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PubMed1983

Metabolic effects of low aflatoxin B1 levels on broiler chicks.

The effects of daily ingestion of aflatoxin B1 (AFB1) on growth, feed intake, plasma glucose, plasma cholesterol, plasma amino acids, plasma albumin, plasma ceruloplasmin, muscle amino acids, liver lipid, and bone strength were studied. For 3 weeks, beginning at an age of 2 days, broiler chicks were dosed daily per os with 50 or 100 micrograms of AFB1 per kg of body weight. Body weight and feed consumption were recorded daily, and metabolic responses were determined at 3 weeks. Treatment with AFB1 did not significantly alter body weight or feed intake. Relative liver weight showed a significant increase at the highest dose, with a significant concomitant increase in liver lipid and decrease in hepatic zinc. Relative spleen and heart weights were not affected by the toxin. Plasma glucose and cholesterol were significantly elevated at the highest dose. AFB1 significantly decreased plasma lysine and histidine and significantly increased muscle histidine, arginine, and valine. AFB1 decreased plasma albumin and markedly increased plasma ceruloplasmin. Dimensions of the long bones (femur and tibiotarsus) were not altered by the toxin. However, AFB1 caused a significant linear decline in the resistance of bone to breakage ("bone breaking strength"). The results indicate that low levels of AFB1 reduced bone strength in broiler chicks. The alterations in blood parameters indicated that AFB1 can disrupt metabolism even at low levels.

Aflatoxin B1↗
PubMed1986

Identification of an activated c-Ki-ras oncogene in rat liver tumors induced by aflatoxin B1.

Weanling male Fischer rats were administered 40 intraperitoneal injections of aflatoxin B1 (25 micrograms per animal per day) over a 2-month period. This chronic dosing regimen resulted in the sequential formation of hyperplastic foci, preneoplastic nodules, and hepatocellular carcinomas in all of the animals treated. The presence of transforming DNA sequences was detected by formation of anchorage-independent foci after transfection of tumor-derived DNA in NIH 3T3 mouse fibroblasts. Transfection of genomic DNA isolated from individual tumors from eight animals resulted in specific transforming activities ranging from 0.05 to 0.2 foci per micrograms of DNA. Primary transfectant DNAs were analyzed by Southern blot hybridization with DNA probes homologous to c-Ha-ras, c-Ki-ras, and N-ras oncogenes. A highly amplified c-Ki-ras oncogene of rat origin was detected in transformants derived from tumors in two of the eight animals tested. There was no evidence to suggest the presence of c-Ha-ras or N-ras sequences in any of the transformants. Analysis of primary liver tumor DNA showed no Ki-ras DNA amplification when compared to control liver DNA samples. Increased levels of c-Ki-ras p21 proteins were detected in 3T3 transformants containing activated rat c-Ki-ras genes. The presence of c-Ki-ras sequences of rat origin capable of inducing transformed foci can be taken as evidence that the c-Ki-ras gene has been activated in the primary liver tumors.

Aflatoxin B1↗
PubMed1986

Fumaric acid enhances DNA synthesis of rat hepatocytes by counteracting the toxicities of mitomycin C and aflatoxin B1.

The effect of fumaric acid was examined on DNA synthesis in hepatocytes or hepatoma cells from rats treated with toxic agents. Male Donryu rats were injected with mitomycin C or aflatoxin B1, singly or in combination with fumaric acid. After a specified period, hepatocytes were isolated from the liver by the collagenase perfusion method and placed in culture, and their activities for DNA synthesis were measured. The iv injection of rats with mitomycin C (0.5 mg/kg) reduced the semiconservative DNA synthesis of the hepatocytes, but simultaneous dosing of fumaric acid (40 mg/kg) enhanced the recovery of the DNA synthesis. The DNA synthesis of hepatoma cells, a 3'-methyl-4-(dimethylamino)azobenzene-induced transplantable cell line growing in the abdominal ascites of rats, was also reduced by the iv injection of mitomycin C but, in contrast to that of the hepatocytes, was little influenced by the simultaneous dosing of fumaric acid. The ip injection of fumaric acid also reduced the toxicity of aflatoxin B1 (0.25 mg/kg, ip), preventing the reduction of DNA synthesis as well as the occurrence of nuclear degenerative changes in the aflatoxin B1-exposed hepatocytes.

Aflatoxin B1↗
PubMed1977

Enzyme-linked immunosorbent analysis for aflatoxin B1.

An enzyme-linked immunosorbent analysis (ELISA) permitted the detection of less than 10 pg of aflatoxin B1 per ml. The antitoxin was most specific for aflatoxins B1 and B2alpha, and least specific for aflatoxin G1.

Aflatoxins↗
PubMed1985

[Paraclinical research on broiler chickens treated with aflatoxin B1 and microbiological studies of the meat and liver obtained from them].

Studied were some paraclinical indices of the blood of 50 broiler birds treated with aflatoxin B1. It was found that the effect of the mycotoxin used in concentrations of 25.0 and 37.5 micrograms in the course of thirty days and in conc. of 50.0 micrograms in the course of five days with three test groups of birds (as compared to a group of controls) consisted in the drop of total protein and the rise of the activity of GOT, GPT, and total bilirubin. It was demonstrated that the use of feeds containing aflatoxin B1 had a bearing on the microbiologic status of the meat and liver. There was no increase in the total count of aerobic mesophile organisms.

Aflatoxin B1↗
PubMedDate not supplied

In vivo effect of dietary factors on the molecular action of aflatoxin B1: role of copper on the catalytic activity of liver microsome.

Wealing rats were kept on a synthetic copper-free diet for 9-13 weeks and subsequently on the same diet but supplemented with copper at different levels for 2 weeks. The ability of liver microsomes to catalyze reactions of aflatoxin B1 leading to its activation and DNA adduct formation was measured after each period of experimental feeding. An increased molecular reactivity of aflatoxin B1 was evident during deficiency such that the degree of its conversion to its reactive metabolite and subsequent DNA adduct formation was higher with microsomes from copper deficient rats as compared to rats maintained on a normal supply of copper. These activities of microsomes returned to normal after supplementation of the diet with a small level of copper. The results emphasize the role of copper in the activation, and hence in modulating the carcinogenicity of aflatoxin B1.

Aflatoxin B1↗
PubMed1976

[Effect of aflatoxin B1 in vitro and in vivo].

The direct and transplacental action of aflatoxin B1 was studied on organic cultures of the embryonic pulmonary tissue of mice of the A line, BD-IX rats and golden hamsters (Cricetus auratus W.). Its toxic action on the cultures and the absence of any blastomogenic effect was demonstrated. In experiments on mice the transplacental penetration of aflatoxin B1 led to an increase in the incidence of the breast tumours in the progeny.

Aflatoxins↗
PubMed1985

A comparative study of monooxygenase activity in elasmobranchs and mammals: activation of the model pro-carcinogen aflatoxin B1 by liver preparations of calf, nurse shark and clearnose skate.

Liver microsome preparations of the elasmobranchs Ginglymostoma cirratum (nurse shark) and Raja eglanteria (clearnose skate) were examined for monooxygenase activity using aflatoxin B1 as substrate. At equiprotein concentrations, elasmobranch microsomes were less than 20% as active as calf liver in producing mutagenic metabolites of aflatoxin B1.

Aflatoxin B1↗
PubMed1999

Occurrence of Aspergillus section flavi and aflatoxin B1 in corn genotypes and corn meal in Argentina.

A study has been carried out in Argentina on samples of corn genotypes from a breeding station as well as in commercially available corn meal. All samples were analyzed for fungal infection and aflatoxin B1. Mycological analysis of corn genotypes showed the presence of three principal genera of filamentous fungi Fusarium (100%), Penicillium (67%) and Aspergillus (60%). In the genus Fusarium three species were identified, F. moniliforme (42%), F. nygamai (56%) and F. proliferatum (1.8%). Eight species of Penicillium were identified, the predominant species isolated were P. minioluteum, P. funiculosum and P. variabile. In the genus ranked third in isolation frequency, two species were identified, A. flavus and A. parasiticus, the percentage of infection was 78% and 21%, respectively. Only one corn genotype was contaminated with aflatoxin B1 at a level of 5 ppb. The corn meal samples showed great differences in fungal contamination, the values ranging from 1 x 10(1) to 7 x 10(5) cfu g-1. Fusarium (68%), Aspergillus (35%) and Penicillium (21%) were the most frequent genera isolated. Among the genus, Aspergillus, A. parasiticus (38%) was the most frequent species isolated. All the samples of corn meal were negative to aflatoxin B1. These results indicate a low degree of human exposure to aflatoxins in Argentina through the ingestion of maize or corn meal.

Aflatoxin B1↗
PubMedDate not supplied

Long-term administration of low doses of mycotoxins to poultry. 1. Residues of aflatoxin B1 and its metabolites in broilers and laying hens.

A study was performed to determine aflatoxin residues in tissues and organs of male broilers and hens that had been fed a diet contaminated with 50 micrograms/kg aflatoxin B1 (AFB1). Residue levels of AFB1, aflatoxicol (Ro), aflatoxin M1 (AFM1) and aflatoxin B2a (AFB2a) were determined by an HPLC method and, with the exception of AFB2a, were detected in the liver, kidney and thigh of both male broilers and hens. The highest levels found were for Ro in liver (1.10 and 0.60 micrograms/kg for male broilers and hens, respectively). On the other hand no detectable amounts of aflatoxins were found in any tissue after withdrawal periods of 14 and 33 days for male broilers and laying hens respectively.

Aflatoxin B1↗
PubMed1980

Effects of sequential exposure to aflatoxin B1 and diethylnitrosamine on vascular and stomach tissue and additional target organs in rats.

Male weanling rats were given a standard amount (375 micrograms) of aflatoxin B1; some were then exposed to dietary diethylnitrosamine (DEN) in varying concentrations ranging from 5 to 80 ppm for 20 weeks. They were maintained for an additional period of time following DEN exposure and then killed for gross and microscopic examination. DEN at 5 ppm did not enhance aflatoxin B1 liver carcinogenesis. Ten ppm or more of DEN, however, enhanced liver carcinogenesis and introduced two additional target organs; angiosarcomas of the lung and squamous cell carcinomas of the stomach types of tumors which have not been observed after treatment with DEN alone, were noted.

Aflatoxin B1↗
PubMed1980

[Method for the simultaneous determination of aflatoxins B1 and M1 in the liver of slaughter animals].

The method used by Egmond et al. (1979) was chosen from a number of methods recommended for the determination of aflatoxins in raw materials of animal origin. This method is described in detail to facilitate its use in practice in cases of forced slaughters of animals suspected of aflatoxicosis. The sensitivity of the method for aflatoxin B1 and M1 is about 0.05 micrograms . kg-1. On the whole, 88 liver samples were examined for the presence of the aflatoxins B1 and M1. The samples had been obtained from the slaughtered pigs (52), bulls (23), cows (6), calves (5), and from deceased pigs (2). Positive findings were obtained in five of sixteen pork liver samples and in two of the tested five samples of calf liver. All of these animals were suspected of aflatoxicosis. At current slaughter, only one case of 36 examined pigs was found to be positive. Aflatoxin M1 was found more frequently than aflatoxin B1. However, the findings never exceeded the concentration of 100 ng . kg-1; this is less by 1.5 orders than the proposed tolerated concentration for adult animals (5 micrograms . kg-1).

Aflatoxins↗
PubMed1987

[Effect of aflatoxin B1 on ultrastructural changes of biliary epithelial cells in mice experimentally infected with Clonorchis sinensis]

The present study was carried out to examine the effect of a carcinogen, aflatoxin B1 on the ultrastructural changes of biliary epithelial cells in mice infected with Clonorchis sinensis. A total of 93 male albino mice(BALB/c strain) was divided into 3 groups; group I, treated with 1.0 ppm aflatoxin B1 for 12 weeks; group II, given 50 C. sinensis metacercariae, and group III, given 50 metacercariae and treated with 1.0 ppm aflatoxin B1 for 12 weeks. Three mice served for untreated-uninfected controls. From 4 weeks after the treatment and/or infection, three mice from each group were sacrificed at 4 week intervals up to the 40th week, and their hepatobiliary tissues were prepared for transmission electron microscopy. The most prominent ultrastructural changes in group I were remarkable enlargement of nuclear size, separation of nucleolus, dispersed chromatin granules in nuclei and increased dense granules along the inner membrane of nuclei. In the cytoplasm there was slight proliferation of mitochondria and endoplasmic reticulum (ER) at earlier stage. At the 12th week separation of fibrillar and granular components of the nucleolus was a characteristic finding. As the time elapsed, epithelial cells showed flattened-cuboidal form and a tendency of atrophy. Most of the nuclei were elongated and polygonal in shape. In group II the appearance of elaborate interwoven folds of lateral cytoplasm forming a labyrinth of interconnected intercellular space and variety in nuclear shape were the prominent findings at earlier stage. The cytoplasm showed slight proliferation and dilatation of mitochondria and ER, and a small number of mucin droplets. In the basement membrane scanty fibrous cells were seen. With time, variety in nuclear shape, marked proliferation and dilatation of rough ER and some collagen fibrils were demonstrated. Other features of intracellular organelles and mucin droplets persisted. In group III cuboidal epithelial cells showed their remarkably enlarged and irregular nuclei, increased chromatin granules in the nuclei, separated nucleoli, proliferated and dilated rough ER. With time, sequestered mitochondria showed bleb-like evaginations which lacked cristae and dense matrix, and were limited by a single membrane. Since the 20th week, microvilli were relatively scanty and poorly developed. Organelles and inclusions in the cytoplasm of metaplastic cells were poor. Nuclei were variable in shape. The most prominent changes at later stage were separation of nuclei from the cytoplasm, and appearance of numerous and irregularly angled electron dense granules in the nuclei.

Journal Article↗
PubMed1982

Toxicology of aflatoxin B1, warfarin, and cadmium in young pigs: clinical chemistry and blood coagulation.

The purpose of this experiment was to compare the toxic effects of aflatoxin B1 (AFB1) and warfarin in pigs and to determine whether these have an additive effect in these pigs fed dietary Cd. Cadmium was provided daily through the diets of 2 concentrations (0 or control, and 83 micrograms/g of diet) during the 40 days of the experiment. At the start of the 5th week, AFB1 and warfarin were given in 5 daily doses (each dose 0.2 mg/kg of body weight) and the effects were determined for 10 days (starting with the 1st treatment day). Aflatoxin B1 given to the pigs fed the control diet (0 Cd) was toxic, inducing significantly increased alkaline phosphatase, sorbitol dehydrogenase, and aspartate aminotransferase activities and the prothrombin time (PT) and activated partial thromboplastin time (APTT) and significantly decreased values in serum total protein, alpha-globulin, beta-globulin, gamma-globulin, and fibrinogen. There was no effect on blood urea nitrogen. The treatment with warfarin was more effective in producing earlier and significantly longer PT and APTT. In the pigs fed the diet with the added Cd, differences in activity of alkaline phosphatase, sorbitol dehydrogenase, aspartate aminotransferase values, but not blood urea nitrogen, as well as differences in intensity and duration of response in PT and APTT occurred when pigs were dosed daily for 5 days after AFB1 or warfarin. It is concluded that dietary Cd (83 micrograms/g of diet) in young pigs has an inhibitory effect on AFB1 toxicity and an enhancing synergistic effect with warfarin.

Aflatoxin B1↗
PubMed1990

[A rapid and simple approach for radioimmunochemical determination of aflatoxin B1 in cereals and feed using a commercial analysis kit].

In order to facilitate a practical large-scale introduction of the radioimmunochemical control of aflatoxin B1 contamination in cereals and feeds a new method of the preparation of sample extracts was verified. In comparison with the procedure used until now when water-nonmiscible chloroform must be evaporated from a chloroform extract and the solids must be dissolved in acetone, while using the tested method the sample is extracted by methyl alcohol or acetone and the extract is diluted by a buffer before the radioimmunoanalysis. This new method of sample extract preparation displays aflatoxin B1 recovery comparable to that of the older method (83-90% for concentrations of 2-20 micrograms per kg), the worse theoretical detection limit (1 microgram per kg vs. 0.2 microgram per kg) but it prevents the result distortion by interfering substances and it makes the whole analytical procedure simpler and expeditious. Radioimmunochemically aflatoxin was quantified by means of commercially produced analytical kits developed in one institute at Kosice.

Aflatoxin B1↗
PubMedDate not supplied

Enzyme-linked immunosorbent assay of aflatoxins B1, B2, and G1 in corn, cottonseed, peanuts, peanut butter, and poultry feed: collaborative study.

A direct competitive enzyme-linked immunosorbent assay (ELISA) screening method for aflatoxins at 20 ng/g was studied by 12 collaborators. Test samples of peanut butter were extracted by blending with methanol-water-hexane (55 + 45 + 100) and heating the test extracts on a steam bath; test samples of the other commodities were extracted by blending with methanol-water (80 + 20). All test extracts were filtered and the filtrates were diluted with buffer to a final methanol concentration of less than 30%. Each diluted filtrate was applied to a cup containing a filter with immobilized polyclonal antibodies specific to aflatoxins B1, B2, and G1. Aflatoxin B1-peroxidase conjugate was added, the cup was washed with water, and a mixture of hydrogen peroxide and tetramethylbenzidine was added. The test sample was judged to contain greater than or equal to 20 ng aflatoxins/g when, after exactly 1 min, no color was observed on the filter; when a blue or gray color developed, the test sample was judged to contain less than 20 ng aflatoxins/g. All collaborators correctly identified naturally contaminated corn and raw peanut positive test samples. No false positives were found for controls containing less than 2 ng aflatoxins/g. The correct responses for positive test samples spiked at levels of 10, 20, and greater than or equal to 30 ng aflatoxins/g (the ratio of B1:B2:G1 was 10:1:3) were 52, 86, and 96%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxin B1↗
PubMed1995

Signal transduction mechanism in response to aflatoxin B1 exposure: phosphatidylinositol metabolism.

A single dose of aflatoxin B1 (7 mg/kg body weight) to male Wistar rats significantly stimulated the hepatic activity of phosphatidylinositol kinase, a key enzyme in the cell signalling mechanism, 1-7 h following its administration. Phosphatidylinositol 4-phosphate kinase activity showed only marginal increase, whereas activities of diacylglycerol kinase and phosphatidylinositol synthetase remained unchanged. The level of diacylglycerol, however, recorded a sharp increase at 1 and 2 h after carcinogen treatment. The stimulation of phosphatidylinositol cycle with faster turnover of active second messengers might be an early step in the manifestation of toxicity and/or carcinogenicity.

1-Phosphatidylinositol 4-Kinase↗
PubMed1985

Characterization of water-soluble glucuronide and sulphate conjugates of aflatoxin B1. 1. Urinary excretion in monkey, rat and mouse.

Water-soluble aflatoxin conjugates prepared from urine samples from rats, mice and rhesus monkeys dosed with [14C]aflatoxin B1 (AFB1) ip or iv were hydrolysed by enzymes (beta-glucuronidase and sulphatase), acid or a combination of both treatments. Different amounts of AFB1 and its metabolites were found in hydrolysates from different sources, indicating the presence of glucuronide, sulphate and possibly mercapturate conjugates of aflatoxins. In addition to aflatoxins M1, P1, Q1 and B2a, AFB1 was frequently identified in the products released from the hydrolysates. These water-soluble aflatoxin conjugates were not mutagenic to Salmonella typhimurium TA98 in the presence of rat-liver S-9 mix. However, chloroform extracts of the hydrolysates from beta-glucuronidase and sulphatase treatment showed mutagenic activity in these bacteria in the presence of S-9 mix. Although very low levels of AFB1 radioactivity were detected in the hydrolysates, the potent mutagenic activity of AFB1 contributed to the high numbers of revertant colonies. AFP1 was detected in urine samples from monkeys that were pretreated with phenobarbital before an iv dose of AFB1. No mutagenic activity was detected in the enzymatic hydrolysate of the sample from these monkeys. The results thus indicate that AFB1 can form glucuronide and/or sulphate conjugate(s) directly and be excreted in the urine.

Aflatoxin B1↗