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PubMed2001

Production of ultrasensitive antibodies against aflatoxin B1.

AIMS: To produce specific antibodies against the haptenic fungal toxin aflatoxin B1 (AFB1) and apply these antibodies in immunochemical assays for aflatoxins. METHODS AND RESULTS: Rabbits were immunized using an AFB1-bovine serum albumin conjugate and serum titres determined by double-antibody enzyme immunoassay. High titres of antibodies with very high affinity for AFB1 were obtained 15 and 4 weeks after the initial immunization and the first booster immunization respectively. The antibodies were employed in enzyme immunoassay (EIA) and immunoaffinity chromatography (IAC) methods for aflatoxins. With a detection limit of 15.8 pg ml(-1) for AFB1, the EIA employing these antibodies is the most sensitive test for AFB1 described so far. In IAC columns, these antibodies provided high binding capacity for all major aflatoxins, including AFB1, AFB2, AFG1 and AFG2. CONCLUSION: The antibodies described here are useful for the analysis of trace levels of aflatoxins. SIGNIFICANCE AND IMPACT OF THE STUDY: Polyclonal antibody-based EIA and IAC methods for aflatoxin analysis offer a suitable alternative to the more expensive monoclonal antibody-based methods.

Aflatoxins↗

PubMed1999

Aflatoxin and liver cancer.

This chapter reviews the data that have been accumulated implicating aflatoxin ingestion as an important risk factor in the aetiology of hepatocellular carcinoma (HCC). Numerous epidemiological studies have observed a correlation between areas of high aflatoxin exposure and a high incidence of HCC. The use of experimental models and specific biomarkers for aflatoxin exposure, such as urinary metabolites or aflatoxin adducts, have validated these findings. Ongoing clinical trials in Qidong, China, have indicated that oltipraz, a chemopreventive agent, can lower the biologically effective dose of aflatoxins by decreasing the metabolism of aflatoxin to its carcinogenic form and increasing the detoxification pathways of these metabolites. Intervention with chemicals such as these, alongside hepatitis B virus immunization programmes and improved storage conditions of staple foods, are prevention measures that can be undertaken to reduce the incidence of HCC in high-risk regions.

Aflatoxins↗

PubMed2004

Chemoprevention of hepatocellular carcinoma in aflatoxin endemic areas.

Hepatocellular carcinoma is one of the most common cancers worldwide. Infection with hepatitis B virus and exposure to aflatoxins in the diet act synergistically to amplify risk. From a public health perspective, hepatitis virus vaccination programs and efforts to both reduce aflatoxin exposures and to attenuate the toxicological consequences of unavoidable exposures should have major impacts on the global incidence of this disease. Experimentally, aflatoxin-induced hepatocarcinogenesis can be inhibited by over a score of different chemopreventive agents with multiple mechanisms of action. One agent, oltipraz, is a potent inducer of phase 2 enzymes involved in the detoxication of carcinogens including aflatoxin. A second agent, chlorophyllin, impedes the bioavailability of carcinogens by forming molecular complexes and enhances their elimination in the fecal stream. This review highlights the findings of recent randomized clinical trials with oltipraz and chlorophyllin conducted in individuals exposed to dietary aflatoxins and at high risk for development of liver cancer. Both chemopreventive agents modulated levels of aflatoxin biomarkers in the study participants in manners consonant with protection. Although pharmacological approaches establish proof of principle and help identify key molecular targets for interventions, food-based approaches that also use these molecular targets may be the most practical for widespread application in high-risk populations.

Aflatoxins↗

PubMed2002

Dominant role of hepatitis B virus and cofactor role of aflatoxin in hepatocarcinogenesis in Qidong, China.

We assessed the separate and combined effects of hepatitis B virus (HBV), hepatitis C virus (HCV), and aflatoxin in causing hepatocellular carcinoma (HCC) in Qidong, China. A consecutive series of 181 pathologic-diagnosed HCC cases were studied for hepatitis B surface antigen (HBsAg), anti-HBc, HBV X gene sequence, anti-HCV, the 249ser-p53 mutation, and chronic hepatitis pathology. Each of the 181 incident HCC cases had markers for HBV infection and hepatitis pathology; only 6 of 119 cases were coinfected with HCV. The 249ser-p53 mutation was found in 54% (97/181) of HCC cases and in all 7 cases with tissue for analysis from the hepatitis cohort but in none of 42 matched cases from Beijing. The estimated cumulative dose of aflatoxin B1 in these 7 cases ranged from 0.13 to 0.49 mg/kg. Follow-up data through 13.25 years on a cohort of 145 men with chronic HBV hepatitis showed that the relative risk from aflatoxin exposure was 3.5 (1.5-8.1). A similar relative risk was found using 249ser-p53 mutation as a marker for aflatoxin exposure. In conclusion, HBV hepatitis is ubiquitous in Qidong HCC cases, whereas HCV contributes little to its risk. The 249ser-p53 mutation appears to result from coexposure to aflatoxin and HBV infection. Even modest levels of aflatoxin exposure tripled the risk of HCC in HBV-infected men.

Adult↗

PubMed1976

Mutagenicity of aflatoxins related to their metabolism and carcinogenic potential.

Aflatoxins and their animal biotransformation products were screened for carcinogenic potential using the Ames' in vitro microbial detection system for carcinogens as bacterial mutagens [B. N. Ames et al. (1973) Proc. Natl. Acad. Sci. USA 70,2281-2285]. Aflatoxicol, aflatoxins G1 and M1, aflatoxicol H1, and aflatoxins Q1, B2, P1, G2, B2a, and G2a, listed in order of decreasing mutagenic potency, were all less active than aflatoxin B1. No compound possesses activity in the absence of the rat liver preparation, and this indicates none of the animal metabolites are the ultimate mutagenic and/or carcinogenic species. The relative mutagenic potency observed with this in vitro system qualitatively correlates with in vivo carcinogenic data. Comparison of both methods indicates: (i) aflatoxin B1 possessed the structure optimal for both mutagenicity and carcinogenicity, (ii) the decreased carcinogenicity of various animal metabolites is associated with their decreased mutagenicity, and (iii) the 2,3-double bond is involved in both the mutagenic and carcinogenic activity of aflatoxins. The Ames' assay has been demonstrated to be an extremely promising (toxicological) tool for the analysis of mycotoxins for mutagenic and/or carcinogenic activity.

Aflatoxins↗

PubMed1977

Structural identification of the major DNA adduct formed by aflatoxin B1 in vitro.

The covalent binding of the hepatocarcinogen aflatoxin B1 by rat liver microsomes to calf thymus DNA resulted in a binding level equal to one aflatoxin residue per 60 DNA nucleotides. An aflatoxin derivative-guanine adduct was efficiently liberated from DNA with formic acid. Analytical reversed-phase high-pressure liquid chromatography of the DNA hydrolysate revealed that approximately 90% of the carcinogen bound to DNA could be accounted for as a single component. Preparative high-pressure liquid chromatography was used to isolate sufficient quantities of the adduct for structural analysis from large quantities (340 mg) of DNA. A combination of spectral and chemical data indicates that the major product of the interaction of metabolically activated aflatoxin B1 and DNA is 2,3-dihydro-2-(N7-guanyl)-3-hydroxyaflatoxin B1 with the guanine and hydroxyl functions possessing a trans configuration. The structural data support the hypothesis that the putative 2,3-oxide of aflatoxin B1 is quantitatively important as an intermediate in the binding of aflatoxin B1 to nucleic acids.

Aflatoxins↗

PubMed1996

Mutational properties of the primary aflatoxin B1-DNA adduct.

The mutagenic activity of the major DNA adduct formed by the liver carcinogen aflatoxin B1 (AFB1) was investigated in vivo. An oligonucleotide containing a single 8,9-dihydro-8-(N7-guanyl)-9-hydroxyaflatoxin B1 (AFB1-N7-Gua) adduct was inserted into the single-stranded genome of bacteriophage M13. Replication in SOS-induced Escherichia coli yielded a mutation frequency for AFB1-N7-Gua of 4%. The predominant mutation was G --> T, identical to the principal mutation in human liver tumors believed to be induced by aflatoxin. The G --> T mutations of AFB1-N7-Gua, unlike those (if the AFB1-N7-Gua-derived apurinic site, were much more strongly dependent on MucAB than UmuDC, a pattern matching that in intact cells treated with the toxin. It is concluded that the AFB1-N7-Gua adduct, and not the apurinic site, has genetic requirements for mutagenesis that best explain mutations in aflatoxin-treated cells. While most mutations were targeted to the site of the lesion, a significant fraction (13%) occurred at the base 5' to the modified guanine. In contrast, the apurinic site-containing genome gave rise only to targeted mutations. The mutational asymmetry observed for AFB1-N7-Gua is consistent with structural models indicating that the aflatoxin moiety of the aflatoxin guanine adduct is covalently intercalated on the 5' face of the guanine residue. These results suggest a molecular mechanism that could explain an important step in the carcinogenicity of aflatoxin B1.

Aflatoxin B1↗

PubMed1979

The influence of vitamin A status on the response of chickens to aflatoxin B1 and changes in liver lipid metabolism associated with aflatoxicosis.

1 A series of experiments were conducted to investigate the effects of dietary retinol status on chickens ingesting aflatoxin B1. The effects of dietary supplementation with biotin and alpha-tocopherol were also examined. 2. Aflatoxin B1 levels greater than 1 mg/kg diet had a detrimental effect on 'liveability', body-weight gain, food intake and food conversion efficiency. When fed for more than 2 weeks aflatoxin increased relative liver weight and liver lipid concentration. These effects were less pronounced with avitaminotic A chickens. 3. A synergistic effect on hydropericardium development was observed between aflatoxin B1 and retinol. This effect was not observed when the dietary level of alpha-tocopherol was increased tenfold. 4. The specific activities of certain hepatic lipogenic and amino acid-metabolizing enzymes were influenced by aflatoxin ingestion. A reduction in lipogenic enzyme activity was observed before a reduction in the activities of amino acid-metabolizing enzymes. 5. Liver fatty acid composition was significantly influenced by aflatoxin B1. The extent of these changes was reduced by the inclusion of additional dietary biotin.

Aflatoxins↗

PubMed1999

Effect of sodium bentonite on the performance and blood variables of broiler chickens intoxicated with aflatoxins.

1. This study was conducted to evaluate the protective effect of natural sodium bentonite (NaB) in the prevention of toxic effects of aflatoxins. Five hundred and twenty-eight 1-d-old Ross male broiler chickens were housed in pens (22 chickens per pen) for 42 d. There were 3 inclusion rates of NaB (0, 2.5, and 5 g/kg) and 2 of aflatoxins (0 and 3 mg/kg food). Each treatment had 4 replicates of 22 chickens. 2. All chickens treated with aflatoxin and without bentonite were adversely affected. NaB treatment at 5.0 g/kg improved body weights at 42 d of age by 31.3%, increased food intake by 23.8% and improved productive efficiency by 40.1%. Weights of liver, heart, pancreas and crop and biochemical variables were not affected by dietary NaB. However, serum phosphorous concentration was reduced by 30% compared with chickens that received aflatoxin. 3. NaB caused no adverse effects on chickens that did not receive aflatoxin. 4. It is concluded that NaB at pH 7.9 partially neutralises the effects of aflatoxins on broiler chickens when included at 5.0 g/kg in the diet.

Alanine Transaminase↗

PubMed1981

Susceptibility of various poultry species to dietary aflatoxin.

1. The relative sensitivities of broiler chicks, White Leghorn chicks, quail chicks, goslings and turkey poults to increasing dietary contents of aflatoxin from 1 to 21 d of age were determined. Aflatoxin was included in the diets at three concentrations (0.7, 1.4 and 2.1 mg aflatoxin B1 equivalents/kg). 2. Data were analysed for species differences in food consumption, body weight, food utilisation, mortality and liver pathology. 3. There were no significant effects of aflatoxin in broiler and Leghorn chicks. Aflatoxin at 0.7 mg/kg decreased the body weight of turkey poults but tended to increase the growth rate of goslings. At 1.4 mg aflatoxin/kg food consumption, body weight and weight gain of goslings were adversely affected. 4. Liver damage occurred in goslings and quail chicks at all inclusions of aflatoxin and was extensive at 2.1 mg/kg. 5. Poults and goslings appeared to be the most sensitive, quail were intermediate and domestic chicks were most resistant.

Aflatoxins↗

PubMed2001

Aflatoxins B1 in different grades of chillies (Capsicum annum L.) in India as determined by indirect competitive-ELISA.

Samples of the three grades of chilli pod (grades 1 to 3) were collected during surveys in 1998 and 1999 from the principal market yards and cold storage facilities of the major chilli-growing areas of Andhra Pradesh (AP), India. Chilli powders were collected from different supermarkets in Hyderabad, AP. They were analysed for aflatoxin B1 (AFB1) content by an indirect competitive ELISA. To avoid the influence of interfering substances present in chilli extracts, it was necessary to prepare the aflatoxin standards in methanol extracts of chillies free from aflatoxins. For nine representative samples there was good agreement between ELISA and HPLC estimations of AFB1 and the results suggested that the ELISA procedure adopted was dependable. Of the 182 chilli samples tested, 59% of the samples were contaminated with AFB1 and 18% contained the toxin at non-permissible levels. The highest AFB1 concentration of 969 microg/kg was found in one sample representing grade 3. Overall the maximum percentage of chilli pods showing AFB1 levels higher than 30 microg/kg (non-permissible levels) was in grade 3. Chilli pods stored in refrigerated rooms showed the lowest proportion of samples containing aflatoxin. Nearly 9% of the chilli powders sold in supermarkets contained non-permissible aflatoxin levels. This report highlights the importance of using grade 1 chilli pods to minimize aflatoxin contamination.

Aflatoxin B1↗

PubMed2001

Proficiency testing for the evaluation of the ability of European Union-National Reference laboratories to determine aflatoxin M1 in milk at levels corresponding to the new European Union legislation.

In 1992, the European Union set up a network of National Reference Laboratories and charged the Community Reference Laboratory with the responsibility to design a proficiency testing scheme for assessing the analytical ability of laboratories involved in the official control of aflatoxin M1 in milk. Since 1996, two exercises of proficiency testing have been performed on samples of milk powder and liquid milk at various levels of aflatoxin M1 contents. The trials were conducted according to ISO Guide 43, in particular for the homogeneity testing of sample batches and for the calculation of laboratory z-scores. The National Reference Laboratories officially designated by their governments participated in this programme. Samples were naturally-contaminated milk obtained by feeding cows with aflatoxin B1-contaminated feed. The levels of aflatoxin M1 in the samples ranged from 0.2 to 0.7 microg/kg in milk powder and from 0.05 to 0.07 microg/l in liquid milk. These levels were chosen as being close to the European Union-regulated limit of 0.05 microg of aflatoxin M1 per litre. The results produced by laboratories were compiled and statistically analysed to detect any outlying results and to calculate the individual z-scores. Except for one laboratory in each exercise, all laboratories exhibited acceptable or questionable z-scores. The interlaboratory relative standard deviation for reproducibility (RSDR) obtained for both 1996 and 1998 exercises were in the range 15.7-30.3%. Compared with other published studies, this indicates a very good precision for the performance of this laboratory network in the analysis of traces of aflatoxin M1 in milk.

Aflatoxin M1↗

PubMedDate not supplied

The effect of aflatoxins on the electron transport chain of chloroplasts from Zea mays L. and Pisum sativum L.

The influence of aflatoxins B1, B2, G1, and G2 was studied on the electron transport chain (from water to methyl viologen) of freshly lysed chloroplasts from maize (Zea mays L.) and peas (Pisum sativum L.). A partially purified extract containing all four toxins was added to a chloroplast suspension. Basal, phosphorylating, and uncoupled electron transport were assessed immediately after its addition and 4 min later. In maize chloroplasts, all three types of electron transport were inhibited by the mixture. The inhibition did not increase with time. The basal electron transport of pea chloroplasts was inhibited very slightly (20%) by the aflatoxin mixture. Commercially purified aflatoxins B1, B2, G1, and G2 were tested individually. Only aflatoxins B1 and B2 showed effects on the chloroplasts of both species. With 16 microM/ml of aflatoxin B2 in the assay medium, the three kinds of electron transport were drastically inhibited both in maize (75%) and pea (60%) chloroplasts. Aflatoxin B1 showed no effect on maize chloroplasts; however, a slight increase (31%) was observed on the electron transport rate of pea chloroplasts. Differential response between electron transport rate in maize and pea could be related to the toxin's chemical structure, with a slight difference between molecules resulting in enormous differences in activity.

Aflatoxins↗

PubMedDate not supplied

Selection for resistance to aflatoxin formation in maize through seed inoculation.

The efficiency of selection for resistance to aflatoxin development caused by Aspergillus flavus L. ex Fries, in maize (Zea mays L.) grain was studied in three CIMMYT lowland tropical maize populations. Seed samples of each population were inoculated with a spore suspension of cultures of Aspergillus spp. known to produce aflatoxins. Inoculated seeds were maintained at 85% RH in plastic boxes kept at room temperature. At 50% germination, seed samples were planted in the field. At flowering time, selected plants were bulk pollinated. After three cycles of selection, gains for tolerance to aflatoxin formation and improvement for agronomic characters were evaluated. The results indicate there are differences in aflatoxin accumulation between different genotypes and cycles of selection. Populations 22 (DMR) and 28 (DMR) were the most damaged and Population 31 DMR suffered the lowest infection. The study suggests that there are differences in aflatoxin production between the maize genotypes tested. However, our results failed to show that tolerance to aflatoxin development can be accumulated through a recurrent selection breeding scheme.

Aflatoxins↗

PubMed1996

A survey of the natural occurrence of aflatoxins and zearalenone in Argentine field maize: 1983-1994.

A survey was carried out from 1983 to 1994 to determine the natural occurrence of aflatoxins and zearalenone in maize samples from Buenos Aires and Santa Fe provinces, Argentina. Among 2271 samples analysed, 1214 (53.5%) were contaminated with mycotoxins. Aflatoxin B1 was identified in 445 samples (19.6%), aflatoxin B2 was identified in 92 samples (4.1%) and zearalenone was identified in 676 samples (29.8%). Aflatoxin G1 was detected in only one sample and none of the samples contained detectable amounts of aflatoxin G2. Aflatoxin contamination was not detected in the 1988, 1993 and 1994 harvests and, in the other years, with the exception of 1989, the contamination levels were low. Zearalenone was found in every year.

Aflatoxins↗

PubMed1987

Aflatoxins and kwashiorkor in Kenya: a hospital based study in a rural area of Kenya.

Aflatoxin analyses were undertaken on sera and urines of 41 children admitted to a rural hospital in Kenya with kwashiorkor, marasmus, marasmic kwashiorkor or normal nutrition (Wellcome Classification). Aflatoxins were detected most frequently and at highest concentrations in the sera of kwashiorkors who, conversely, showed aflatoxins least frequently in their urine and in concentrations that were disproportionately low compared with serum/urine aflatoxin levels in other groups. These findings indicate altered aflatoxin metabolism in kwashiorkor and support the hypothesis that there are special relationships between aflatoxins and kwashiorkor.

Aflatoxins↗

PubMed1995

Neonatal jaundice, aflatoxins and naphthols: report of a study in Ibadan, Nigeria.

This study set out to investigate the prevalence of naphthols and aflatoxins in the sera of babies with neonatal jaundice and their mothers in order to determine whether they contribute to the occurrence of unexplained neonatal jaundice in Ibadan. Blood was obtained from 327 jaundiced neonates and 80 of their mothers, and 60 non-jaundiced controls and seven of their mothers admitted to hospital between April 1989 and April 1991. Blood group, bilirubin concentration, erythrocyte G6PD status, aflatoxin and naphthol concentrations in blood were measured. Altogether, 30.9% of the jaundiced neonates were G6PD-deficient, compared with 13.3% of controls (chi 2 = 6.88; p = 0.009). Aflatoxins were detected in 27.4% of jaundiced neonates, 17% of their mothers, 16.6% of controls and 14.4% of control mothers. Naphthols were detected in 7.2% of jaundiced babies, 6.3% of their mothers, 6.25% of control babies and 14.4% of their mothers. Analysis of the data revealed that either G6PD deficiency or the presence of any serum aflatoxin is a risk factor for neonatal jaundice; odds ratio were 2.97 (95%) confidence intervals (CI): 1.31-6.74) and 2.68 (CI: 1.18-6.10), respectively. This study demonstrates that G6PD deficiency and/or the presence of serum aflatoxins are risk factors for neonatal jaundice in Nigeria. Aflatoxins are an additional risk factor not previously reported.

Aflatoxins↗

PubMed1979

Effects of the aflatoxins on ATPase activities in mouse and rat liver.

The effects of the aflatoxins on ATPase activities in mouse and rat tissues were investigated in vitro. The hepatic oligomycin-sensitive (O.S.) Mg++ ATPase was inhibited significantly. The order of inhibition was G1 greater than B1 greater than G2 greater than B2. Mouse O.S. Mg++ ATPase was more sensitive than the corresponding rat enzyme. The oligomycin-insensitive (O.I.) Mg++ ATPase activities in rat and mouse liver were not altered. Although aflatoxins G1 and B1 were more potent inhibitors of hepatic O.S. Mg++ ATPase, no concentration-response was observed, whereas aflatoxins G2 and B2 inhibited enzyme activity in a concentration-dependent manner. Spectral analysis of aflatoxin G1 solutions suggested that solubility was not related to the observed effects. In addition, the effects of aflatoxin B1 and G1 on mouse brain microsomal Na+-K+ ATPase were examined. Although aflatoxin B1 was more potent that G1, both mycotoxins significantly inhibited enzyme activity in a concentration-dependent fashion.

Adenosine Triphosphatases↗