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PubMed2004

[Monitoring the important mycotoxin biomarkers (ochratoxin A, aflatoxin M1) in the Czech population].

BACKGROUND: In among mycotoxins, secondary metabolites of toxinogenic moulds, ochratoxin A and aflatoxins occupy a prominent place. These mycotoxins have been--as etiologic agents-- associated with a wide numbers of acute and chronic human diseases including mycotoxicoses like Balkan endemic nephropathy or liver cancer. While the risk of acute toxic effects of ochratoxin A and aflatoxin B1 is usually considered to be minimal in the Czech Republic, the situation is different as far as the risk of the late toxic effects (particularly carcinogenic), which result from a single or repeated intake of low doses of these mycotoxins from foodstuffs is concerned. METHODS AND RESULTS: The presence of ochratoxin A and aflatoxins in human environment has been monitored within the program "Monitoring the health state of the population". As for ochratoxin A, 2206 samples of blood serum were investigated, 2077 (94 %) of them turned out to be positive (with levels > or = 0.1 microg x l(-1)), the average was 0.28 microg x l(-1), the median was 0.2 microg x (l(-1), and the percentile (90%) was 0.5 microg x l(-1). The ochratoxin A levels ranged from 0.1 to 13.7 microg x l(-1) of sera. The presence of ochratoxin A was also analyzed in 30 samples of human kidneys; 12 samples were positive (with levels > or = 0.1 microg l(-2), the average was 0.07 microg x kg(-1), the median was 0,05 microg x kg(-1). As for aflatoxins, in 1997-1998 the presence of aflatoxin M1 was investigated in 205 samples of human urine; 118 samples (58%) were positive (with levels >125 pg x l(-1) of urine). CONCLUSIONS: When calculated to a concentration of creatinine in urine, the average was 391 pg x g(-1), the median was 127 pg x g(-1), and the percentile (90%) was 585 pg x g(-1). The aflatoxin M1 levels ranged from 19 to 19 219 pg x g(-1) of creatinine.

Aflatoxin M1↗

PubMedDate not supplied

Characterization of the toxicity of the mycotoxins aflatoxin, ochratoxin, and T-2 toxin in game birds. II. Ringneck pheasant.

Ringneck pheasants were fed diets containing 1.25, 2.5, or 5 ppm aflatoxin; 1, 2, or 4 ppm ochratoxin A (OA); or 4, 8, or 16 ppm T-2 toxin. Severe toxin-induced mortality was seen during the first to third weeks with 2.50 and 5.00 ppm aflatoxin (92.5% and 97.5%, respectively), compared with the mortality in control pheasants fed no toxin (0%). Slight mortality (less than or equal to 5%) was seen with OA and T-2 toxin. Body weights were significantly decreased by the lowest level (1.25 ppm) of aflatoxin by 2 weeks of age, by the two highest levels of aflatoxin by 1 week of age, and by 16 ppm T-2 toxin by 1 week of age. The feed-conversion ratio was increased by 2.50 and 5.00 ppm aflatoxin compared with the feed-conversion ratio in controls, although high mortality may have influenced the results. Aflatoxin had no effect on liver weight, but OA increased kidney weight in 3-week-old pheasants. Mouth lesions were seen in some of the pheasants fed T-2 toxin.

Aflatoxins↗

PubMedDate not supplied

Characterization of the toxicity of the mycotoxins aflatoxin, ochratoxin, and T-2 toxin in game birds. III. Bobwhite and Japanese quail.

Bobwhite and Japanese quail were fed diets containing 1.25, 2.50, or 5.00 ppm aflatoxin; 1, 2, or 4 ppm ochratoxin A (OA); or 4, 8, or 16 ppm T-2 toxin. Aflatoxin induced mortality in bobwhites during the second and third week with 1.25 ppm (10%), 2.50 ppm (30%), and 5.00 ppm (40%), and during the same period with T-2 toxin at 8 ppm (20%) and 16 ppm (22.5%). Body weights of bobwhite quail were significantly decreased by the two higher levels of aflatoxin by 2 weeks of age, and by the two higher levels of T-2 toxin by 1 week of age. In Japanese quail, only the highest level of aflatoxin and T-2 toxin reduced body weight (by 3 weeks and by 1 week of age, respectively), and even then to a much lesser extent than in bobwhites (less than 10%). Aflatoxin did not affect feed-conversion ratio (FCR) in bobwhite quail, but the two higher levels of T-2 toxin increased FCR. None of the toxins induced mortality or increased the FCR in Japanese quail. Aflatoxin increased liver weight in both bobwhite and Japanese quail. OA increased kidney weight in 3-week-old Japanese quail but had no effect on the kidney weight of bobwhite quail. Mouth lesions were progressively more severe in bobwhite quail fed increasing levels of T-2 toxin, but lesions were far less severe in Japanese quail.

Aflatoxins↗

PubMed2006

Clinical significance of aflatoxin, mutant P53 gene and sIL-2 receptor in liver cirrhosis and hepatocellular carcinoma.

The incidence of hepatocellular carcinoma (HCC) varies widely worldwide. Chronic infection with hepatitis B virus (HBV) and exposure to aflatoxins in foodstuffs are the main risk factors. AAG to AGT transversion at codon 249 of the P53 gene arg-ser (249ser) has been identified as a hotspot, reflecting DNA damage caused by aflatoxin B1 metabolites in HCC. Because HBV infection is often endemic in high aflatoxin exposure areas, it is still not clear whether HBV acts as a con-founder or as a synergistic partner in the development of the 249ser P53 mutation. Serum levels of soluble interleukin 2 receptor (sIL-2R) correlated with the progression of liver cirrhosis independently of its etiology. This fact may reflect the stimulation of T-lymphocytes, monocytes and macrophages in liver cirrhosis. The inter-relationship among aflatoxin exposure, HBV & HCV infections, P53 & sIL-2R in patients with liver cirrhosis and hepatocellular carcinoma was studied. The results revealed significant increase in serum levels of mutant P53, sIL-2R and aflatoxin B1 in patients with cirrhosis and those with HCC compared to the controls. HCC patients showed levels of all the three parameters significantly higher than both cirrhotics and controls (P<0.001). Correlations were found between serum aflatoxin B1, mutant P53 and sIL-2R in HCC group. The results were discussed.

Aflatoxin B1↗

PubMedDate not supplied

Black tea ameliorates aflatoxin-induced lipid peroxidation in the kidney of mice.

Oral administration of 25 and 50 mg of aflatoxin in 0.2 mL olive oil/animal/day for 30 days caused dose-dependent and significantly higher lipid peroxidation in the kidney of aflatoxin-treated mice than in the controls. The levels of non-enzymatic antioxidant such as glutathione as well as the enzymatic antioxidants such as superoxide dismutase, glutathione peroxidase and catalase were significantly lower in the kidney of aflatoxin-treated mice than in the controls. Black tea extract (2%) treatment significantly ameliorates aflatoxin-induced lipid peroxidation, which could be due to higher enzymatic and non-enzymatic antioxidants in the kidney of mice as compared with that given aflatoxin alone. These findings suggest that black tea extract treatment significantly ameliorates aflatoxin-induced lipid peroxidation in the kidney of mice.

Aflatoxins↗

PubMed2003

The effect of bread making steps on the degradation of aflatoxins produced as a result of single inoculation with Aspergillus flavus and combined inoculation with Aspergillus flavus and Aspergillus ochraceus.

This study aimed to determine the effect of bread making steps on the stability of aflatoxin. Sakha 8 wheat and Gemaiza 5 wheat cultivars, were used in the present study. They were inoculated with a dense spore suspension of toxigenic fungal species of Aspergillus flavus and a non toxigenic species of Aspergillus ochraceus singly and combined. Aflatoxin concentration was determined in the whole wheat grain, after milling, after fermentation, and after bread-baking process. Results showed that the highest reduction percentage for the total aflatoxins (81, G1 and G2), was in Sakha 8 (32.96%) (single treatment), Gemaiza 5 (19.54%) (single treatment ), Gemaiza 5 (18.65%) (combined treatment), and finally in Sakha 8 (16.49%) (combined treatment). There was no significant difference (p < 0.05) in aflatoxins content between Sakha 8 and Gemaiza 5 treated singly and in a combined way before and after milling process. In the mean time, the percentage of AFB1, AFG1 and AFG2 were reduced by 31.98%, 44.53% and 35.35%, respectively, while the total aflatoxins concentration were reduced by 41.17% after baking. Results also showed the presence of a significant difference at p < 0.05 among the whole grain, after milling and after baking concerning AFG1, AFG2 and the total aflatoxins content. No significant difference was found in case of AFB1.

Aflatoxins↗

PubMedDate not supplied

Comparison of an ELISA-based screening test with liquid chromatography for the determination of aflatoxins in corn.

An enzyme-linked immunosorbent assay (ELISA) screening test (CITE PROBE) was compared to liquid chromatography (LC) for the determination of aflatoxins in naturally contaminated corn samples. The CITE PROBE, with a positive/negative cutoff of 5 ng/g aflatoxin B1, was correct (based on LC results) on 47 of 51 samples. Two of the incorrect responses by the CITE PROBE were false positives on samples containing 4.4 ng/g and 4.1 ng/g aflatoxins by LC. Another incorrect response was a false negative on a sample containing 5.5 ng/g aflatoxins by LC. The fourth incorrect response was a false positive on a sample containing 1.9 ng/g aflatoxins by LC. On the basis of these results, the CITE PROBE was determined to be a reliable screening method for the detection of greater than or equal to 5 ng/g aflatoxins in corn.

Aflatoxins↗

PubMed1977

Repair of DNA in human cells after treatment with activated aflatoxin B1.

Repair replication was examined in cultured human cells exposed to the hepatocarcinogen aflatoxin B1 using the combined bromodeoxyuridine density label and radioisotopic label method. Semiconservative DNA synthesis was strongly inhibited, and the repair replication mode was stimulated in diploid fibroblasts (W138) and in their SV40 transformants (VA13) only when exposure to aflatoxin B1 was in the presence of an activating system containing rat liver microsomal enzymes. The maximum amount of repair synthesis was about 20% of that obtained after saturating doses of ultraviolet light (UV). The time course of repair synthesis was similar to that seen after UV, and most of the synthesis was in 30- to 50-nucleotide "short patches." A line of SV40-transformed xeroderma pigmentosum cells (Group A) deficient in repair after exposure to UV was similarly deficient in repair replication after aflatoxin treatment. Treatment with aflatoxin resulted in a 25 to 45% inhibition of UV-induced repair replication, suggesting that in addition to producing lesions in DNA, which are substrates for the excision repair system, the toxin also inhibits excision repair. CsC1 gradients of DNA treated in vitro with activated aflatoxin demonstrated binding of the drug to DNA. Alkaline sucrose gradient sedimentation gave no indication that single-strand breaks or alkali labile bonds were introduced into DNA by treatment of cells with activated aflatoxin.

Aflatoxins↗

PubMedDate not supplied

Primary liver cancer and aflatoxin intake in Transkei.

Transkei has an intermediate primary liver cancer (PLC) rate that is unusually high for a corn-based subsistence economy. The situation is complicated by a very high esophageal carcinoma incidence rate and known exposure to hepatocarcinogenic N-nitrosamines. A total of 623 cooked food samples were collected from two northeastern and two southern districts over two seasons, in a single-sample grid pattern, for aflatoxin analysis. Aflatoxin B1 was quantitated in 26% of all samples during 1976, resulting in a mean contamination rate of 0.65 microgram/kg wet food. Mean contamination during 1977 was 0.66 microgram/kg, and 24% of samples were positive. Thus for both years a mean aflatoxin B1 intake of 16.5 ng/kg body weight per day was calculated. When the data were plotted on our published PLC incidence-aflatoxin intake graph constructed with standardized data from four countries, Transkei was well within the 95% confidence limits. Individual district comparisons are handicapped by as yet inadequate PLC incidence data, but rank order correlations (rs) between aflatoxin intakes and the PLC incidence in goldminers originating from the study districts were significant (P less than .05). Corn was the basis of 95% of the meals and was also the main source of contamination. Six of 23 samples of home-brewed corn beer were positive for aflatoxin, resulting in an overall contamination of 0.69 microgram/L.

Aflatoxins↗

PubMedDate not supplied

Comparison of two immunochemical methods with thin-layer chromatographic methods for determination of aflatoxins.

Three different methods were compared for the determination of total flatoxins in corn and peanuts naturally contaminated with aflatoxins and in corn, peanuts, cottonseed, peanut butter, and poultry feed spiked with aflatoxins B1, B2, and G1. The 3 methods were an enzyme-linked immunosorbent assay (ELISA) screening test; a monoclonal antibody-affinity column-solid-phase separation method; and the AOAC official thin-layer chromatography (TLC) methods for all except poultry feed, for which Shannon's TLC method for mixed feed was used. The ELISA test is designed to provide only positive results for total aflatoxins at greater than or equal to 20 ng/g or negative results at less than 20 ng/g. The affinity column separation is coupled with either bromination solution fluorometry to estimate total aflatoxins or liquid chromatography (LC) to quantitate individual aflatoxins. Fluorodensitometry was used to determine aflatoxins in commodities analyzed by the TLC methods. The LC and TLC results were in good agreement for all the analyses. The results for the affinity column using bromination solution fluorometry were similar except those for cottonseed, which were about 60% higher. The ELISA screening method correctly identified naturally contaminated corn and peanut positive samples. No false positives were found for controls. The correct response for spiked corn, raw peanuts, peanut butter, and cottonseed at greater than or equal to 20 ng aflatoxins/g was about 90%. The correct response for spiked poultry feed at greater than or equal to 20 ng aflatoxins/g was about 50%.

Aflatoxins↗

PubMed1989

[Studies on chemical analysis of mycotoxin (XX). Chemical analysis of aflatoxins in corn and corn-products].

The investigation was carried out to analyze aflatoxins contaminated corn. 1) Methanol, chloroform and acetonitrile were used as the extraction solvents for aflatoxins added to corn. As the result, the method using acetonitrile was found to be effective to extract and detect aflatoxins. 2) The Rapid detection of aflatoxins was made possible by using the affinity column (containing monoclonal antibodies against aflatoxins bound onto agarose) and the mini-column. The detection-limit was 20 ppb of aflatoxins in samples.

Aflatoxins↗

PubMed1989

Ultrastructure of hepatic and renal lesions in chickens fed aflatoxin.

Male broiler chicks were given feed and water ad libitum from hatching through 3 weeks of age. The feed contained 0, 1.25, 2.5, and 5.0 micrograms of aflatoxin/g of feed. The chicks were killed by cervical dislocation and specimens of liver and kidney were obtained for electron microscopy on days 3, 6, 9, 17, and 21. In chicks fed 5.0 micrograms of aflatoxin, the primary lesions in liver were hepatocellular lipidosis, enlargement of bile canaliculi, reduction in mitochondrial size, mild lymphocytic infiltration, and hepatocellular degeneration and necrosis. Similar lesions were noticed in some chicks fed 2.5 micrograms of aflatoxin, but none was observed in chicks fed at 1.25 micrograms of aflatoxin. At 5 micrograms of aflatoxin, the most consistent lesion in the kidney was thickening of the glomerular basement membrane. Similar glomerular lesions were observed at 2.5 micrograms of aflatoxin, but not at 1.25 micrograms of aflatoxin. Some foot processes of the glomerular epithelial cells were poorly developed. Fusion of foot processes was not observed and fibrous material was not evident in the basement membrane. The pseudopodia of endothelial cells lining the thickened basement membrane were depleted in number or were absent. Degenerative changes also were observed in the cells of the proximal convoluted tubules, but these were less consistent than those of the glomerulus.

Animals↗

PubMedDate not supplied

Simulation of aflatoxin testing plans for shelled peanuts in the United States and in the export market.

The 1987 United States aflatoxin testing plan for shelled peanuts was designed with a final accept level of 25 parts per billion (ppb) total aflatoxin. Some of the importers of U.S. peanuts use aflatoxin testing plans with accept levels lower than 25 ppb. For example, the accept level of a testing plan used in The Netherlands is 5 ppb B1 or 10 ppb total aflatoxin. Whenever export lots are re-tested for aflatoxin by an importing country, some lots accepted in the United States will be rejected by the importing country's aflatoxin testing plan. Computer models were developed to determine the effects of decreasing the final accept level of the U.S. testing plan on the number of lots accepted and rejected in the United States and the number of exported lots accepted and rejected by The Netherlands testing plan. Decreasing the final accept level of the U.S. testing plan from 25 to 5 ppb increased the number of lots rejected in the United States by 371% while reducing the number of exported lots rejected by 51%. For every additional 8.3 lots rejected in the United States, one less export lot will be rejected.

Aflatoxins↗

PubMedDate not supplied

Aflatoxin B1 and aflatoxicol metabolism in rainbow trout (Salmo gairdneri) and the effects of dietary cyclopropene.

Aflatoxin M1 was identified as a minor metabolite formed by the in vitro incubation of aflatoxin B1 with the postmitochondrial fraction or microsomes from rainbow trout (Salmo gairdneri) liver. Fresh, whole trout liver converted perfused aflatoxin B1 to aflatoxicol and aflatoxin M1, and converted perfused aflatoxicol to aflatoxin B1 and aflatoxin M1. AFB1 reductive activity was found in the 105,000 xg supernatant, while activity converting AFL to AFB1 was distributed about equally in the 105,000 xg supernatant and in the microsomal pellet. Transformation of AFL to AFB1 was not inhibited by CO, but formation of AFM1 was completely blocked. Cyclopropene fatty acids (CPFA)-fed fish produced only one-half to one-third as much AFL from AFB1 as controls, and they produced no detectable AFM1. Most of the unreacted AFB1 was recovered by extraction of the incubation medium by organic solvent whereas, in controls, much of it remained bound to the protein. There was no difference in conversion of AFL to AFB1 when results were expressed in terms of postmitochondrial protein levels. CPFA-fed fish had lower microsomal protein and cytochrome P-450 levels and NADPH-cytochrome c reductase and aldrin epoxidation activities than did controls.

Aflatoxins↗

PubMed1979

Laser fluorometric determination of aflatoxin B1 in corn.

A 2-step chromatographic separation, using both thin layer chromatography (TLC) and high pressure liquid chromatography (HPLC), in conjunction with the high sensitivity of laser fluorometry permits extension of the detection limits of aflatoxin contamination in corn to 0.1 ppb (microgram/kg) with a 26% root mean square variation. Aflatoxin B1 is extracted from corn with water-methanol and cleaned up by TLC. The recovery of aflatoxin from the TLC plates was linear from 10 to 1000 pg. Aflatoxin B1 is converted to the more highly fluorescent B2A derivative by treatment with 1N HCl. Experiments with aflatoxin B1 standard establish a constant conversion to B2A over approximately 3 orders of magnitude in B1 concentration. An extract of the B2A aflatoxin derivative is injected onto a reverse phase HPLC column. A flowing droplet of eluant is irradiated by an amplitude-modulated 325 nm He-Cd ion laser beam, and fluorescence from the droplet is detected by a lock-in amplifier in phase with the laser modulation. Several chromatograms are presented that demonstrate the capability of this procedure for removing interfering components in the corn extract.

Aflatoxins↗

PubMed1979

Extraction, cleanup, and quantitative determination of aflatoxins B1 ANd M1 in beef liver.

A method for the determination of aflatoxin B1 in eggs was applicable for aflatoxin B1 in liver, but ineffective for aflatoxin M1 in liver because of poor recovery of added aflatoxin and interferences in thin layer chromatography. The method was modified by the addition of citric acid to the extracting solvent and ammonium sulfate to the extract solution for removing protein. The elution system for silica gel column cleanup was also changed by substituting methanol for acetone, and adding a step for confirmation of aflatoxin M1 identity. The method has been used successfully for survey and research on aflatoxin residues in animal tissues.

Aflatoxins↗

PubMed1977

[Contamination of cotton seeds and of cotton seed cake by aflatoxin].

Following the discovery of aflatoxin M in cow's milk in the previous study, the contamination with aflatoxin of cotton-seed and cotton-seed cake which constitute the principal feed of local animals was measured. The samples were taken from 2 factories. The grain from the 1st factory was grown in the centre of the country in dry climate, and those from the 2nd source originated from the humid region of the north of Iran. The grain and cotton-seed cake from the 1st factory did not contain aflatoxin before storage. During storage the sample contamination amount and percent increased with time in both regions, with the dry less than the humid. In conclusion, Iranian cotton-seed and cotton-seed cake appear to be contaminated with aflatoxin B in 2 processes. The 1st is aflatoxin contamination before harvest, in the humid region of Iran; the 2nd is general storage aflatoxin contamination in both regions in which humidity and length of storage appear to be the principal factors.

Aflatoxins↗

PubMed1982

High pressure liquid chromatographic determination of aflatoxins in peanut butter using a silica gel-packed flowcell for fluorescence detection.

A high pressure liquid chromatographic method has been developed for determining aflatoxins B1, B2, G1, and G2 in peanut butter. The method is based on extraction with acidified aqueous methanol, partition of the aflatoxin into methylene chloride, and purification of the extract on a 2 g silica gel column. The extracted aflatoxins are resolved on a microparticulate (10 micrometer) porous silica gel column in ca 10 min with a water-washed chloroform-cyclohexane-acetonitrile solvent that contains 2% isopropanol. The fluorescence detection system determines aflatoxins B1, B2, G1, and G2 at low levels, i.e., 0.25 ppb B1, 0.5 ppb G1, and 0.2 ppb B2 and G2. Multiple assays of 5 samples of naturally contaminated peanut butters containing total aflatoxins (B1 + B2 + G1 + G2) at levels of 1, 2, 3, 9, and 17 ppb gave intralaboratory coefficients of variation of 7, 4, 4, 11, and 3%, respectively. Samples spiked at levels of 5, 9, and 17 ppb total aflatoxins showed recoveries of 79, 81, and 81%, respectively.

Aflatoxins↗