Abstract Aflatoxin B1 Research Articles

Some studies on the relationship between the cytotoxicity of aflatoxin B1 to rat hepatocytes and metabolism of the toxin.

Aflatoxin B1 (AFB1) caused marked, rapid (1 h) inhibition of RNA synthesis and subsequent cytotoxic response in isolated and primary cultured hepatocytes, from control rats, which are known to metabolise AFB1. A rat liver-derived cell line, BL8L, was much less susceptible to these effects of AFB1. These cells have no detectable AFB1 metabolising capacity, but a less potent, anti-mitotic action of AFB1 was observed in the BL8L cell line. Thus AFB1 would seem to require metabolism to exert its acute cytotoxic action which is found at very low AFB1 concentrations, although a direct antimitotic effect, independent of metabolism, is seen in dividing cells. Phenobarbitone and 3-methylcholanthrene in vivo pretreatments, known inducers of AFB1 metabolism, resulted in reduced AFB1 inhibition of RNA synthesis and cytotoxicity in hepatocytes, but only at lower concentrations of AFB1 used, whereas cells from AFB1 fed rats were much less susceptible to AFB1 toxicity at all concentrations used. This resistance to cytotoxicity of AFB1 would appear to involve detoxification mechanisms, primarily the formation of polar conjugates of AFB1 metabolites, particularly glutathione conjugates. These cell culture systems are useful for studying association between metabolism and cytotoxicity of AFB1, and other xenobiotics.

Studies on the efficiency of the Salmonella/rat hepatocyte assay for the detection of carcinogens as mutagens: activation of 1,2-dimethyl-hydrazine and procarbazine into bacterial mutagens.

Aflatoxin B1, benzo[a]pyrene, N-nitrosomorpholine, procarbazine (PC) and 1,2-dimethylhydrazine (DMH) were used to investigate the efficiency of the Salmonella/rat hepatocyte assay for detecting carcinogens as mutagens. In this assay, bacteria and the test compound were co-incubated with freshly isolated rat hepatocytes and then plated onto minimal glucose agar. Factors for optimal mutagenicity, including the number of hepatocytes and the number of bacteria, the type of assay medium and the length of incubation in liquid medium were investigated. All the compounds were metabolized into bacterial mutagens. Mediation of the mutagenicity of PC and DMH by rat hepatocytes indicates that freshly isolated cells of this type are a useful alternative metabolic activation system for use in screening chemicals found to be non-mutagenic in the Salmonella/microsome assay.

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.

Implications of seasonal variations in aflatoxin B1 levels in Nigerian market foods.

Aflatoxin B1 levels were determined in Nigerian rural and urban market foods from 1977 to 1978. In general, levels were found to be highest during the peak rainy season, and the data suggest that livestock and humans are at highest risk from aflatoxicosis during this time. The incubation period for humans and nonhumans varies, and the risk to man from seasonal exposure to aflatoxin is assessed and reviewed. Primary hepatocellular carcinoma patients showed first symptoms of tumors during the dry season.

Aflatoxin contamination of Australian animal feeds and suspected cases of mycotoxicosis.

Aflatoxin B1 was detected in 23 of 55 Australian feedstuffs known to be either water damaged or visibly mouldy. The highest contamination was 0.7 mg/kg of feed and the mean concentration 0.14 mg/kg. Of 36 feedstuffs purchased from local manufacturers, only a peanut meal contained aflatoxin B1 (0.5 mg/kg). Eleven feedstuffs were associated with field outbreakds of animal disease and 7 of these contained aflatoxin. However, the level of aflatoxin contamination was insufficient to account for the described disease symptoms.

Aflatoxin production by a variant of Aspergillus oryzae (NRRL strain 1988) on cowpeas (Vigna sinensis).

Aflatoxin B1, B2, G1, and G2 are produced when a variant of Aspergillus oryzae (NRRL strain 1988) is grown on cowpeas or rice. The present study indicates that a strain of Aspergillus oryzae approved for use in food processing is variable and the resulting variant, unlike the parent strain, has a propensity to produce aflatoxin.

The effects of aflatoxin B1 and palmotoxins B0 and G0 on the germination and leaf colour of the cowpea (Vigna sinensis).

Aflatoxin B1, crude aflatoxins and palmotoxins B0 and G0 were tested for seed germination and chlorophyll formation using the cowpea. It was found that aflatoxin B and crude aflatoxins inhibited both chlorophyll formation and seed germination and palmotoxins inhibited these processes to a lesser extent. 3 — Indolylacetic acid reduced the inhibitory effects of the aflatoxins in seed germination and chlorophyll formation in the cowpea.

The effects of aflatoxin B1, citrinin, and ochratoxin A on amino acid uptake and incorporation by cucumber

Both aflatoxin B1 and citrinin, in light and darkness, inhibited leucine uptake and its incorporation into protein by cucumber cotyledon disks. Aflatoxin was more inhibitory in the light and both toxins showed increased inhibition with increasing concentration. At a concentration of 50 μg/ml, citrinin was more inhibitory to amino acid absorption than aflatoxin. Time-course studies showed that a pretreatment time of at least 2 h was necessary with aflatoxin to affect the subsequent incorporation of leucine; citrinin, on the other hand, was inhibitory when it was supplied together with the 14C-leucine. In darkness, ochratoxin A at 10, 50, and 100 μg/ml enhanced leucine uptake but did not affect its incorporation into protein.

Aflatoxin-induced hepatic injury in the African monkey.

Aflatoxin B1, fed to African monkeys (Cereopithecus aethiops) in doses of 0.01 to 1.0 mg daily until death, produced a consistent histological pattern of hepatic toxicity characterized by centrilobutar loss of stainable cytoplasm and necrosis with mid-zonal fatty change, but without hemorrhage, fibrosis, or bile-duct proliferation. This toxic hepatitis, induced for the first time in a primate by aflatoxin, is similar to that occasionally seen in man and was preceded by mild elevations of bilirubin concentration and serum glutamic oxaloacetic transaminase activity, reflecting hepatic necrosis.

Stability of Individual Aflatoxin B1, B2, G1, and G2 Standards in Benzene and Chloroform Solutions

Abstract Aflatoxin B1, B2, G1, and G2 primary standards were stored in benzene and chloroform solutions for 1 year at 28 and –18°C. Storage at either temperature produced only minor changes in molar absorptivity; the decreases ranged from 0.5 to 2.9% and averaged 1.9% at 28°C and ranged from 0.3 to 1.4% and averaged 1.0% at –18°C. Solution fluorescence KQ showed a greater decrease; it ranged from 8 to 22% and averaged 15% at 28°C and ranged from 7 to 19% and averaged 14% at –18°C. Thin layer chromatography of standards stored 1 year showed a single spot for each aflatoxin and the absence of any other fluorescent derivatives.

Zebra Fish Eggs and Larvae as Aflatoxin Bioassay Test Organisms

Abstract Aflatoxin B1 is acutely toxic to embryos and larvae of zebra fish, Brachydanio rerio (Hamilton-Buchanan). These organisms are sensitive to sub-microgram quantities of the toxin and can be used as bioassay test organisms. The larval response is easier to measure than embryonic response, and a standard dosage-mortality curve for the larvae can be developed in 33 hr. As an aflatoxin bioassay test organism, the larvae of zebra fish have several advantages over other test organisms, including ducklings, embryos, and tissue cultures. They require no special skill or equipment and can be obtained easily in the laboratory throughout the year.

Response of Fertilized Eggs of the Mollusk Bankia setacea to Aflatoxin

Abstract Aflatoxin B1 inhibits cell cleavage in fertilized mollusk eggs without preventing fertilization or nuclear division. The reaction is very dramatic and positive since fertilized eggs in the presence of aflatoxin are multinuclear, whereas the controls have multiplied to multicellular larvae. The bioassay requires a minimum of technique and training and is sensitive to concentrations of 0.05 μg/ml. Because the reaction is observed with the aid of a low-powered microscope (70X), the concentration of aflatoxin required can be reduced considerably below 0.05 μg. The test required two to four hours for completion when observing egg division and 18 hours for swimming larvae.