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PubMed1976

Growth and morphology of Streptococcus bovis and of mixed rumen bacteria in the presence of aflatoxin B1, in vitro.

The metabolism of aflatoxin B1 to other fluorescent compounds was studied in rumen organisms. No fluorescent metabolites were found by chromatographic procedures which separate aflatoxin B1 from them. Rumen bacteria (mixtures and Streptococcus bovis) incubated with aflatoxin B1 grew in long chains whereas cells in control cultures were mainly doublets with some short chains. Growth of mixed rumen bacteria and Streptococcus bovis cultures was inhibited by aflatoxin B1 as measured by change in optical density and by incorporation of [carbon-14] adenine into nucleic acids.

Aflatoxins↗

PubMed1994

Development and evaluation of a minicolumn assay for the detection of aflatoxin M1 in milk.

A practical field method for the chemiselective immobilization and detection of aflatoxin M1 in milk has been developed and is being marketed. In this new method, aflatoxin M1 is selectively adsorbed at the interface of a layer of neutral sand and a band of magnesium silicate (Florisil) packed in a glass minicolumn. Aflatoxin M1, at > or = .5 ppb in contaminated milk, can be easily visualized as a band of bright blue fluorescence. Briefly, raw or homogenized and pasteurized milk is diluted with water (1: 1, vol/vol) and passed through a C18 cartridge. Aflatoxin M1 is then partitioned by polarity, eluted with acetone-methylene chloride, and added to the minicolumn. The minicolumn is washed and viewed under long wave UV light. The limit of detection for this assay was .2 ppb, which was similar to the .3 ppb obtained using an immunoaffinity column, followed by minicolumn detection. The assay was accurate, rapid, easy to perform, and stable.

Adsorption↗

PubMed2001

[Proportion of aflatoxin B1 contaminated kernels and its concentration in imported peanut samples].

Moldy and split peanut kernels were separated from peanuts exported from Brazil, Sudan, India and Taiwan by visual inspection. The remaining peanuts from Brazil, Sudan and India were roasted lightly and the skins were removed. Stained peanuts were separated from the others. Aflatoxin was detected in moldy and stained peanuts. There was a positive correlation between % of aflatoxin-contaminated peanut kernels and aflatoxin B1 concentration in whole samples. Aflatoxin concentration of moldy peanuts was higher than that of stained peanut kernels.

Aflatoxin B1↗

PubMed2001

[Application and improvement of aflatoxin analysis in foods using a multifunctional column and HPLC].

In an earlier report, we developed a rapid, sensitive and clean method consisting of non-chloroform extraction, clean-up on a commercial multifunctional cartridge column and HPLC with fluorescence detection for the analyses of aflatoxins. In this report, we applied this method to analyze aflatoxins in nuts, giant corn, cereals, spice and black teas. The method was effective for macadamia nuts, walnuts, hazelnuts, brazil nuts, giant corn, rice, wheat and buckwheat, and the recoveries of aflatoxins B1, B2, G1 and G2 spiked in them at the level of 10 ng/g were 85-106%. However, in the chromatograms of spices and black tea, many background peaks were observed. Therefore, we added a purification step with an affinity column to the clean-up of these samples with the multifunctional cartridge column. After the additional purification, most of the background peaks were gone. The recoveries of aflatoxins B1, B2 and G1 spiked at the level of 10 ng/g were 71-112% except for the case of B2 in white pepper (48%). The recoveries of G2 were 49-95%.

Aflatoxins↗

PubMed1979

Depressed 59 Fe absorption due to dietary aflatoxin.

This study investigated the relationship between 59 Fe absorption and the anemia associated with aflatoxicosis in commercial broilers. A level of 0 or 5 micrograms of aflatoxin per gram of diet was fed for a 21 day period beginning at 1, 7, 14, or 21 days of age in each of two trials. Packed cell volume (PCV) and percent retention of an oral dose of 59 Fe were determined. The feeding of aflatoxin resulted in an anemia when fed from 0 to 3 or 1 to 4 weeks of age. At the conclusion of these treatment periods, percent 59 Fe retention was significantly reduced from the controls. Aflatoxin when fed from 2 to 5 weeks of age resulted in a slight but significant depression in PCV (P less than .05) with a slight but nonsignificant depression in percent 59 Fe retention. At the conclusion of the 3 to 6 week treatment period both percent iron retention and PCV were greater than controls but not significantly so. The iron retentions of birds separated into high and low PCV groups within each treatment combination were compared. Although the iron retentions of the low PCV groups were lower than those of the high PCV groups, none of the differences were statistically significant. However, Pearson correlations of PCV with percent 59 Fe retention were - .28 (P less than or equal to .02, n = 69) for control birds and - .19 (P less than or equal to .14, n = 58) for birds fed aflatoxin, suggesting a relationship between PCV and iron absorption.

Aflatoxins↗

PubMed1980

Additive toxicity of aflatoxin and dietary tannins in broiler chicks.

In two experiments graded levels of either aflatoxin and tannic acid (experiment 1) or aflatoxin and a high-tannin variety of grain sorghum (BR-64) (experiment 2) were incorporated into broiler chick starting diets in a factorial design. When present singly, aflatoxin and both tannic acid and high tannin sorghum significantly depressed chick growth. When present in combination, and deleterious effects of aflatoxin and either tannic acid or high tannin sorghum on chick growth and feed conversion ratios were found to be additive.

Aflatoxins↗

PubMed1982

A delay in blood clotting of chickens and ducks induced by aflatoxin treatment.

Using the thrombotest technique blood clotting times were measured in the duck and the chicken after an intraperitoneal (I.P.) administration of aflatoxin B1 (58 microgram/kg body weight). Six hours after injection, the average thrombotest (blood clotting) time of the blood of the young duck was 194.5 +/- 1.3 sec (control time was 101.5 +/- 1.4, P less than .0001) and that of the young chicken averaged 70.2 +/- sec (control time was 51.7 +/- 2 sec, P less than .001). Corresponding times for the aflatoxin-treated adult birds were 249.5 +/- 1.4 sec (control, 118.5 +/- 1.1 sec; P less than .001) and 82.9 +/- .2 sec (control, 66.8 +/- .1 sec; P less than .001) for the duck and chicken respectively. In addition to the relatively low concentration of blood clotting factors in the plasma of the bird the present results suggest that there is a weak interaction of blood clotting factors II, VII, IX, and X in the avian species during aflatoxin poisoning. There is an inter-species difference in the anticoagulant effects of aflatoxin in the avian class.

Aflatoxins↗

PubMed1985

Aflatoxin effects in white Leghorn chickens selected for response to sheep erythrocyte antigen. 2. Serological and organ characteristics.

Aflatoxin was fed to chickens from lines selected for high and low antibody response to sheep erythrocyte (SRBC) antigen and reciprocal crosses between the two lines. Differences were found among populations for liver, bursa, and thymus weight and antibody production to SRBC but not for spleen weight or heterophil: lymphocyte ratios. Dietary aflatoxin depressed absolute and relative weights of bursae and thymi and absolute weights of livers and spleens. Relative to body weight, however, liver and spleen weights increased. There was a large decrease in liver metabolism and a dramatic increase in heterophil: lymphocyte ratios when 5700 ppb of aflatoxin was fed, but no alteration in antibody production to SRBC antigen was detected. Population by response to aflatoxin interactions were not significant for any of the traits measured except bursa and spleen weights, suggesting a general response to this mycotoxin among lines of chickens known to be immunologically different.

Aflatoxins↗

PubMed1988

Depletion of oxycarotenoid pigments in chickens and the failure of aflatoxin to alter it.

Aflatoxin, a demonstrated cause of pale bird syndrome in chickens, was investigated for its effects on the depigmentation of chickens placed on a diet low in carotenoids. Chickens were pigmented by feeding for 3 wk a white corn-soy diet supplemented with 50 micrograms free lutein and 0 or 4 micrograms aflatoxin/g diet. Then birds were switched to the same diets unsupplemented with lutein. At 0, 1, 2, 3, 6, and 9 days after switching, jejunal contents and mucosa, serum, liver, and toe web of 4 groups of 10 birds were removed for analysis of their carotenoids by high performance liquid chromatography. In control birds the order of decrease in total lutein was jejunal contents greater than jejunal mucosa greater than serum greater than liver greater than toe web. Aflatoxin did not alter the depletion process, except for minor retardation of lutein depletion in the mucosa and liver. Pharmacokinetic analysis of the data indicated that lutein depletion in the integument was accomplished through three sequential reactions (lutein diester----lutein monoester----lutein----serum lutein) and that aflatoxin had no effect on the reactions. These results imply that aflatoxin induces pale bird syndrome by interfering with the accumulation of pigment by chickens rather than by enhancing the depletion of pigment.

Aflatoxins↗

PubMed1988

Toxic synergism between aflatoxin and T-2 toxin in broiler chickens.

The individual and combined effects of aflatoxin and T-2 toxin were studied in male broiler chicks (Hubbard X Hubbard). The experimental design was a 2 X 2 factorial design with dietary treatments of 0 and 2.5 micrograms/g aflatoxin and 0 and 4.0 micrograms/g T-2 toxin. The broilers were obtained at 1 day of age and housed in electrically heated batteries with feed and water available ad libitum until they reached 3 wk of age. Aflatoxicosis in this study was characterized by a significant (P less than .05) reduction in body weight, changes in red blood cell counts and serum levels of protein, albumin, glucose, cholesterol, and calcium, and magnesium, activity of the serum enzymes lactic dehydrogenase and alkaline phosphatase, and a significant (P less than .05) increase in relative weights of the liver, kidney, spleen, pancreas, proventriculus, and heart. Dietary T-2 toxin alone caused oral lesions, a significant (P less than .05) decrease in serum protein, albumin, potassium, and magnesium levels, and a significant (P less than .05) decrease in the activity of the serum enzymes lactic dehydrogenase and alkaline phosphatase. In the combination treatment of aflatoxin and T-2 toxin, significant (P less than .05) interactive effects were seen through a decrease in body weights, increase in the relative weights of the kidney, gizzard, and heart, and decrease in mean corpuscular volume and serum levels of potassium. These data indicate that aflatoxin and T-2 toxin can interact to produce synergistic toxicity. This synergism is a threat to poultry production due to the prevalence of these mycotoxins and severity of the interactive toxicity of these mycotoxins.

Aflatoxins↗

PubMed1991

The individual and combined toxicity of kojic acid and aflatoxin in broiler chickens.

The individual and combined effects of kojic acid and aflatoxin were studied in male broiler chicks (Peterson x Hubbard). The experiment had a two by two factorial arrangement of treatments with dietary treatments of 0 and 2,500 mg kojic acid/kg feed and 0 and 2.5 mg aflatoxin/kg feed. The broilers were obtained at 1 day of age and housed in electrically heated batteries with feed and water available for ad libitum intake until they reached 3 wk of age. The toxicity of kojic acid was characterized by significant (P less than .05) reductions in body weight, the relative weight of the bursa of Fabricius, serum cholesterol concentration, and serum alkaline phosphatase activity, and by significant (P less than .05) increases in the relative weight of the pancreas, proventriculus, and gizzard, and serum concentrations of uric acid and triglycerides. Aflatoxicosis was characterized by significant (P less than .05) reductions in body weight, serum concentrations of total protein, albumin, cholesterol, and inorganic phosphorus, serum glutamic oxalacetic transaminase activity, and mean corpuscular volume, mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration. Significant (P less than .05) increases in the relative weight of the liver, kidney, spleen, pancreas, proventriculus, and heart, and the serum pyruvic transaminase activity were also caused by aflatoxin alone. The only significant (P less than .05) interaction between kojic acid and aflatoxin, which can best be described as antagonistic, was seen through an increase in mean corpuscular hemoglobin and mean corpuscular hemoglobin concentration. These data indicate that kojic acid is not an aflatoxin synergist at the levels used in the present study.

Aflatoxins↗

PubMed1999

Natural and in vitro coproduction of cyclopiazonic acid and aflatoxins.

Eighty samples of animal feeds of different origins were screened for the natural co-occurrence of cyclopiazonic acid (CPA) and aflatoxins in Portugal. Forty-five strains of Aspergillus flavus were collected from those samples and studied for their ability to produce these mycotoxins, in vitro. CPA was detected by thin-layer chromatography using Erhlich's reagent for confirmation. Aflatoxins were determined by high-pressure liquid chromatography with postcolumn iodination. Only 5 of the 80 samples (6.2%) were naturally contaminated with cyclopiazonic acid (0.16 mg/kg) and 36 (45.0%) with aflatoxin B1 (AFB1) (from 0.001 to 0.016 mg/kg). An in vitro study of the 45 strains of A. flavus was performed in cracked corn at 25 degrees C (water activity, a(w) = 0.96), incubated for 21 days to CPA production. For in vitro production of aflatoxins, the same substrate was incubated at 28 degrees C for 14 days. Nineteen of the strains (42.2%) produced CPA (ranging from 0.5 to 1.45 mg of CPA/kg) and 23 of them (51.1%) produced AFB1 (from 0.001 to 0.844 mg/kg). Only 10 isolates (22.2%) produced both CPA and AFB1 (0.05 to 0.10 mg/kg and 0.001 to 0.230 mg/kg, respectively). Thirteen strains did not produce either CPA nor AFB1.

Aflatoxins↗

PubMed1999

Inhibition of aflatoxin-producing fungi by Welsh onion extracts.

Welsh onion ethanol extracts were tested for their inhibitory activity against the growth and aflatoxin production of Aspergillus flavus and A. parasiticus. The survival of spores of A. flavus and A. parasiticus depended on both the extract concentration and the exposure time of the spores to the Welsh onion extracts. The mycelial growth of two tested fungi cultured on yeast extract-sucrose broth was completely inhibited in the presence of the Welsh onion ethanol extract at a concentration of 10 mg/ml during 30 days of incubation at 25 degrees C. The extracts added to the cultures also inhibited aflatoxin production at a concentration of 10 mg/ml or permitted only a small amount of aflatoxin production with extract concentration of 5 mg/ml after 2 weeks of incubation. Welsh onion ethanol extracts showed more pronounced inhibitory effects against the two tested aflatoxin-producing fungi than did the same added levels of the preservatives sorbate and propionate at pH values near 6.5.

Aflatoxins↗

PubMed2000

Binding of aflatoxin B1 to bifidobacteria in vitro.

Aflatoxins are mycotoxins that cause health and economic problems when they contaminate food and feed. One potential method for reducing human health effects due to aflatoxin ingestion is to block uptake via binding by bacteria that either make up the normal gut flora or are present in fermented foods in our diet. These bacteria would bind aflatoxin and make it unavailable for absorption in the intestinal tract. Bifidobacteria comprise a large fraction of the normal gut flora, are thought to provide many probiotic effects and are increasingly used in fermented dairy products. These qualities targeted bifidobacteria for studies to determine if various strains of heat-killed bifidobacteria can bind aflatoxin B1 (AFB1) in vitro. The AFB1 binding affinities of various strains of bifidobacteria, Staphylococcus aureus, and Escherichia coli were quantitated utilizing enzyme-linked immunosorbent and [3H]AFB1 binding assays. The bacteria analyzed were found to bind significant quantities of AFB1 ranging from 25% to nearly 60% of the added toxin. The data also suggest that there are reproducible strain differences in AFB1 binding capacity.

Aflatoxin B1↗

PubMed2002

Occurrence of aflatoxins and ochratoxin A in Indian poultry feeds.

From 1998 to 2001, 216 ingredients intended for incorporation into chicken feed, which included groundnut cake, maize, millets, rice bran, sorghum, soybean, sunflower, and mixed feeds, were assayed for aflatoxins and ochratoxin A contamination using an indirect competitive enzyme-linked immunosorbent assay. Thirty-eight percent of the samples were contaminated with aflatoxins and 6% with ochratoxin A. The incidence scores of aflatoxin contamination in excess of 10 microg/kg were 41 of 95 for maize, 18 of 30 for mixed feeds, 10 of 37 for groundnut, 6 of 29 for sorghum, 5 of 10 for sunflower, 3 of 14 for rice bran, and 1 of 8 for millet. Ochratoxin A contamination, in excess of 10 microg/kg, was found in 9 of 29 sorghum samples, 1 of 27 groundnut samples, 1 of 14 rice bran samples, 1 of 10 sunflower samples, and 2 of 8 millet samples. Ochratoxin A was not found in maize and mixed feeds. None of the three soybean samples contained ochratoxin A. This is the first report, to our knowledge, of co-occurrence of aflatoxins and ochratoxin A in Indian poultry feeds. The results confirm the importance of analysis of ingredients before incorporating them into mixed feeds.

Aflatoxins↗

PubMed2005

Microbiological and aflatoxin evaluation of Brazil nut pods and the effects of unit processing operations.

Harvesting of Brazil nuts not only helps to preserve the Amazon rainforest but also provides income to individuals who would otherwise have little means of making a livelihood. Recently, the European Community has tightened the quality requirements for Brazil nuts, particularly with regard to aflatoxin levels and microbiological contamination. The objectives of this research were to gain a better understanding of the origin of aflatoxins on Brazil nuts and to microbiologically evaluate some of the operations involved in processing. In this regard, five Brazil nut pods were aseptically picked from trees located in each of three concessions of the Peruvian Amazon rainforest (Madre de Dios province). The exteriors of the pods and the nuts were examined for yeast and molds, including Aspergillus flavus and Aspergillus parasiticus, and for bacteria, including Salmonella and Escherichia coli. Brazil nuts obtained from various commercial process operations located in Peru were similarly evaluated. Exteriors of all Brazil nut pods did not contain A. parasiticus, and only pods from one concession yielded A. flavus isolates. All isolates tested were aflatoxigenic (630 to 915 ppb total aflatoxin). Coliforms, E. coli, and salmonellae were not recovered from any of the pods. Whole, in-shell nuts obtained after opening the pods yielded no A. flavus or A. parasiticus. Aflatoxins were not detected (detection limit 1.75 ppb) in any of the nuts. Whole, in-shell and shelled nuts from various process operations were all positive for A. flavus but negative for E. coli and salmonellae. Soaking of whole, in-shell nuts before cracking or shelling increased coliform numbers, whereas levels of A. flavus decreased. In order to gain a better understanding of the sanitary performance of the unit process operations, additional evaluations should be conducted on product lots processed on different days. Also, the microbiology of product processed from common lots should be followed through the various unit operations and compared.

Aflatoxins↗

PubMed2006

Occurrence of aflatoxins, ochratoxin A, and fumonisins in retail foods in Japan.

We conducted a survey of aflatoxin B1, B2, G1, and G2, ochratoxin A, and fumonisin B1, B2, and B3 contamination in various foods on the retail market in Japan in 2004 and 2005. The mycotoxins were analyzed by high-performance liquid chromatography, liquid chromatography-mass spectrometry, or high-performance thin-layer chromatography. Aflatoxins were detected in 10 of 21 peanut butter samples; the highest concentration of aflatoxin B1 was 2.59 microg/kg. Aflatoxin contamination was not found in corn products, corn, peanuts, buckwheat flour, dried buckwheat noodles, rice, or sesame oil. Ochratoxin A was detected in oatmeal, wheat flour, rye, buckwheat flour, green coffee beans, roasted coffee beans, raisins, beer, and wine but not in rice or corn products. Ochratoxin A concentrations in contaminated samples were below 0.8 microg/kg. Fumonisins were detected in popcorn, frozen corn, corn flakes, and corn grits. The highest concentrations of fumonisins B1, B2, and B3 in these samples were 354.0, 94.0, and 64.0 microg/kg, respectively.

Aflatoxins↗

PubMed1995

Aflatoxin contamination of corn used as bait for deer in the southeastern United States.

Samples of shelled corn used for wildlife feed were taken from bait piles and storage bins in North Carolina and South Carolina (USA) from 29 September through 28 November 1993, and were analyzed for aflatoxin. Twenty (51%) of 39 samples were positive, with aflatoxin levels ranging from a trace to 750 parts per billion. Based on the high prevalence of aflatoxin-contaminated corn, exposure of wild-life to aflatoxin undoubtedly occurs, although the effects of such exposure are largely unknown.

Aflatoxins↗