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PubMedDate not supplied

Review of the decontamination of aflatoxins by ammoniation: current status and regulation.

Ammoniation of corn, peanuts, cottonseed, and meals to alter the toxic and carcinogenic effects of aflatoxin contamination has been the subject of intense research effort by scientists in various government agencies and universities, both in the United States and abroad. Results of these studies have been well documented over the last 20 years. Engineers have devised workable systems of treatment of whole seeds, kernels, or meals; chemists have identified and characterized products formed from the reaction of aflatoxin B1 with ammonia with and without a meal matrix; biochemists have studied the biological effects of these compounds in model systems; and nutritionists have studied animal responses to rations containing ammoniated or non-ammoniated components. This review describes these studies. Results demonstrate overwhelming support for the efficacy and safety of ammoniation as a practical solution to aflatoxin detoxification in animal feeds.

Aflatoxins↗

PubMedDate not supplied

Rapid determination of aflatoxins in raw peanuts by liquid chromatography with postcolumn iodination and modified minicolumn cleanup.

A method is described for rapid cleanup followed by reverse-phase liquid chromatographic (LC) quantitation of aflatoxins in raw peanuts. A modified minicolumn cleanup is used for sample preparation, and a preliminary estimation of aflatoxin content by minicolumn can be made so that highly contaminated samples can be diluted before LC analysis. The use of the simple, quick minicolumn cleanup eliminates the need for further column or cartridge cleanup, thus greatly reducing sample preparation time. Sensitive quantitation is achieved using a phenyl column, a mobile phase of water-tetrahydrofuran (80 + 20, v/v), and postcolumn derivatization with water-saturated iodine followed by fluorescence detection. The recoveries of aflatoxins B1, B2, G1, and G2 from peanut meal spiked at 3 levels ranged from 71.7 to 88.3% (average 80%) with coefficients of variation from 2.7 to 10.4%.

Aflatoxins↗

PubMedDate not supplied

Relationship of serum alpha-amylase to aflatoxin resistance in Japanese quail.

Serum alpha-amylase (S alpha A) activities were examined in a non-selected population (NS) of Japanese quail and in two lines genetically selected for resistance to aflatoxin. Normal S alpha A activities of both selected lines were significantly lower than that of the NS line (P less than or equal to 0.05). An oral dose of 2.5 mg aflatoxin/kg body weight significantly lowered S alpha A activity in NS quails after 24 hours; 18.0 mg/kg body weight was required to decrease the activity in selected lines to a similar degree. The two selected lines did not differ significantly in response. Disc tube gel electrophoresis of the serum revealed eight bands of S alpha A activity and six S alpha A zymogram phenotypes in the total population using an iodine-staining technique. Neither migration distance nor band width varied with genetic line, but the frequency of quails with at least one of three specific anodic bands was significantly higher in the selected lines (75% and 100%) than in the NS line (27%). The frequencies of the zymogram phenotypes with these bands were similarly increased in the resistant populations. Although there are differences in total S alpha A activity between the selected aflatoxin-resistant lines and the NS line, the presence of specific electrophoretic anodic band types and the S alpha A zymogram may be more useful indicators of aflatoxin resistance.

Aflatoxins↗

PubMed1978

[The biochemical activity of the aflatoxins (author's transl)].

Results of experiments with the Salmonella typhimurium-liver microsome technique make it evident that the mutagenic and carcinogenic metabolite of aflatoxin B1 is aflatoxin B1-2,3-oxide. This compound forms adducts with guanine in DNA. There is a close relationship between the mutagenic activity and the hepatocarcinogenic property of the different aflatoxin derivatives.

Aflatoxins↗

PubMed1986

Dietary aflatoxins, intelligence and school performance in southern Georgia.

In a region of southern Georgia known for poor school performance, the mothers of the mentally retarded children had diets that differed from the average in terms of foods, but did not differ in terms of critical nutrients. The consumption of large amounts of corn, rice, peanuts and milk (foods potentially high in aflatoxins) was significantly related to mental retardation of children in one county having high levels of aflatoxins in the food supply. However, no such relationship was found in a county having trivial levels of aflatoxins in the diet.

Aflatoxins↗

PubMed1985

[Susceptibility of hybrid varieties of sunflower to the formation of aflatoxins].

Aflatoxin is produced on sunflower varieties and hybrids. Since it has been demonstrated that sunflower seed are a natural substrate for aflatoxin production in our country, 4 varieties and 11 hybrids were studied to determine aflatoxin susceptibility. The samples were analyzed after 7 days of inoculation with A. parasiticus NRRL 2999. The varieties and hybrids showed different capacity of toxin production being the varieties more susceptible than the hybrids.

Aflatoxins↗

PubMed1979

[Elimination of aflatoxin B1 by clays from contaminated substrates].

It has been proved that clays were able to absorb aflatoxin B1. The amount of adsorbed aflatoxin depended on the nature of clay. The adsorbing power of the clays was checked in relation to some environmental factors. From this study, it is claimed that clays are suitable for détoxification of liquid food-stuffs poisoned by aflatoxin.

Adsorption↗

PubMed1977

["Milk aflatoxin" and transfer of toxicity].

Diet including 20 p. 100 of lyophilised milk produced by Goat who consumes peanut meals containing 1,530, 79 and 54 microng/kg aflatoxins with 1,136, 64 and 54 microng/kg aflatoxin B1, is given to duckling during 23 days. There is no influence of this diet on growth, feed efficiency and liver or kidney histology. In contrast, direct consummation of Peanut meal, with the highest level of aflatoxins, produces 18 p. 100 mortality and characteristic injuries of aflatoxiocsis.

Aflatoxins↗

PubMed1977

Aflatoxin and liver cancer in Karachi, a preliminary survey.

A cause and effect relationship of Aflatoxin and liver cancer is well established. The incidence of liver cancer is 3.6% in Karachi (Zuberi et al., 1976) and Aflatoxins have been detected in 43% of 28 samples of food analysed in this study. The long term ingestion of aflatoxin with food may have some effect on the existing pattern of liver cancer in Karachi.

Aflatoxins↗

PubMed1977

[Selection of screening methods for the detection of aflatoxins in animal feed].

Five different screening methods of the detection of aflatoxin B1 are compared as to their usability in ten feeds, feed concentrates, and complete feed mixtures. Method II, i. e. the author's modification of the method of Pons et al. (1973) was found to be the best for the highest number of different feeds. Aflatoxin B1-positive findings were obtained in samples of groundnut cake and protein concentrates a) for laying hens and b) for breeding pigs. No aflatoxins were detected in other feed samples: soya, sunflower, maize, fish meal, complete feed mixtures--table trout trout feed, carp stock feed, table carp feed, duckling fattening mixture.

Aflatoxins↗

PubMed1979

Comparative study of two methods for extraction of aflatoxin from peanut meal and peanut butter.

The difference between the CB and Best Foods methods in extracting aflatoxins from peanut products has been studied. The CB method yields 60, 121, 35, and 22% higher results for aflatoxins B1, B2, G1, and G2, respectively for 4 samples of peanut meal and 6 samples of peanut butter studied. Both reverse phase liquid chromatography and thin layer chromatography were used to quantitate the extracted aflatoxins.

Aflatoxins↗

PubMed1979

Distribution of aflatoxins B1 and M1 in contaminated calf and pig livers.

The determination of aflatoxins B1 and M1 in multiple sections of livers from 4 calves and 1 pig exposed to high levels of aflatoxins showed a uniform distribution of the aflatoxins in each liver, within the precision of the analytical method used. The thin layer chromatographic method has an expected within-laboratory coefficient of variation of 15%.

Aflatoxins↗

PubMed1984

Synergism between hepatitis B virus and aflatoxin in hepatocellular carcinoma.

Epidemiological data have suggested that environmental factors play a major role in hepatocellular carcinoma (HCC). Such factors include hepatitis B virus (HBV), infection, chemical carcinogens and parasites. The available data provide compelling evidence of the causative association of HBV with HCC but its exact role has not been defined. Similarly, field studies have indicated the importance of aflatoxin contamination of foodstuffs in areas with high prevalence rates of HCC. The precise role of this mycotoxin has been the subject of debate. The hypothesis that aflatoxin and HBV can interact and cause HCC synergistically has been challenged by those who postulate that aflatoxin merely suppresses cell-mediated immunity, thereby permitting persistence of HBV in the liver.

Aflatoxins↗

PubMed1977

[Antibacterial properties of aflatoxin B1: cytotoxic effects on Bacilus thuringiensis (Berliner)].

In a sensitive strain of Bacillus thuringiensis (Berliner), aflatoxin B1 inhibited growth with a dose above 5.0 microgram/ml. With subinhibitory levels (0.5 - 5.0 microgram/ml) physiological damage (decreased growth rate) and cellular alteration (filamentous cells) were noted. With these doses the mycotoxin disturbs various metabolisms : DNA synthesis (gradual blockage of the specific bacteriophage multiplication and dispersion of nuclear apparatus in giant cells); protein synthesis (decrease of protease secretion (2.0 microgram/ml), thuricin excretion (3.0 microgram/ml) and inhibition of endotoxin formation (4.0 microgram/ml); specific activities (bacterial motility, flagellar arrangment and sporulation were respectively affected with 1.0, 0.5 and 4.0 microgram/ml). The mycotoxin did not affect the metabolism of a resistant mutant isolated in the presence of a lethal dose of aflatoxin B1 (mutation rate : 1.10(8) with 20 microgram/ml). The numerous bacterial responses to aflatoxin B1 indicate that the probable site of its toxic binding may not be restricted to a particular locus on the DNA. On the contrary these observations suggest that there exist many combining affinities of the mycotoxin for intracellular sites or interference with a key-function such as the messenger-RNA synthesis.

Aflatoxins↗

PubMed1977

Mutagenic effect of aflatoxin B1.

The present work aimed to study the mutagenic effect of aflatoxin B1 on human chromosomes. The experiments showed that aflatoxin B1 is a strong chromosome damaging agent. The treated cells showed a high rate of aberrations mainly breaks and interchanges. Using Giemsa banding technique, the study showed that the distribution of breakage points on individual chromosomes was significantly non-random. The study of sister chromatid exchanges (SCEs) indicated that the high incidence of breakage rate was paralled by an increased SCE rate. Some chromosomes were very sensitive to the mutagenic effect of aflatoxin B1, while other chromosomes were very resistant. The present data provides an additional consideration in assessing the risks of exposure to this agent.

Aflatoxins↗

PubMed1977

Aflatoxin and encephalopathy with fatty degeneration of viscera (Reye).

In the past 5 years we have observed 27 children at the age from 3 days to 8 years who died on the encephalic syndrome with fatty degeneration of the viscera (Reye). According to the morphological changes in the liver and to the clinical course, we have divided our cases into 3 groups. In the first group there were 20 children who died within 2-10 days after the first symptoms of the disease appeared. In their liver diffuse fatty degeneration was found. In the second group there were 3 children who died within 1-2 months after the acute onset of the disease. In their liver fibrosis with bile duct proliferation and steatosis were found. In the third group there were 4 children who died within 2-4 months after the first symptoms. Their liver showed cirrhosis. The bacteriological and virological investigations in all cases were negative, but in the most of them direct contacts with viral infections were proved. In the liver specimens of the children in all 3 groups the presence of aflatoxin B1 chromatographically and spectrophotometrically was found. The source of the intoxication in 5 cases was aflatoxin contaminated milk food. Our observations of 2 - 3 - days old newborns with the morphological changes similar to that of Reye's syndrome seems to support our hypothesis about the possibility of the intrauterine intoxication. We suggest that aflatoxin represents an important factor in the etiology of this syndrome and a high risk for human health.

Aflatoxins↗

PubMedDate not supplied

Mycotoxins in grain dust: method for analysis of aflatoxins, ochratoxin A, zearalenone, vomitoxin, and secalonic acid D.

A multimycotoxin method is presented to quantitate aflatoxins, ochratoxin A, zearalenone, secalonic acid D, and vomitoxin in grain dust. Dust spiked with these mycotoxins was extracted sequentially with methylene chloride followed by acetonitrile-water (86 + 14). Vomitoxin was recovered in the latter extract and all other mycotoxins were recovered in the methylene chloride. Aflatoxins and ochratoxin were quantitated by fluorescence measurement on silica thin layer chromatographic plates. The other mycotoxins were quantitated after cleanup by reverse phase liquid chromatography and ultraviolet detection. Recoveries from dust spiked in the parts per billion (ng/g) range were approximately 80% (SD = 15-29%) for all mycotoxins. Minimum detectable amounts ranged from less than 0.5 ng/g for aflatoxins to 20 ng/g for zearalenone.

Aflatoxins↗

PubMed1980

Survey for aflatoxins and Zearalenone in canned and frozen sweet corn.

Aflatoxins and zearalenone were determined in 263 samples of canned or frozen sweet corn, collected from packing plants during the 1976 and 1977 packing seasons. As anticipated from geographic, agronomic, and microbiological considerations, no aflatoxin or zearalenone was found. Based on this sampling, the highest incidence of detectable aflatoxin that could be statistically anticipated in the major packing areas is 1.5%.

Aflatoxins↗