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 1,081 records · Page 60Linked to original sources

PubMed1987

Degradation of aflatoxin by Aspergillus flavus.

Aflatoxin degradative activity was demonstrated in 6- to 12-d-old intact mycelium and cell-free extracts of Aspergillus flavus. The addition of cycloheximide, SKF 525-A or metyrapone to cultures of A. flavus prevented subsequent degradation of the aflatoxins, while in cell-free extracts degradation was inhibited by SKF 525-A, metyrapone and cytochrome c but not by KCN. In cell-free extracts, aflatoxin degradation was enhanced by NADPH and NaIO4. The results suggest the involvement of cytochrome P-450 monooxygenases in the aflatoxin degradative activity of A. flavus.

Aflatoxin B1↗

PubMed1986

Drug resistance patterns and susceptibility to aflatoxin B1 of strains of Escherichia coli and Staphylococcus aureus.

The antibacterial properties of aflatoxin B1 have been evaluated against antibiotic-resistant clinical isolates of Escherichia coli and Staphylococcus aureus. The inhibition of growth ranged from 11.5 to 60.0% and 4.5 to 18.5% in the strains of S. aureus and E. coli, depending on the extent of drug resistance. Aflatoxin-B1 binding varied with toxin concentration, the presence of surfactants (Tween-80 or EDTA) as well as with the antibiotic-resistance pattern; binding was maximal in antibiotic-sensitive strains and least in the most resistant strains. Binding of aflatoxin B1, correlated with growth inhibition. Aflatoxin B1 also caused leakage of cell contents and decrease in inulin uptake, effects which were also concentration dependent.

Aflatoxin B1↗

PubMed1982

Occurrence of aflatoxins in oilseeds providing cocoa-butter substitutes.

Four oilseeds providing cocoa-butter substitutes--shea, pentadecima, illipe, and salseed--when tested as substrates for aflatoxin production by two strains of Aspergillus parasiticus, gave varying levels of aflatoxin. Aflatoxins were found at low levels occurring naturally in moldy shea-nuts, but none of 21 commercial shea-nut samples contained greater than 20 micrograms of aflatoxin B1 per kg.

Aflatoxin B1↗

PubMed1984

Aspergillus parasiticus growth and aflatoxin production on black and white pepper and the inhibitory action of their chemical constituents.

Aspergillus parasiticus Speare NRRL 2999 growth and aflatoxin production in black and white pepper and the penetration of the fungus in black pepper corn over various incubation periods were studied. Also, the effects of piperine and pepper oil on growth and aflatoxin production were studied. Under laboratory conditions, black and white pepper supported aflatoxin production (62.5 and 44 ppb (ng/g), respectively) over 30 days of incubation. Fungal growth measured in terms of chitin was considerably less in white pepper than in black pepper. A histological study of black pepper corn showed the fungus penetrating up to the inner mesocarp and establishing itself in the middle mesocarp. Piperine and pepper oil were found to inhibit fungal growth and toxin production in a dose-dependent manner. Thus, both black and white pepper could be considered as poor substrates for fungal growth and aflatoxin production.

Aflatoxin B1↗

PubMed1985

Mechanism of action of aflatoxin B1 in Bacillus megaterium.

Bacillus megaterium cells from various growth phases were equally susceptible to the lethal effects of aflatoxin B1. Known surfactants (EDTA and Tween-80) accentuated the effects of aflatoxin B1. Viability and inulin uptake in aflatoxin B1-exposed cells decreased considerably. The effect was concentration dependent. A straight-line relationship observed in the death curve indicated a single target for aflatoxin B1 action in B. megaterium. Leakage of intracellular constituents in B. megaterium was also concentration dependent, and this can be related to the extent of cell membrane damage.

Aflatoxin B1↗

PubMed1987

Averufanin is an aflatoxin B1 precursor between averantin and averufin in the biosynthetic pathway.

Wild-type Aspergillus parasiticus produces, in addition to the colorless aflatoxins, a number of pigmented secondary metabolites. Examination of these pigments demonstrated that a major component was an anthraquinone, averufanin. Radiolabeling studies with [14C]averufanin showed that 23% of the label was incorporated into aflatoxin B1 by the wild type and that 31% of the label was incorporated into O-methylsterigmatocystin by a non-aflatoxin-producing isolate. In similar studies with blocked mutants of A. parasiticus the 14C label from averufanin was accumulated in averufin (72%) and versicolorin A (54%) but not averantin. The results demonstrate that averufanin is a biosynthetic precursor of aflatoxin B1 between averantin and averufin.

Aflatoxin B1↗

PubMed1988

Presence of aflatoxin M1 in commercial ultra-high-temperature-treated milk.

Forty-seven samples of commercial ultra-high-temperature-treated milk from a dairy facility in the northwest part of Spain were analyzed for the presence of aflatoxin M1. A total of 14 samples (29.8%) were positive for aflatoxin M1 (4 in May, 3 in November, 3 in December, 1 in January, 1 in April, 1 in July, and 1 in August), 29 (61.7%) were negative, and 4 (8.5%) were doubtful, i.e., they showed trace quantities of aflatoxin M1. The range of aflatoxin M1 content was 0.02 to 0.1 ng/ml.

Aflatoxin M1↗

PubMed1988

Biosynthetic relationship among aflatoxins B1, B2, G1, and G2.

Aspergillus parasiticus NIAH-26, a UV-irradiated mutant of A. parasiticus SYS-4 (NRRL 2999), produces neither aflatoxins nor precursors. When sterigmatocystin (ST) or O-methylsterigmatocystin was fed to this mutant in YES medium, aflatoxins B1 (AFB1) and G1 (AFG1) were produced. When dihydrosterigmatocystin (DHST) or dihydro-O-methylsterigmatocystin was fed to this mold, aflatoxins B2 (AFB2) and G2 (AFG2) were produced. The reactions from ST to AFB1 and DHST to AFB2 were also observed in the cell-free system and were catalyzed stepwise by the methyltransferase and oxidoreductase enzymes. In the feeding experiments of strain NIAH-26, the convertibility from ST to AFB1-AFG1 was found to be remarkably suppressed by the coexistence of DHST in the medium, and the convertibility from DHST to AFB2-AFG2 was also suppressed by the presence of ST. When some other mutants which endogenously produce a small amount of aflatoxins (mainly AFB1 and AFG1) were cultured with DHST, the amounts of AFB1 and AFG1 produced were significantly decreased, whereas AFB2 and AFG2 were newly produced. In similar feeding experiments in which 27 kinds of mutants including these mutants were used, most of the mutants which were able to convert exogenous ST to AFB1-AFG1 were also found to convert exogenous DHST to AFB2-AFG2. These results suggest that the same enzymes may be involved in the both biosynthetic pathways from ST to AFB1-AFG1 and DHST to AFB2-AFG2. The reactions described herein were not observed when the molds had been cultured in the YEP medium.

Aflatoxin B1↗

PubMed1998

Characterization of aflJ, a gene required for conversion of pathway intermediates to aflatoxin.

The genes encoding the aflatoxin biosynthetic pathway enzymes have been localized as a cluster to a 75-kb DNA fragment. The enzymatic functions of the products of most of the genes in the cluster are known, but there are a few genes that have not yet been characterized. We report here the characterization of one of these genes, a gene designated aflJ. This gene resides in the cluster adjacent to the pathway regulatory gene, aflR, and the two genes are divergently transcribed. Disruption of aflJ in Aspergillus flavus results in a failure to produce aflatoxins and a failure to convert exogenously added pathway intermediates norsolorinic acid, sterigmatocystin, and O-methylsterigmatocystin to aflatoxin. The disrupted strain does, however, accumulate pksA, nor-1, ver-1, and omtA transcripts under conditions conducive to aflatoxin biosynthesis. Therefore, disruption of aflJ does not affect transcription of these genes, and aflJ does not appear to have a regulatory function similar to that of aflR. Sequence analysis of aflJ and its putative peptide, AflJ, did not reveal any enzymatic domains or significant similarities to proteins of known function. The putative peptide does contain three regions predicted to be membrane-spanning domains and a microbodies C-terminal targeting signal.

Aflatoxin B1↗

PubMed1981

Prevention by estradiol of aflatoxin-induced cytotoxicity in cultured chick embryo liver cells.

Aflatoxin B1 at a final concentration of 10(-5) M depressed the sytheses of DNA, RNA and protein in cultured chick embryo liver cells. The same dose produced ultrastructural changes in the nucleus, such as nucleolar compactness or segregation of fibrillar and granular components and in the cytoplasmic area, such as vesiculation, dilatation or degranulation of endoplasmic meticulum. These acute toxic effects of aflatoxin B1 were partially decreased by an addition of 4 X 10(-5) M estradiol-17 beta. Namely estradiol-17 beta significantly reduced the nucleolar compactness and segregation of fibrillo-granular components but did not improve the vesiculation, dilatation and degranulation of endoplasmic reticulum. Estradiol-17 beta also protected the liver cells from the aflatoxin B1-induced inhibition of nucleic acid and protein synthesis. These results suggest that the protective effect of estradiol-17 beta against the acute hepatotoxicity of aflatoxin B1 is mainly due to an antagonistic interaction of both compounds on the synthesis of nucleic acid in nucleolus.

Aflatoxin B1↗

PubMed1987

Strain differences in the metabolic activation of aflatoxin B1 in the rat.

It has been reported that female Fischer rats are much more susceptible to the hepatocarcinogenic effects of aflatoxin B1 than female DA rats. Female Fischer rats are approximately twice as active as female DA rats in producing adducts of aflatoxin B1 with DNA in vivo, in freshly isolated hepatocytes and with hepatic microsomal fractions. There was no difference between the hepatic microsomal fractions from Fischer and DA rats in the production of adducts between aflatoxin B1 and microsomal protein. The difference between the strains in the formation of adducts with DNA was not due to either the activity of glutathione S-transferases or to the selective destruction of cytochrome P-450 in the DA strain. None of the differences reported here was of sufficient magnitude to explain the difference in susceptibility of the rat strains to the hepatocarcinogenic effects of aflatoxin B1.

Aflatoxin B1↗

PubMed1991

Effect of subchronic aflatoxin exposure on growth and progression of Ehrlich's ascites tumor in mice.

The present investigation was undertaken to assess whether aflatoxin B1 (AFB1) has any modulatory effect on the growth and progression of Ehrlich's ascites tumor (EAT) in mice or not. Male Swiss albino mice were treated with 0, 70, 350 and 700 micrograms AFB1/kg body weight in 0.2 ml corn oil on alternate days, orally, for two weeks. Treated animals were challenged with 1 x 10(6) cells of Ehrlich's ascites tumor. Animals were monitored for the appearance of palpable tumor, body weight gain as a measure of tumor burden, mortality profile and tumor cell population. Some parameters of cell mediated immunity (CMI), humoral immunity and non-specific immunity were also studied in aflatoxin treated animals in order to find out the mechanism of action of AFB1 on host immunity. It was observed that AFB1 treatment resulted in an early appearance of tumor, enhanced mortality, appreciable increase in body weight gain and EAT cell population following tumor challenge, in comparison with the control animals. Aflatoxin treatment caused suppression of CMI including an impairment of macrophage function, while humoral immunity was not much affected. It may be concluded that impaired CMI and macrophage function might be contributing to the increased growth of EAT in the AFB1 treated animals. Our findings may be relevant in that when a host is exposed to aflatoxins concomitantly with other carcinogens and cancer causing situations.

Aflatoxin B1↗

PubMed1981

Aflatoxin M1 in manufactured dairy products produced in the United States in 1979.

In a 1979 survey of manufactured dairy products (992 samples of nonfat dry milk, vanilla ice cream, yogurt, Cheddar cheese, and cottage cheese) for aflatoxin M1 contamination, one sample, a cottage cheese, had detectable aflatoxin equivalent to .08 ng/ml in the milk from which the product was made. Samples were taken by Food and Drug District inspectors from randomly selected establishments at three times throughout the year. The distribution of sample quotas to each District was weighted to double the representation of establishments in the southern tier of states. The conclusion from this survey is that in a "normal" year aflatoxin M1 should not be in a manufactured dairy product in the United States at a level in excess of that from milk with .1 ng aflatoxin M1/ml.

Aflatoxin M1↗

PubMed1985

Effect of purified aflatoxin on turkeys.

Purified aflatoxin B1 (AFB1) or AFB1 plus aflatoxin B2 (AFB2) was given daily for 5 weeks in gelatin capsules to 2-week-old Nicholas X Nicholas turkeys. In Experiment 1, pure AFB1 was given in dosages equivalent to the quantity of toxin received if diets containing either 0, 200, 500, or 1000 ppb of AFB1 were consumed. In Experiment 2, either pure AFB1 or AFB1 plus AFB2 was given in capsules equal to the quantity of toxin received if a diet containing either 0, 100, 150, or 200 ppb of AFB1 was consumed. In Experiment 1, pure AFB1 administered by capsule equal to 500 and 1000 ppb was highly toxic and by the second week, it resulted in 100% morbidity, mortality, and gross and microscopic lesions. Aflatoxin B1 at 200 ppb caused none of these changes. However, it did cause a significant depression in feed conversion, but not weight gain, during all weeks and also a reduction in cell-mediated immunity (CMI) as measured by a delayed hypersensitive skin test to mycobacterium. Results in Experiment 2 were similar to the first. Aflatoxin B1 and AFB1 plus AFB2 as high as 200 ppb resulted in no morbidity, mortality, or gross or microscopic lesions. Also, no significant reductions in either weight gain or feed conversion were evident in any level of either AFB1 or AFB1 plus AFB2. However, numerical, but not statistically significant, dose-related reductions in all CMI tests were noted in birds receiving either AFB1 or AFB1 plus B2 at as low as 100 ppb.

Administration, Oral↗

PubMedDate not supplied

Determination of aflatoxins in grains and raw peanuts by a rapid procedure with fluorometric analysis.

A rapid, quantitative, inexpensive, and efficient method was developed to determine aflatoxins in corn, corn meal, popcorn, rice, wheat, cottonseed, and peanuts. Samples are ground and extracted with methanol-water (80 + 20). A portion of the extract is cleaned up by passage through a solid-phase separatory column, 500 microL purified extract is derivatized with a bromine reagent, and fluorescence of the solution is immediately quantified with a calibrated fluorometer containing a broad wavelength pulsed xenon light source. This method can quantify aflatoxin from 5 to 5000 ppb without dilution and was linear when applied to samples of noncontaminated corn spiked at 0 to 5000 micrograms aflatoxin B1/g. Correlation coefficients of the method with LC for multiple analyses for corn (n = 34), cottonseed (n = 32), and peanuts (n = 11) were 0.999, 0.995, and 0.980, respectively. Individual analyses may be conducted in less than 5 min, and grouping of samples is unnecessary. The sensitivity of the method for corn is 5 ppb and the fluorometer, under the operating conditions, has a limit of detection of 0.6 ng aflatoxin B1.

Aflatoxin B1↗

PubMed1999

[Aflatoxins in food: tests of decontamination of peanut cakes by ionizing treatment].

The efficacy of ionising treatment for decontaminating peanut cakes was tested. The influence of cakes water content and the effect of ionisation dose rate were studied. The results obtained after a reverse phase liquid chromatographic determination of B1, B2, G1 and G2 aflatoxins have revealed an important contamination of the peanut cakes (up to 1000 ppb of total aflatoxin's contents). After ionising treatment at 25 kGy, the aflatoxins degradation in peanut cake's was less important in dried samples (about 5-10% at 0.55 water activity: aw) than in the humid ones (40-60% degradation at 0.95 water activity). At this dose, any indicative difference of the degradation rate of aflatoxins, with regard to the ionising process was observed. The efficacy of ionising treatment for decontaminating peanut cakes could probably be improved, however the economic interest of such process as alternative of the treatment with ammonia is questionable.

Aflatoxin B1↗

PubMedDate not supplied

Liquid chromatographic analysis of aflatoxin using post-column photochemical derivatization: collaborative study.

Aflatoxin analysis, with post-column derivatization using a photochemical reactor for enhanced detection (PHRED) system for derivatization, has been compared to the officially recognized iodine and Kobra cell derivatization systems. This photochemical system has been extensively used for screening peanuts by some U.S. Department of Agriculture laboratories for many years. From their periodic method checks, using standard spiked samples, an 80 sample series with each of the 3 derivatization methods was statistically analyzed. Paired comparisons, using the same sample extract, were also made between the PHRED and one of the other 2 methods, among laboratories in 4 different countries, on a variety of naturally contaminated commodity products. The differences between the techniques were not significant for peanuts, but for corn the photochemical system consistently gave slightly higher values for aflatoxins B1 and B2 than the Kobra cell method. However, a comparison of all sample results showed no significant differences between methods. The Pearson correlation coefficients for aflatoxin B1 in 102 test samples and aflatoxin B2 in 94 test samples were 0.9994 and 0.9874, respectively. The probability factor was P < 0.0001, and the t-tests were not significantly different except for the corn. These indicated that the PHRED system is equivalent to the iodine and Kobra cell methods for peanuts relative to the current official procedures, but the PHRED system has a slightly high bias for corn compared to the iodine and Kobra cell systems.

Aflatoxin B1↗

PubMed1990

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

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

Aflatoxin B1↗