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PubMedDate not supplied

Modification of aflatoxin B1-induced changes in certain mitochondrial enzymes and lipids by medroxyprogesterone acetate.

The effect of a single dose of 5 mg/kg body weight of aflatoxin B1 on rat liver mitochondrial enzymes, succinate dehydrogenase (SDH) and Mg++ adenosine triphosphatase (Mg++-ATPase) and on certain lipids were studies at various intervals of time from 3 to 24 hours. A significant decrease in the specific activity of SDH was observed after 6, 12, 18 and 24 hr treatment. The Mg++-ATPase activity remained unaffected up to 12 hr but appreciably decreased after, 18 and 24 hr of the treatment. The level of phospholipids and cholesterol were not altered after 3, 6 and 12 hr treatment, thereafter (18 and 24 hr) an increase was observed in both the lipids following the aflatoxin treatment. Medroxyprogesterone acetate (MPA) did not cause any alteration in the specific activities of these enzymes as well as levels of cholesterol and phospholipids. The treatment with MPA caused significant increase in contents of cytochromes P-450, b5 and activities of Arylhydrocarbon hydroxylase (AHH), UDP-glucuronyl transferase (UDP-GT) and NADPH-cytochrome C-reductase of hepatic microsomes. It was observed that pretreatment with medroxyprogesterone acetate (MPA) could significantly minimuze the depression caused in mitochondrial SDH and Mg++-ATPase activities by aflatoxin B1.

Aflatoxin B1↗

PubMed1987

Aflatoxin, viral hepatitis and primary liver cancer.

Thirty-eight cases of primary liver cancer (PLC) from the Department of Pathology, Charles University, Hradec Kralové were investigated. The viral hepatitis HBsAg antigen was found in the sera of 8 of the 38 patients. Radioimmunoassay demonstrated aflatoxin in 27 of 34 cases. Fluorescence microscopy revealed a fluorescence characteristic of aflatoxin and its fluorescent metabolites in the peritumoral tissue and the tumor for all of the cases studied. This study emphasizes the increasing incidence of PLC over the last 15 years. In addition, this type of cancer now appears to develop in a different manner: reduction in the number of cases with cirrhosis, progressive rise in the number of women affected, and occurrence of PLC in children and adolescents. These observations tend to indicate that aflatoxin might play a significant role in the genesis of PLC.

Adenoma, Bile Duct↗

PubMed1986

Measurement of aflatoxin B1, its metabolites, and DNA adducts by synchronous fluorescence spectrophotometry.

Sensitive and specific methods are needed for measuring human exposure to carcinogens. Synchronous fluorescence spectrophotometry can be used to measure fmol of aflatoxins, their metabolites, and DNA adducts. Computer-assisted analysis of spectra of these agents obtained by synchronous fluorescence spectrophotometry can be displayed as contour maps which are highly specific for each agent. Individual agents in mixtures, e.g. aflatoxins B1 and M1, can be identified by fourth derivative spectral analysis. This physical method should complement immunological and other methods to measure aflatoxin B1, its metabolites, and nucleic acid adducts.

Aflatoxin B1↗

PubMedDate not supplied

Interaction of aflatoxin B1 with bacterial DNA: possible relationship to bacteriophage induction in lysogenic Bacillus megaterium.

Studies were conducted to determine possible interactions between aflatoxin B1 and deoxyribonucleic acid (DNA) and induction of bacteriophage formation in lysogenic Bacillus megaterium NRRL-B-3695. At pH 7.4, the spectrophotometric characteristics of B1 with various concentrations of calf thymus DNA were altered with both a hypochromic shift and a shift of the wavelength for maximum absorbance of the toxin. Aflatoxin B1 apparently interacted with DNA as indicated by spectrophotometric analysis and ultrafiltration studies. Under alkaline conditions (pH 10.0), spectrophotometric characteristics of this interaction were altered from those observed at pH 7.4. Toxin incubated at pH 7.4 could induce bacteriophage formation but failed to do so at pH 10. Preincubation of toxin with calf thymus DNA did not block subsequent induction. It is proposed that a bacterial DNA-toxin interaction, involving an alkaline-labile bond of aflatoxin B1, is necessary to cause induction of bacteriophage formation in lysogenic B. megaterium.

Aflatoxin B1↗

PubMedDate not supplied

Production and isolation of aflatoxin M1 for toxicological studies.

One hundred mg aflatoxin M1 was produced and purified for toxicological studies. Aspergillus flavus NRRL 3251 was cultured on rice to produce aflatoxins B1, B2, M1, and M2, B1 and B2 were separated from M1 and M2 by a normal phase low pressure liquid chromatography (LC) column. M1 was then separated from M2 by a reverse phase low pressure LC column. Recoveries of aflatoxins from the LC columns were about 90%. The purified M1 was confirmed by ultraviolet-visible spectrometry, mass spectrometry, nuclear magnetic resonance spectrometry, optical rotation, and its mutagenicity to Salmonella typhimurium TA98.

Aflatoxin M1↗

PubMed1986

Aflatoxins in the livers of children with kwashiorkor in Ghana.

Autopsy liver specimens from 22 kwashiorkor children in Ghana were analysed for the presence of aflatoxins using both high performance liquid chromatography and thin layer chromatography. Aflatoxin B1 was found in the livers of 20 subjects and aflatoxicol in the livers of the remaining two subjects. These results confirm previous findings of aflatoxin B1 and aflatoxicol in the livers of children with kwashiorkor and provide further evidence of associations between these toxic compounds and kwashiorkor which might have relevance to the aetiology and pathogenesis of this disease which as yet remain mysterious.

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↗

PubMed1986

Investigation of aflatoxin contamination in commercial Spanish peanuts.

In the present study aflatoxin contamination was investigated with 102 peanut samples. Only 11 samples showed contamination by that mycotoxin. Concentration was less than 15-20 micrograms/kg in all the contaminated samples. Aflatoxin B1, B2, G1, and G2 were detected in the above-mentioned samples. No significant difference was found between shell and shelled peanuts owing to aflatoxin contamination.

Aflatoxin B1↗

PubMedDate not supplied

Thin layer chromatographic confirmation of aflatoxin M1 extracted from milk.

Aflatoxin M1 can be confirmed directly on a thin layer plate by reacting the toxin with a mixture of reagents containing p-anisaldehyde. This confirmatory procedure requires only 2 elutions in the same direction using 2 different solvents. The mixture containing p-anisaldehyde is overspotted on M1 after the plate has been developed in toluene-ethyl acetate-ethyl ether-formic acid (25 + 35 + 40 + 5). The plate is heated at 110 degrees C for 10 min and then developed in hexane-acetone-chloroform (15 + 50 + 35). The Rf value of the green fluorescent derivative is less than that of the M1 standard. This confirmatory procedure requires only one-dimensional TLC, so several sample extracts and the standard can be run simultaneously. The minimum detectable quantity of aflatoxin M1 on the TLC plate with this test is 0.3 ng. p-Anisaldehyde reagent solution may also be used as a spray reagent for the confirmation of aflatoxin M1. The procedures described were satisfactory for confirming the mycotoxin in spiked samples of powdered and liquid milk.

Aflatoxin M1↗

PubMed1986

The mutagenicity of aflatoxin Q1 to Salmonella typhimurium TA 100 with or without rat or human liver microsomal preparations.

An investigation of the mutagenicity of aflatoxin Q1 in the Salmonella-mutagenicity test is reported. This mammalian metabolite of aflatoxin B1 was marginally mutagenic to strain TA 98 when either rat or human liver microsomes were present in the test. However, it was mutagenic to TA 100 with the same liver activation sources in the assay. Moreover, it was mutagenic to TA 100 in the absence of liver microsomes. This Q1 mutagenesis, presumably a direct acting base substitution effect, was nearly equal to the liver activated mutagenesis. It was also greater in this respect than aflatoxin B1 or aflatoxicol.

Aflatoxin B1↗

PubMed1987

[SH group content and hydrolase activity of the small intestine mucosa in chickens fed a mixture containing aflatoxin B1].

The effect of aflatoxin B1 on the content of SH-groups and the activity of leucinamino peptidase, Mg (Na+, K+), ATP, and glucoamylase in the mucous membrane of the small intestine of birds was studied. The experiment was carried out with three groups of male broilers. The controls were given starter and finisher mixtures with 21.6 and 19.5 per cent protein, with no aflatoxin B1. The birds of the test groups (II and III) were offered one and the same mixture containing 0.250 and 0.600 ppm of aflatoxin B1. By the end of the finisher period on the 49th day mucosa homogenate was used to determine the content of SH-groups and the activity of leucinamino peptidase, Mg (Na+, K+), ATP, and glucoamylase. It was found that rates of 0.600 ppm in the feed suppressed the activity of Mg (Na+, K+) ATP in the mucosa of the small intestine. Lower amounts (0.250 ppm) produced no effect on the activity of this enzyme. Leucinamino peptidase, glucoamylase, and the SH-groups did not change essentially their activity at the two rates of the toxin.

Aflatoxin B1↗

PubMed1987

Prevalence of aflatoxin B1 in commercial poultry rations in Nigeria.

122 samples of commercial poultry feed from 5 southern states of the Republic of Nigeria were investigated for their content of aflatoxin B1.57.4% of all samples examined contained aflatoxin B1. The relative prevalence levels in chick, broiler starter, broiler finisher, layers, and growers rations were 33.3, 50.0, 58.4, 68.6, and 52.1%, respectively. The aflatoxin content of the samples analysed varied between 0.57 and 2.55 micrograms/g.

Aflatoxin B1↗

PubMedDate not supplied

Optimum conditions for formation of aflatoxin M1-trifluoroacetic acid derivative.

Because thin-layer chromatographic (TLC) confirmation of identity and reverse-phase liquid chromatographic (LC) determination with fluorescence detection of aflatoxin M1 both require the derivative formed in the reaction of M1 and trifluoroacetic acid (TFA), various reaction conditions were studied to obtain complete derivative formation. Of the various organic solvents tested, the reaction between M1 and TFA proceeded best in the nonpolar solvents hexane and isooctane. Other parameters investigated were reaction temperature and time, aflatoxin M1 concentration, and solvent volume. The following procedure is considered optimum: 200 microL each of hexane and trifluoroacetic acid are mixed with M1 standard in a silylated glass vial or with milk residue in a regular glass vial with a Teflon-lined screw cap and heated 10 min at 40 degrees C. The mixture is evaporated to dryness under N2, and the derivative is saved for TLC or LC. No unreacted aflatoxin M1 was detected by reverse-phase LC after this procedure was incorporated for analysis of milk samples.

Aflatoxin M1↗

PubMed1988

An epidemiological investigation associating aflatoxin M1 with milk production in dairy cattle.

An attempt was made to utilize the analysis for aflatoxin M2 in milk, instead of aflatoxin B1 in feed for a pilot epidemiological study addressing the association of M1 levels and various production parameters. Four dairy farms, representing above average to below average management practices, were identified with 10 animals being randomly selected from each farm for this study. Milk samples and production data were evaluated from these animals in order to gain insight into the possible effects of low level mycotoxin ingestion on production and to test whether or not this approach offered potential for future epidemiological studies. Feed samples were basically negative for the presence of aflatoxin B1, yet milk analysis revealed the presence of M1 in a large percentage of the animals. Further, the M1 levels appeared to be associated with a decrease in daily milk production. This study indicates that employing M1 analysis in milk for epidemiological investigations of low level mycotoxin ingestion effects, instead of B1 feed analysis, is feasible and offers a potential for more definitive studies in this area.

Aflatoxin M1↗

PubMed1988

DNA strand scission and apurinic sites induced by photoactivated aflatoxins.

Covalent binding of photoactivated aflatoxins to DNA in vitro under close-to-physiological conditions resulted in the formation of apurinic sites and in strand scission. Linearized pBR322 DNA was randomly fragmented, and supercoiled DNA was relaxed during the binding reaction. A primary amine facilitated fragmentation and relaxation. Quantitative measurements of relaxation revealed that the probability of a binding event to be converted into a DNA chain break was approximately 3-5% in the absence of a primary amine. The presence of the latter increased the probability approximately 2- to 3-fold. The results are compatible with the model that photoactivated aflatoxins bind to guanines on DNA; some of these guanine adducts are released, creating apurinic sites. The latter are converted into DNa chain breaks at physiological pH and temperature. Thus, apurinic sites and DNA chain breaks must be considered as quantitatively important (genotoxic) DNA damage induced by aflatoxins.

Aflatoxin B1↗

PubMed1988

Gene-specific differences in the aflatoxin B1 adduction of chicken erythrocyte chromatin.

Mature and immature chicken erythrocyte nuclei were treated with activated aflatoxin B1 (2,3-dichloroaflatoxin B1), producing covalently bound DNA adducts. This reaction produces alkali-labile sites in the DNA which can be identified by using a variation of the Maxam-Gilbert sequencing procedure. We determined the aflatoxin B1 accessibility of defined regions of the erythroid genome by using different specific probes and monitoring the disappearance of similar-sized fragments generated by restriction enzyme digestion. The genes studied were the erythroid-specific beta-globin and histone H5 genes, which are potentially active in mature erythroid nuclei and transcriptionally active in immature erythrocytes, and the vitellogenin and ovalbumin genes, which are both transcriptionally inactive in these cells. The beta-globin and histone H5 genes were more accessible than the repressed vitellogenin and ovalbumin genes to aflatoxin B1 modification in mature and immature erythroid chromatin. Micrococcal nuclease was used to probe the nucleosomal organization of active (beta-globin and histone H5) and repressed (vitellogenin and ovalbumin) genes in chicken erythrocytes. The vitellogenin and ovalbumin genes show a canonical nucleosome repeat pattern in mature and immature chicken erythrocyte nuclei. In contrast, the beta-globin and histone H5 genes lack a distinct nucleosomal repeat pattern in these cells. These results support the hypothesis that transcriptionally active genes are preferentially accessible to carcinogen modification because of their disrupted chromatin structure.

Aflatoxin B1↗

PubMed1988

Detection of exposure to aflatoxin in an African population.

Urinary excretion of 8,9-dihydro-8-(7'-guanyl)-9-hydroxyaflatoxin (AFB-Gua) was studied in areas of different liver cancer incidence in Kenya. Of 983 urine samples analysed for AFB-Gua by high-performance liquid chromatography, 12.6% gave positive results. The chemical identity of AFB-Gua was verified by synchronous scanning fluorescence spectrophotometry. A moderate degree of correlation between prevalence of exposure to aflatoxin B1 and liver cancer incidence could be established in Bantu. People living in areas with high exposure to aflatoxin B, form antibodies that recognize an aflatoxin B1 epitope.

Aflatoxin B1↗

PubMedDate not supplied

Modification of the rapid screening method for aflatoxin in corn for quantitative use.

A study was made to determine if the official AOAC method for screening of aflatoxin in corn could be modified for use as a quantitative method. Several different corn products were analyzed using the modified method, with an average savings of over 1 h/sample vs the CB method. Average recoveries for aflatoxin B1 were 94% for the low level spiked samples and 108% for the high level. Samples of corn and corn products containing naturally incurred aflatoxin were also analyzed with the modified method, and the results compared favorably with those obtained by the CB method.

Aflatoxin B1↗