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PubMed1977

Mode of action and human health aspects of aflatoxin carcinogenesis.

The toxicity and carcinogenicity of the aflatoxins have been studied extensively in the rat. In this species these compounds are recognized as some of the most active hepatocarcinogens. The early lesions induced by the aflatoxins have been studied in an attempt to recognize the developing malignant neoplasm prior to the presence of metastasis. The relationship of focal hyperplasia to neoplasia will be discussed in comparison with other recognized carcinogens. The pattern of human hepatic neoplasia will be compared with that of neoplasia induced by the aflatoxins in order to add weight to the "mycotoxin hypothesis" of the aetiology of hepatic neoplasia. The role of dietary modification will also be discussed.

Aflatoxins↗
PubMed1993

Metabolic activation of aflatoxin B1 by human placental microsomes.

The metabolic activation of aflatoxin B1 by human placental microsomes was studied. Aflatoxin B1 showed relatively high mutagenic activity in Ames test when incubated with human placental microsomes. Addition of alpha-naphthoflavone or aminoglutethimide, known inhibitors of cytochrome P450 1A and P450 19, respectively, into the test system partially inhibited the mutagen-producing activity. It was suggested that the activation of aflatoxin B1 in human placental microsomes is mediated by at least these two forms of cytochrome P450.

Aflatoxin B1↗
PubMed2001

Aflatoxin B1 binding by dairy strains of lactic acid bacteria and bifidobacteria.

Various food commodities including dairy products may be contaminated with aflatoxins, which, even in small quantities, have detrimental effects on human and animal health. Several microorganisms have been reported to bind or degrade aflatoxins in foods and feeds. This study assessed the binding of aflatoxin B1 (AFB1) from contaminated solution by 20 strains of lactic acid bacteria and bifidobacteria. The selected strains are used in the food industry and comprised 12 Lactobacillus, five Bifidobacterium, and three Lactococcus strains. Bacteria and AFB1 were incubated (24 h, +37 degrees C) and the amount of unbound AFB1 was quantitated by HPLC. Between 5.6 and 59.7% AFB1 was bound from solution by these strains. Two Lactobacillus amylovorus strains and one Lactobacillus rhamnosus strain removed more than 50% AFB1 and were selected for further study. Bacterial binding of AFB1 by these strains was rapid, and more than 50% AFB1 was bound throughout a 72-h incubation period. Binding was reversible, and AFB1 was released by repeated aqueous washes. These findings further support the ability of specific strains of lactic acid bacteria to bind selected dietary contaminants.

Aflatoxin B1↗
PubMed1978

Aflatoxin production on high moisture corn and sorghum with a limited incubation.

Samples of ground, cracked, or whole kernels of sorghum or corn were inoculated with Aspergillus flavus no. 15546. The samples were incubated at 25 or 30 C and 90% relative humidity for 48 or 72 h. In all treatments, the 72-h samples contained more aflatoxins B1 and B2 than the 48-h samples. Cracked sorghum at 30 C for 72 h and whole sorghum at 25 C for 72 h contained more aflatoxins than any other treatment. Even in these short incubation periods, enough aflatoxin could be produced to be harmful to livestock.

Aflatoxins↗
PubMed1975

Interaction of aflatoxin and paratyphoid infections in broiler chickens.

There was a significant (P less than 0.05) interaction resulting in increased mortality in chickens fed aflatoxin and infected with Salmonella worthington, S. thompson, S. derby, or S. typhimurium var. copenhagen which cause paratyphoid. There was no interaction on body weight or spleen weight; however, there wan an interaction with all four Salmonella species resulting in enlarged livers from which Salmonella could be isolated with increased frequency. Aflatoxin caused a decrease in total serum proteins but a dramatic increase in anti-Salmonella agglutinins in infected birds. These results suggest that aflatoxin impairs some component of the immune system other than that forming humoral antibodies and perhaps other than the reticuloendothelial system which have been reported previously to be impaired during aflatoxicosis in the chicken.

Aflatoxins↗
PubMed1975

Effects of dietary aflatoxin on certain egg yolk parameters.

Aflatoxicosis was induced in laying hens by incorporating graded amounts of aflatoxin into a commercial layer ration (0, 1.25, 2.5, 5.0, and 10.0 mug./g. of feed). After four weeks liver size and liver lipid were increased by aflatoxin while egg production and egg size were decreased (P less than 0.05). Total yolk weight and the yolk as percent of total egg weight were lowered (P less than 0.05). The dry weight and lipid content of the yolk were not affected. Yolk and plasma carotenoid concentrations were elevated (P less than 0.05). The data suggest that plasma and yolk lipids respond to the inhibition of lipid synthesis and transport from the liver by aflatoxin, but plasma and yolk carotenoids which are dietary in origin necessarily increase when egg production decreases during aflatoxicosis.

Aflatoxins↗
PubMed1977

The effect of various antifungal agents on aflatoxin production and growth characteristics of Aspergillus parasiticus and Aspergillus flavus in liquid medium.

Various antifungal agents were added to a medium of 2% yeast extract-4% sucrose. Spores of a toxigenic strain of Aspergillus parasiticus were inoculated into the medium and incubated at 26 degrees C. for 10 days. Growth of the mold and aflatoxin formation were monitored every 48 hours during the experiment. Of the antifungal agents evaluated, propionic acid and crystal violet were the most effective compounds in retarding mold growth. Propionic acid was fungicidal at concentrations greater than 3.0 microgram/ml. whereas crystal violet exhibited a mold retarding activity at levels greater than 2,0 microgram/ml. Crystal violet retarded the growth rate of the mold during the initial stages of growth, however, this retardation was overcome after 10 days of incubation. Crystal violet also retarded aflatoxin production and sporulation of Aspergillus parasiticus; however, aflatoxin production was the most sensitive parameter. A survey involving 12 toxigenic isolates of A. parasiticus and A. flavus indicated that these species vary markedly in susceptibility to crystal violet.

Aflatoxins↗
PubMed1980

Strain variation in hematological response of broilers to dietary aflatoxin.

The response of clinical blood values to graded levels of dietary aflatoxin was studied in three populations of chickens. Male chicks of two commercial broiler strains, one color-sexed and the other feather-sexed, and a randombred strain were fed dietary aflatoxin at levels of 0, 1.25, 2.50 or 5.0 microgram/g of diet from 1 to 21 days of age. At the conclusion of the 21-day treatment period, all remaining birds were bled by cardiac puncture and packed cell volume (PCV), erythrocyte counts (RBC), hemoglobin concentration (Hb), mean corpuscular volume (MCV), mean corpuscular hemoglobin concentration (MCHC), total plasma protein, and total plasma cholesterol were determined. All strains of broilers were susceptible to aflatoxicosis as detected by total plasma protein and cholesterol. Anemia associated with aflatoxicosis was induced in the two commercial broiler lines, but not in the randombred line. The PCV, RBC, and Hb were diminished from control values in a dose-related fashion by graded levels of aflatoxin in the commercial broilers, but not in the randombred line. Decreases in MCV with no significant changes in MCHC were observed in all strains.

Aflatoxins↗
PubMed1981

Effect of dietary aflatoxin on hemostasis of young turkey poults.

Young turkey poults fed graded levels of aflatoxin (0, 125, 250, and 500 microgram/kg) from hatching for 3 weeks displayed altered hemostasis, manifested in prolonged prothrombin times at 2 and 3 weeks of age. Body weights were only affected in those groups receiving 500 microgram/kg. Total plasma protein, fibrinogen, and plasma calcium were reduced in response to dietary aflatoxin. In comparison with chickens, which exhibit similar hemostatic dysfunction concomitant with reduced body weight, turkeys receiving aflatoxin at lower levels exhibited an altered hemostatic response without exhibiting depressed body weights. Thus, the turkey hemostatic system is a better indicator of aflatoxicosis than is body weight gain.

Aflatoxins↗
PubMed1983

Individual and combined effects of aflatoxin and ochratoxin A on bruising in broiler chickens.

A 2 x 2 factorial design with treatments of 0 and 2.5 microgram/g aflatoxin and 0 and 2.0 microgram/g ochratoxin A was used to evaluate the individual and combined effects of these mycotoxins on bruising and blood thigh syndrome in broiler chickens. Trial 1 consisted of four replicate pens of 10 broilers per replicate, which were maintained on these dietary treatments from 0 to 3 weeks of age. At 3 weeks of age two replicate pens per treatment were randomly selected and placed on toxin-free feed with two replicate pens remaining on toxin feed until they were 6 weeks of age when the trial was concluded. In Trial 2 three replicate pens of 38 broilers per treatment were maintained on toxin feed from 0 to 3 weeks of age. At 3 weeks of age 13 broilers per replicate were placed on toxin-free feed with 25 broilers per replicate remaining on toxin until they reached 7 weeks of age when Trial 2 was concluded. These data indicate that a synergistic toxicity exists between aflatoxin and ochratoxin A to significantly (P less than .05) decrease body weight. Body weights of broilers on aflatoxin or ochratoxin A diets for only 3 weeks partially recovered by 6 or 7 weeks of age; however, the body weights of broilers on the interaction treatments for only 3 weeks remained significantly (P less than .05) depressed at 6 and 7 weeks of age.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗
PubMed1985

The effect of aflatoxin on complement activity in broiler chickens.

Groups of broiler chickens were fed rations containing .625, 1.25, or 2.5 micrograms total aflatoxin/g of feed from one day to 42 days of age. Treatment groups were segregated according to sex and control groups were maintained. The chickens were bled at 14-day intervals, and serum was collected for assay of total complement (C) activity using a radial hemolytic procedure. No significant differences were found in C titers between males and females of the same age group. For the sexes combined, mean C titers of chickens fed aflatoxin were compared to mean titers of controls. For each age group, significant differences in C titers existed only between the control group and those chickens fed 2.5 micrograms/g aflatoxin. Complement is a major component of the humoral immune response and this study adds to the evidence that aflatoxin can be immunosuppressive to chickens.

Aflatoxins↗
PubMed1985

Aflatoxin effects in white Leghorn chickens selected for response to sheep erythrocyte antigen. 1. Body weight, feed conversion, and temperature responses.

Chickens from lines selectively bred for high and low antibody response to sheep red blood cell antigen and reciprocal crosses between them were fed diets containing 0, 1, 2, 3, and 6 micrograms of total aflatoxin/g diet from 2 to 42 days of age. Low-line birds, although larger, did not differ from the high-line birds in feed consumption, feed conversion, surface, or cloacal temperatures. Differences between crosses and parental lines varied according to the particular trait. Responses to dietary aflatoxin were similar regardless of population. Aflatoxin depressed body weight, feed consumption, and feed conversion at 14 days and subsequent ages with the effect on body weight and feed consumption occurring at lower levels than that noted for feed conversion. Although aflatoxin did not alter cloacal temperatures, there were progressive decreases in surface temperatures at 2 micrograms/g and higher.

Aflatoxins↗
PubMed1985

Aflatoxin-antioxidant effects on growth of young chicks.

Butylated hydroxytoluene (BHT), an antioxidant, was provided to chicks at 8 X, 30 X and 80 X the normal concentrations in their feed beginning at 1 day of age and continuing for the next 6 weeks. The ability of these birds to resist the adverse effects of dietary aflatoxin (3000 ppb, beginning Day 8) was measured by weight gain and feed efficiency over the 6-week period of study. Birds on aflatoxin-contaminated feed did not gain weight as rapidly or as efficiently as birds on uncontaminated feed. Depression of growth caused by aflatoxin was significantly less in birds given BHT than in those fed the diet not containing antioxidant.

Aflatoxins↗
PubMed1981

Aflatoxins and disease.

These days it is widely believed by experts that most cancers are caused by environment factors. The epidemiology of most of these suspected factors is still equivocal. One such factor which has been widely studied is aflatoxin, a chemical produced by the fungus Aspergillus flavus. Because of the widespread distribution of this agent, its known toxicity, and its frequent ingestion by humans, aflatoxin may well be a significant cause of cancer worldwide. This paper attempts to summarize some of the historical and epidemiological evidence regarding aflatoxins and disease.

Aflatoxins↗
PubMed1998

Physicochemical alterations enhance the ability of dairy strains of lactic acid bacteria to remove aflatoxin from contaminated media.

Lactobacillus rhamnosus GG and Lactobacillus rhamnosus LC-705, previously shown to effectively bind to aflatoxin B1, were subjected to various chemical and physical treatments to examine the effects of these treatments on the binding affinity of these strains toward aflatoxin B1. Treatment of bacterial pellets of both strains with hydrochloric acid significantly (P < 0.05) enhanced the binding ability to bind aflatoxin B1 was also observed when the bacterial pellets were subjected to heat treatment by either autoclaving or boiling at 100 degrees C in a water bath, put the impact of these two treatments was not as effective as the acid treatment. Ethanol, UV radiation, sonication, alkaline, or pH treatments either had not effect or reduced the binding ability of the bacteria.

2-Propanol↗
PubMed2000

Preliminary evidence that degradation of aflatoxin B1 by Flavobacterium aurantiacum is enzymatic.

The ability of crude protein extracts from Flavobacterium aurantiacum to degrade aflatoxin B1 (AB1) in aqueous solution was evaluated. Crude protein extracts (800 microg of total protein per ml) degraded 74.5% of AB1 in solution. An average of 94.5% of AB1 was recovered after incubation with heat-treated crude protein extracts (800 microg of total protein per ml). DNase I-treated crude protein extracts degraded 80.5% of AB1 in solution, suggesting that removal of aflatoxin by F. aurantiacum is not due to nonspecific binding with the bacterium's genomic DNA. Proteinase K-treated crude protein extracts degraded 34.5% of AB1, providing evidence that degradation of aflatoxin is linked to a protein that is possibly an enzyme. Solution pH affected the amount of AB1 degraded by crude protein extracts after 24 h. Maximum degradation was observed at pH 7 (pH levels tested: 5, 6, 7, and 8), with some AB1 degradation occurring at pH levels as low as 5 and as high as 8. Acidic pH levels were more detrimental to the ability of crude protein extracts to degrade AB1 than was basic pH. The results of this work indicate that the degradation of AB1 by F. aurantiacum may be enzymatic.

Aflatoxin B1↗
PubMed2001

Comparison of constitutive and inducible maize kernel proteins of genotypes resistant or susceptible to aflatoxin production.

Maize genotypes resistant or susceptible to aflatoxin production or contamination were compared for differences in both constitutive and inducible proteins. Five additional constitutive proteins were found to be associated with resistance in over 8 of the 10 genotypes examined. Among these, the 58- and 46-kDa proteins were identified as globulin-1 and globulin-2, respectively. Differences in the ability to induce specific antifungal proteins, such as the higher synthesis of the 22-kDa zeamatin in resistant genotypes, were also observed between resistant and susceptible kernels incubated under germinating conditions (31 degrees C, 100% humidity). Both constitutive and inducible proteins appear to be necessary for kernel resistance. Embryo-killed kernels (unable to synthesize new proteins) supported the highest level of aflatoxins, whereas imbibed kernels (to hasten protein induction) supported the lowest among all treatments. This suggests that the synthesis of new proteins by the embryo plays an important role in conferring resistance. However, significantly lower levels of aflatoxin production in embryo-killed resistant kernels than in susceptible ones suggest that, in reality, high levels of constitutive antifungal proteins are indispensable to kernel resistance.

Aflatoxins↗