxin B1 metabolites in different species may elucidate why animal species vary widely in sensitivity to aflatoxin B1 carcinogenicity, in addition to offering some perspective on how sensitive man may be to the carcinogenic effects of this mycotoxin. Scientific literature comparing the ability of cellular fractions from different species to metabolize aflatoxin B1 is reviewed. However, in vitro studies exclude components for multiple metabolic pathways, eliminating the possibility of competition between metabolic activation and detoxification. Quantification of metabolic activation by different species from these studies is therefore limited. The species-specific carcinogenic potency of aflatoxin B1 may be reflected in levels of aflatoxin B1-DNA adducts generated in vivo. The current paucity of quantitative information on human DNA adduct levels does not permit comparisons between different species on this basis.

Aflatoxins↗

PubMed2006

The aflatoxin pathway regulator AflR induces gene transcription inside and outside of the aflatoxin biosynthetic cluster.

Aflatoxin contamination of food and feed is a major concern due to the carcinogenic properties of this mycotoxin. Previous studies using classical approaches have identified a cluster of genes responsible for aflatoxin production under the control of the pathway-specific transcriptional regulator aflR, but it is unknown whether aflR controls expression of other genes within the genome. Transcription profiling comparing wild type and DeltaaflR strains of Aspergillus parasiticus grown under conditions conducive for aflatoxin production identified only 23 upregulated genes in the wild type. These included 20 genes in the aflatoxin biosynthetic cluster, and three additional genes outside the aflatoxin biosynthetic cluster (nadA, hlyC, and niiA), all with AflR binding sites. This report is the first to demonstrate genes outside the biosynthetic cluster as being associated with aflR expression.

Aflatoxins↗

PubMed1996

Identification of aflatoxin biosynthesis genes by genetic complementation in an Aspergillus flavus mutant lacking the aflatoxin gene cluster.

Aspergillus flavus mutant strain 649, which has a genomic DNA deletion of at least 120 kb covering the aflatoxin biosynthesis cluster, was transformed with a series of overlapping cosmids that contained DNA harboring the cluster of genes. The mutant phenotype of strain 649 was rescued by transformation with a combination of cosmid clones 5E6, 8B9, and 13B9, indicating that the cluster of genes involved in aflatoxin biosynthesis resides in the 90 kb of A. flavus genomic DNA carried by these clones. Transformants 5E6 and 20B11 and transformants 5E6 and 8B9 accumulated intermediate metabolites of the aflatoxin pathway, which were identified as averufanin and/or averufin, respectively. These data suggest that avf1, which is involved in the conversion of averufin to versiconal hemiacetal acetate, was present in the cosmid 13B9. Deletion analysis of 13B9 located the gene on a 7-kb DNA fragment of the cosmid. Transformants containing cosmid 8B9 converted exogenously supplied O-methylsterigmatocystin to aflatoxin, indicating that the oxidoreductase gene (ord1), which mediates the conversion of O-methylsterigmatocystin to aflatoxin, is carried by this cosmid. The analysis of transformants containing deletions of 8B9 led to the localization of ord1 on a 3.3-kb A. flavus genomic DNA fragment of the cosmid.

Aflatoxins↗

PubMed2000

Reduction of aflatoxins by Korean soybean paste and its effect on cytotoxicity and reproductive toxicity--part 1. Inhibition of growth and aflatoxin production of Aspergillus parasiticus by Korean soybean paste (Doen-jang) and identification of the active component.

The inhibitory effect of methanol extract of Korean soybean paste on the mold growth and aflatoxin production of a toxigenic strain of Aspergillus parasiticus ATCC 15517 was studied using different concentrations of the extract in yeast-extract sucrose broth. While inhibition in mold growth due to increasing the concentration of the extract was observed, the more remarkable effect was the inhibition of aflatoxin production. Reduction of mycelial weight as a result of addition of the extract was observed to range between 1.5 to 12.9% while reduction of aflatoxin production quantified by high-performance liquid chromatography ranged from 14.3 to 41.7%. Five percent of the extract significantly reduced aflatoxin production at the end of the incubation period (P < 0.05), although the effect on mycelial growth was less pronounced. This study indicates that soybean paste could also be an effective inhibitor of aflatoxin production even though mycelial growth may be permitted. The main active component identified by gas chromatography-mass spectroscopy was linoleic acid.

Aflatoxins↗

PubMedDate not supplied

Testing shelled corn for aflatoxin, Part II: modeling the observed distribution of aflatoxin test results.

The suitability of several theoretical distributions to predict the observed distribution of aflatoxin test results in shelled corn was investigated. Fifteen positively skewed theoretical distributions were each fitted to 18 empirical distributions of aflatoxin test results for shelled corn. The compound gamma distribution was selected to model aflatoxin test results for shelled corn. The method of moments technique was chosen to estimate the parameters of the compound gamma distribution. Mathematical expressions were developed to calculate the parameters of the compound gamma distribution for any lot aflatoxin concentration and test procedure. Observed acceptance probabilities were compared to operating characteristic curves predicted from the compound gamma distribution, and all 18 observed acceptance probabilities were found to lie within a 95% confidence band. The parameters of compound gamma were used to calculate the fraction of aflatoxin-contaminated kernels in contaminated lots. At 20 ppb, it was estimated that about 6 in 10,000 kernels are contaminated.

Aflatoxins↗

PubMedDate not supplied

Testing shelled corn for aflatoxin, Part III: evaluating the performance of aflatoxin sampling plans.

The effects of changes in sample size and/or sample acceptance level on the performance of aflatoxin sampling plans for shelled corn were investigated. Six sampling plans were evaluated for a range of sample sizes and sample acceptance levels. For a given sample size, decreasing the sample acceptance level decreases the percentage of lots accepted while increasing the percentage of lots rejected at all aflatoxin concentrations, and decreases the average aflatoxin concentration in lots accepted and lots rejected. For a given sample size where the sample acceptance level decreases relative to a fixed regulatory guideline, the number of false positives increases and the number of false negatives decreases. For a given sample size where the sample acceptance level increases relative to a fixed regulatory guideline, the number of false positives decreases and the number of false negatives increases. For a given sample acceptance level, increasing the sample size increases the percentage of lots accepted at concentrations below the regulatory guideline while increasing the percentage of lots rejected at concentrations above the regulatory guideline, and decreases the average aflatoxin concentration in the lots accepted while increasing the average aflatoxin concentration in the rejected lots. For a given sample acceptance level that equals the regulatory guideline, increasing the sample size decreases misclassification of lots, both false positives and false negatives.

Aflatoxins↗