Aflatoxins, hepatitis B virus, and hepatocellular carcinoma.
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Carcinoma, Hepatocellular↗
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Aflatoxin and Reye's syndrome: a study of livers from deceased cases.
In order to reinvestigate a strong reported association, we attempted to identify aflatoxin in the livers of 12 children who presumably died of Reye's Syndrome and in the liver of one child who died accidentally. Aflatoxins were detected, but not confirmed in only one of the liver specimens (limits of detection 20 ppt). In addition, the microscopic appearance of the livers was reviewed. Although most of the cases fit the clinical definition of Reye's Syndrome, the microscopic appearance of the liver was varied. We conclude that aflatoxin is not regularly recoverable from cases of Reye's Syndrome at a high rate, and question the proposed etiologic relationship. We confirm the varied appearance of the liver late in the course of Reye's Syndrome; however, microvesicular fat was present in most cases.
Aflatoxins↗
Broiler aflatoxicosis with recovery after replacement of the contaminated diet.
Broiler chickens were fed a diet containing 2057 and 1323 micrograms/kg feed of aflatoxins B1 and B2, respectively, for 35 d. Effects of aflatoxins on growth, food consumption, efficiency of food utilisation and manifestations of aflatoxicosis were compared with control birds at the end of the feeding trial and at 1, 2, 4, 8 and 16 d after replacing the contaminated feed. No difference in food consumption was observed between the controls and the aflatoxin-fed chickens, but efficiency of food utilisation was decreased from 2.2 for the controls to 2.4 g food/g gain for the group fed aflatoxins. Aflatoxins caused depressed growth and enlargement of the kidney, liver, heart and gall bladder. Haemorrhagic spots were present on the surface of the muscles and some of the livers. Most livers from aflatoxin-fed birds were pale and infiltrated with lipid. After withdrawal of the food containing aflatoxins, all apparent gross lesions of aflatoxicosis disappeared, with no evidence of any lesions 8 d after removal of the contaminated diet.
Aflatoxin B1↗
Blood biochemical profiles in induced aflatoxicosis of cockerels.
1. Experimental intoxication induced in cockerels with varying doses of aflatoxin fed at the rate of 2.5 micrograms, 5.0 micrograms, and 10.0 micrograms per g of food resulted in appreciable changes in blood biochemical profiles. 2. At all doses the aflatoxin caused decreases in serum total proteins, albumin: globulin ratio, serum total cholesterol, serum calcium and phosphorus and increase in serum globulins, alanine amino transferase (ALT) and aspartate amino transferase (AST) concentrations. 3. No changes in serum bilirubin were observed. 4. Possible mechanisms for such blood biochemical changes are discussed and related to liver cellular damage caused by the aflatoxin toxicity.
Animals↗
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↗
Handling toxicoses of unknown origin.
A strategy is presented for investigating toxicoses of unknown origin and following a disease-oriented approach. The strategy is derived from and illustrated by experience of three large scale outbreaks of disease involving aflatoxicosis in India, intoxication by pyrrolizidine alkaloids from Heliotropium spp. in Afghanistan and from Crotalaria spp. in India. Investigation of such cases involves a descriptive phase (case definition, descriptive pattern of disease), hypothesis generation (based on pathologic studies and indications from environmental and epidemiological investigations), hypothesis testing and confirmatory studies. After establishing a causal relationship, steps need to be taken to transmit information to health authorities, to disseminate knowledge to health delivery personnel and the general public, to identify borderline cases and plan management, to identify mechanisms of exposure/contamination and relevant measures to remove or minimize exposure to the causal agent.
Afghanistan↗
Aflatoxin and outcome from acute lower respiratory infection in children in The Philippines.
Aflatoxin is immunosuppressive in experimental conditions. This study addressed its potentially contributory role in the poor outcome of acute lower respiratory infections (ALRI) in children in The Philippines. The catchment area included peri-urban slums and middle-class housing. One hundred and fifteen children (mean age 2.1, range 0.08-12 years) were enrolled and their serum and urine obtained at presentation with ALRI. Aflatoxins in serum and aflatoxin metabolites in urine were measured by previously validated ELISA tests. Using the 1986 WHO criteria for the severity of ALRI, 31% had mild, 12% moderate, 49% severe and 8% severe complicated pneumonia. Eighty of 97 (82%) chest radiographs were abnormal. Ninety per cent of the children were below average weight for age, using Filipino standards, with a mean of 79% (range 27-157%). Thirteen (11%) children died. Aflatoxin in their serum, reflecting recent ingestion, was detected in 33%, with a mean positive value of 462 pg/ml. Aflatoxin metabolites (reflecting chronic ingestion) were detected in 64 of 65 urines collected, with a mean value of 0.1-4.77ng/ml. None of the children with detectable serum aflatoxin died. Anorexia and impaired consciousness were strongly associated with a poor outcome (prolonged fever or death). There was a strong association between undetectable serum aflatoxin concentrations and death (p = 0.004), perhaps reflecting anorexia. There was no relationship between the concentration of urinary aflatoxin metabolites and outcome. Serum was also obtained from 29 mothers on admission and none contained detectable aflatoxin. As virtually all the children had evidence of exposure to aflatoxin, a potentially immunosuppressive role in the context of pneumonia cannot be excluded.
Aflatoxins↗
Two unusual cases of kwashiorkor: can protein deficiency explain the mystery?
Two children with unusual features of kwashiorkor are reported. One, an exclusively breastfed 7-month-old girl, had been admitted earlier, treated for pneumonia and discharged 3 weeks before she presented with kwashiorkor. The other was an identical twin who was admitted for kwashiorkor and gastro-enteritis. The twin sister was underweight but relatively well. Both children died. Potent aflatoxins were detected in the organs of these children on post-mortem examination. The occurrence of kwashiorkor in a fully breastfed infant and in an identical twin does not accord with the extant belief that the aetiology of kwashiorkor is wholly nutritional, but suggests a disease probably of multifactorial origin.
Aflatoxins↗
Determinants of the variability of aflatoxin-albumin adduct levels in Ghanaians.
Hepatocellular carcinoma (HCC) is a multifactorial disease with various host and environmental factors involved in its etiology. Of these, aflatoxin exposure has been established as an important risk factor in the development of HCC; the presence of aflatoxin-albumin (AA) adducts in the blood serves as a valuable biomarker of human exposure. In this study, the relationship between a variety of different HCC host factors and the incidence of AA adduct levels was examined in a Ghanaian population at high risk for HCC. These factors included age, gender, hepatitis virus B (HVB) and hepatitis C virus (HCV) status, and genetic polymorphisms in both microsomal epoxide hydrolase (mEH) and glutathione S-transferases (GSTs). Blood samples were analyzed for AA adducts and HBV and HCV status. GSTM1 and GSTT1 deletion polymorphisms and mEH exon 3 and exon 4 single-nucleotide polymorphisms (SNPs) were determined from urine samples. In univariate analysis, age, HBV and HVC status, and GSTT1 and mEH exon 3 genotypes were not associated with AA adduct levels. However, mean adduct levels were significantly higher in both females and individuals typed heterozygous for mEH exon 4 (vs. wild types). Stratification analysis also showed that gender along with mEH exon 4 genotype and HBV status had a significant effect on adduct levels. Both females typed HBsAg+ and males with mEH exon 4 heterozygote genotypes showed significantly higher adduct levels as compared to the HBsAg- and wild types, respectively. Understanding the relationships between these host factors and the variability in aflatoxin-adduct levels may help in identifying susceptible populations in developing countries and for targeting specific public health interventions for the prevention of aflatoxicoses in populations with HCC and chronic liver diseases.
Adult↗
Effect of raising dietary protein, amino acids and/or energy levels as an attempt to alleviate severity of the chronic aflatoxicosis by broiler chicks. 1. Performance and toxicity symptoms.
In an attempt to alleviate the aflatoxicosis symptoms by broiler chicks fed on low (50 ppb) aflatoxin-contaminated diet; the dietary nutrients were elevated by 2.6% for protein, 0.54 MJ ME/kg for energy or 0.5% for each of methionine and lysine. These supplements were mixed altogether and applied as well. All the experimental diets were offered for a 6-week period followed by a 2-week period on aflatoxin--free diet without supplements as a withdrawal period. It was proved after the treatment period that the raising of energy concentration was beneficial to overcome the aflatoxin effects on the body weight, feed conversion rate, and dressing (eviscerated weight) percentage and stability of relative weights of liver and kidneys. Additionally, the supplements' mixture improved the body weight and the relative weight of the liver comparing with the chicks fed on the aflatoxin diet without additives. All of the contaminated diets, except that of the high energy, caused apparently toxic symptoms besides the internal gross pathology. The high energy diet reflected the lowest mortality rate, whereas the highest was with the amino acids supplemented one. The withdrawal period resulted in lower differences among treatments in the body weight. It improved also the dressing percentage (significantly) and to some extent the results of the post-mortem examination.
Amino Acids↗
Effect of raising dietary protein, amino acids and/or energy levels as an attempt to alleviate severity of the chronic aflatoxicosis by broiler chicks. 2. Biochemical characteristics.
Aflatoxin caused some reduction in moisture contents of chest and liver, lipids of thigh and blood, blood glucose, muscular protein and GOT in liver. It led also to increase of moisture contents of thigh and kidneys; chest lipids; blood cholesterol; protein of liver, kidneys and blood and blood creatinine. The different supplements used herein led to increasing moisture of muscles, liver and kidneys (except on oil addition); lipids of muscles (except of chest on high energy diet) and blood (except on amino acids-supplemented diet); blood cholesterol (except on high energy one); protein of thigh (except on high protein one) and blood (except on high energy or amino acids diets) and liver GPT (except on high energy diet). The additives led also to low blood glucose; protein of chest (except on high energy), liver, and kidneys; blood creatinine; liver GOT (particularly with high energy or amino acids); plasma GOT (on high amino acids) and plasma GPT. The 2-week withdrawal period led to low moisture contents of muscles and kidneys of most treatments, although they continued higher than in the control for chest, liver and kidneys. It increased blood glucose and cholesterol with continuous higher lipid content of muscles and blood and blood cholesterol than in the control. It led to elevated protein content of muscles, liver (except on the control or supplements mixture), kidneys (on the aflatoxin alone or with the amino acids) and blood (except on the control or aflatoxin alone or with high protein) and blood creatinine (except on the control or on the high energy or the supplements mixture).(ABSTRACT TRUNCATED AT 250 WORDS)
Alanine Transaminase↗
Dietary aflatoxin exposure and chemoprevention of cancer: a clinical review.
Exposure to dietary aflatoxins is considered to be an important risk factor for the development of hepatocellular carcinoma in certain regions of the world. Significant advances have recently been made in understanding the clinical toxicology of aflatoxins. These include the development and validation of biomarkers of exposure and genotoxic effect. These biomarkers are currently being utilized to explore the potential that pharmaceutical interventions may have in modifying the toxicokinetics of dietary aflatoxin exposure. Preliminary results of clinical trials with the drug oltipraz suggest that it may modify the genotoxic effects of aflatoxin B1 by inhibiting bioactivation pathways and stimulating detoxification pathways. More recent results of a clinical trial with chlorophyllin suggest that this drug may have a role in preventing dietary exposure to aflatoxin B1 by reducing its oral bioavailability. The preliminary results of these chemoprevention studies may ultimately have implications for cancer prevention in high-risk populations in the future.
Aflatoxins↗
Some recent studies in the Nutrition Research Laboratories, Hyderabad.
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Adolescent↗
Cirrhosis in children from peanut meal contaminated by aflatoxin.
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Arachis↗
A case-control dietary study of primary liver cancer risk from aflatoxin exposure.
UNLABELLED: The dietary intakes of 90 confirmed primary liver cancer cases were compared against 90 age-sex matched controls. Dietary recall, obtained by the same nutritionist, was taken for each change of residence lasting one year or more. The frequency and amounts of food items consumed were calculated into units of aflatoxin load per day using a Philippine table of aflatoxin values of these items. Of the total subjects' aflatoxin load, 51.2% came from cassava, 20.3% from corn, 6.8% from peanuts and 5.8% from sweet potato. The mean aflatoxin load per day of the cases as found to be 440% that of the controls. Upon grouping dietary aflatoxin loads (and alcohol intakes) into Heavy and Light, and upon comparing cases versus controls, the relative risk (RR) of developing primary liver cancer was found to be statistically significant in the following order of rank: cassava, peanuts, sweet potato, corn and alcohol. Boiled rice which had negligible aflatoxin content gave no difference in risk. Combining aflatoxin load and alcohol intake gave a synergistic and a statistically significant effect on RR with Light Aflatoxin, Light Alcohol as RR = 1. RESULTS: Light Aflatoxin, Heavy Alcohol RR = 3.9; Heavy Aflatoxin, Light Alcohol RR = 17.5; Heavy Aflatoxin, Heavy Alcohol RR = 35.0.
Adolescent↗
Determinants of aflatoxin exposure in young children from Benin and Togo, West Africa: the critical role of weaning.
BACKGROUND: Dietary exposure to high levels of the fungal toxin, aflatoxin, occurs in West Africa, where long-term crop storage facilitates fungal growth. METHODS: We conducted a cross-sectional study in Benin and Togo to investigate aflatoxin exposure in children around the time of weaning and correlated these data with food consumption, socioeconomic status, agro-ecological zone of residence, and anthropometric measures. Blood samples from 479 children (age 9 months to 5 years) from 16 villages in four agro-ecological zones were assayed for aflatoxin-albumin adducts (AF-alb) as a measure of recent past (2-3 months) exposure. RESULTS: Aflatoxin-albumin adducts were detected in 475/479 (99%) children (geometric mean 32.8 pg/mg, 95% CI: 25.3-42.5). Adduct levels varied markedly across agro-ecological zones with mean levels being approximately four times higher in the central than in the northern region. The AF-alb level increased with age up to 3 years, and within the 1-3 year age group was significantly (P = 0.0001) related to weaning status; weaned children had approximately twofold higher mean AF-alb adduct levels (38 pg AF-lysine equivalents per mg of albumin [pg/mg]) than those receiving a mixture of breast milk and solid foods after adjustment for age, sex, agro-ecological zone, and socioeconomic status. A higher frequency of maize consumption, but not groundnut consumption, by the child in the preceding week was correlated with higher AF-alb adduct level. We previously reported that the prevalence of stunted growth (height for age Z-score HAZ) and being underweight (weight for age Z-score WAZ) were 33% and 29% respectively by World Health Organziation criteria. Children in these two categories had 30-40% higher mean AF-alb levels than the remainder of the children and strong dose- response relationships were observed between AF-alb levels and the extent of stunting and being underweight. CONCLUSIONS: Exposure to this common toxic contaminant of West African food increases markedly following weaning and exposure early in life is associated with reduced growth. These observations reinforce the need for aflatoxin exposure intervention strategies within high-risk countries, possibly targeted specifically at foods used in the post-weaning period.
Aflatoxins↗
Efficacy of various inorganic sorbents to reduce the toxicity of aflatoxin and T-2 toxin in broiler chickens.
Experiments were conducted to determine the efficacy of three inorganic sorbents, S1, S2, and S3, to reduce the toxicity of aflatoxins (AF) and T-2 toxin in male broiler chickens from day of hatch to 21 d of age. The compounds had been reported to bind to AF and T-2 toxin in vitro. S1 and S2 were the same basic compound that had been stored for different lengths of time following activation. In Experiments 1, 2, and 3, the appropriate diets were produced to contain no mycotoxins, the specific adsorbent at 0.5% of diet, AF alone at 5 mg/kg of diet, T-2 alone at 8 mg/kg of diet, AF at 5 mg/kg of diet plus the specific sorbent at 0.5% of diet, or T-2 at 8 mg/kg of diet plus the specific sorbent at 0.5% of diet. The specific sorbents used were: 1) Experiment 1, S1; 2) Experiment 2, S1 and S2; and 3) Experiment 3, S3. In Experiments 1 and 3, S1 and S3, respectively, showed no protection against AF or T-2 toxin as measured by BW gain, when compared to AF alone group. In Experiment 2, S1 showed no protection; however S2 reduced the effects of AF on BW gain by 25% as compared to AF alone diet. The data demonstrate that under the conditions of our experiment: 1) one of the sorbents provided some protection against aflatoxicosis; 2) there was variability in protection against aflatoxicosis between two different samples of the same sorbent that had been stored for different lengths of time following activation; 3) protection by the sorbents against the effects of T-2 toxin was not observed.
Adsorption↗