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PubMed1969

Aflatoxin production in meats. I. Stored meats.

Aflatoxins were produced on fresh beef (in which bacterial spoilage was delayed with antibiotics), ham, and bacon inoculated with toxinogenic fungi and stored at 15, 20 and 30 C. Meats stored at 10 C were spoiled by bacteria and yeast before detectable levels of aflatoxins were produced. High levels of aflatoxins were formed in meats stored at 20 C; one sample supported the production of 630 mug of aflatoxins per g of meat, the major portion (580 mug) of which was aflatoxin G(1). Meats stored below 30 C developed higher levels of aflatoxin G(1) than B(1), but at 30 C Aspergillus flavus produced equal amounts of B(1) and G(1), whereas A. parasiticus continued to produce more G(1) than B(1).

Aflatoxins↗

PubMed1971

Influence of fungicides and irrigation practice on aflatoxin in peantus before digging.

Peanuts grown under dryland conditions where drought stress occurred accumulated more aflatoxin before digging than peanuts grown under irrigation. Kernels became more susceptible to Aspergillus flavus and A. parasiticus invasion when the soil moisture in the pod zone approached levels at which moisture moved from the pod into the soil and the kernel moisture dropped below 31%. Isolation frequencies of these aspergilli from fresh-dug kernels were lowest in 1968 (maximum of 3%). In 1967 and 1969, maximum percentages of 100 and 74, respectively, were noted. Kernel infestation was correlated with degree of aflatoxin contamination. Dryland fresh-dug kernels contained a maximum of 35,800 parts per billion aflatoxin while a maximum of 50 parts per billion was detected in kernels from irrigated plots. In 1969 A. flavus infestation was as high as 59% in peanuts from irrigated plots; however, no aflatoxin was detected. Absence of aflatoxin in these samples is attributed to the higher kernel moisture content which reduced the aflatoxin-producing potential of A. flavus. Statistical analysis of the data revealed no significant differences in degree of fungal infestation, production levels, and grade factors between any fungicide treatments.

Acetone↗

PubMed1973

Effects of aflatoxin on seedling growth and ultrastructure in plants.

Nineteen plants belonging to 11 species of the cruciferae were studied to determine the effects of aflatoxin B(1) on seed germination and seedling development. Germination was not inhibited in any test organism at a concentration of 100 mug of aflatoxin per ml of agar substrate. Inhibition of elongation of the hypocotyls and roots in the species studied varied from 29 to 93% and from 22 to 91% in the respective tissues. Lepidium sativum was the most susceptible plant studied and exhibited the maximal inhibitory response noted above at concentrations of 8 mug of aflatoxin per ml. The ultrastructure of Lepidium root cells treated with crystalline aflatoxin B(1) exhibited morphological changes characteristic of those found in aflatoxin-treated animal cells. In addition to changes in the cytoplasmic organelles, numerous ring-shaped nucleoli with prominent nucleolar caps were produced. The effect of aflatoxin on plant cells is compared with similar effects induced by actinomycin D. Seed germination and seedling development is discussed in relation to the effects of both compounds on deoxyribonucleic acid-dependent ribonucleic acid biosynthesis.

Aflatoxins↗

PubMed1975

Production of aflatoxin on soybeans.

Probable factors influencing resistance to aflatoxin synthesis in soybeans have been investigated by using cultures of Aspergillus parasiticus NRRL 3240. Soybeans contain a small amount of zinc (0.01 mug/g) bound to phytic acid. Autoclaving soybeans at 15 pounds (6803.88 g) for 15 min increases the aflatoxin production, probably by making zinc available. Addition of zinc to both autoclaved and nonautoclaved soybeans promotes aflatoxin production. However, addition of varying levels of phytic acid at a constant concentration of zinc depresses aflatoxin synthesis with an increase in the added phytic acid. In a synthetic medium known to give good yields of aflatoxin, the addition of phytic acid (10 mM) decreases aflatoxin synthesis.

Aflatoxins↗

PubMed1967

Antimicrobial activity of aflatoxins.

Antimicrobial activity of a crude aflatoxin preparation and of aflatoxin B(1) was studied. They were found inactive against common gram-positive and gram-negative bacteria at a concentration of 100 mug/ml. Both samples of aflatoxin did, however, exhibit antimicrobial activity, though narrow and limited, against various strains of Streptomyces and Nocardia. The antibiotic action of aflatoxin B(1) was confirmed by bioautogram after thin-layer chromatography. Among seven strains of microorganisms, including aflatoxin-sensitive and -resistant strains, N. asteroides IFM 8 was found to reduce aflatoxin B(1), in addition to other minor fluorescent components in the crude preparation.

Aflatoxins↗

PubMed1980

Aflatoxin B1 in dairy concentrates and other animal feedstuffs.

Over a period of 13 years 740 samples of various animal feedstuffs were analysed for the presence of aflatoxin B1. Nearly 500 were suspected of causing disease in farm animals but aflatoxin B1 could be detected in only 13.6 per cent of them. Groundnut meal samples nearly always contained the toxin but compounded feeds were contaminated to a varying extent. In particular, none could be detected in 62 poultry feeds. Where mycotoxicosis was suspected in dairy cattle, aflatoxin B1 was present at levels of more than 30 micrograms per kg in about 27 per cent of associated feed samples. In other dairy feeds (178 samples) this level of contamination was present in only about 9 per cent of samples. Concentrations of aflatoxin B1 likely to produce toxic effects (100 micrograms per kg and above) were present in about 4 per cent of suspect dairy concentrates but in 1 per cent or less of others. Contamination of dairy concentrates with aflatoxin B1 is usually at such a level that cows probably excrete the toxic metabolite aflatoxin M1 in milk at very low concentrations of 0.1 micrograms per litre or less.

Aflatoxins↗

PubMed1983

Variability of bright, greenish-yellow fluorescent particles and aflatoxin in ground blends of Zea mays.

Developing corn (Zea mays) kernels of single cross B73 X Mo17 grown near Columbia, MO, were inoculated with conidia of Aspergillus flavus or A. parasiticus. After harvest bright greenish-yellow fluorescing (BGYF) kernels were selected under ultraviolet black light (365 nm); they contained 3696 ng/g (A. parasiticus strain NRRL 3145) and 6666 ng/g (A. flavus strain UGA 5337) aflatoxins, respectively. The BGYF-free kernels were obtained from the same hybrid grown in northern Iowa. No BGYF kernels nor aflatoxins were found in 10 assays. To assess the variability in detection of BGYF particles and aflatoxin in ground corn blends, a series was developed by mixing BGYF kernels with BGYF-free kernels in various ratios. In the finely ground samples, standard deviations decreased significantly (P = 0.05) among blends for aflatoxin values in mixtures with higher levels of BGYF particles. Strain 3145 (A. parasiticus) was significantly (P = 0.01) different from strain 5337 (A. flavus) for aflatoxins concentration and the number of grams of BGYF in the blends (r greater than 0.99). The percent fines (passed a 40-mesh screen) in ground, 100% BGYF kernels was significantly (P = 0.01) higher for strain 3145 (A. parasiticus) inoculated samples than for strain 5337 (A. flavus) in spite of equivalent grinding procedures. This observation showed that the relationship between aflatoxin levels determined for a sample and the fraction of BGYF material in the blend was dependent on the fungal-strain source of the BGYF kernels used in the blend.

Aflatoxins↗

PubMed2005

Absence of TP53 codon 249 mutations in young Guinean children with high aflatoxin exposure.

Infection with hepatitis viruses and chronic exposure to high levels of dietary aflatoxins are the major etiologic agents for hepatocellular carcinoma in west Africa. A challenge for the prevention of hepatocellular carcinoma in this region is that both hepatitis B virus and aflatoxin exposures start early in life; indeed, aflatoxin exposures can start in utero and continue unabated throughout childhood. A mutation in the TP53 tumor suppressor gene at codon 249 (TP53 Ser249 mutation) has been reported previously for hepatocellular carcinoma tumors and matched plasma DNA samples in individuals from areas with high aflatoxin exposure. We examined whether the TP53 Ser249 mutation could be observed in DNA found in plasma of young children (ages 2-5 years) from Guinea, west Africa, a region of high aflatoxin exposure. Plasma aflatoxin-albumin adducts were present in 119 of 124 (96%) of the children, geometric mean of positives 9.9 pg/mg albumin (95% confidence interval, 8.8-11.0 pg/mg). This is the level and prevalence of exposure observed previously in adults. Following PCR amplification of plasma-derived DNA and detection using mass spectrometry, none of the samples were found to contain the TP53 Ser249 mutation. Because approximately 50% of the hepatocellular carcinomas in adults in west Africa have this specific TP53 Ser249 mutation, a lack of detection in samples from children ages <5 years may indicate that a window of opportunity for intervention exists that could be exploited to lower hepatocellular carcinoma risk.

Adenoma, Liver Cell↗

PubMed2003

Modification of immune function through exposure to dietary aflatoxin in Gambian children.

Aflatoxins are immunotoxins that frequently contaminate staple foods in The Gambia and other parts of sub-Saharan Africa, resulting in high exposure throughout life. Impaired infant immune system development may be a key predictor of mortality from infectious disease. In this study we aimed to determine the effect of dietary aflatoxin exposure on a number of immune parameters in Gambian children. A cohort of 472 Gambian children 6-9 years of age was recruited. Serum aflatoxin-albumin (AF-alb) adducts were analyzed to provide a measure of exposure. Immune parameters included secretory IgA (sIgA) in saliva, cell-mediated immunity (CMI), determined using the CMI multitest where test antigens are applied to the skin, and antibody responses to both rabies and pneumococcal polysaccharide vaccines. Birth weight, current anthropometry, and micronutrient status were also recorded. AF-alb adducts were detected in 93% of the children (geometric mean level 22.3 pg/mg; range 5-456 pg/mg). AF-alb level was strongly influenced by month of sampling. In a multivariable analysis, sIgA was markedly lower in children with detectable AF-alb compared with those with nondetectable levels [50.4 micro g/mg protein (95% confidence interval [CI] 48.0-52.8) and 70.2 micro g/mg protein (95% CI 61.1-79.2), respectively; p < 0.0001]. Antibody response to one of four pneumococcal serotypes, but not rabies vaccine, was weakly associated with higher levels of AF-alb. There was no association between CMI responses to test antigens and AF-alb. These data confirm that children in rural Gambia are frequently exposed to high levels of aflatoxin. The study provides evidence that sIgA in saliva may be reduced because of dietary levels of aflatoxin exposure. Given the high burden of infection-related mortality in West Africa, further investigation of the immune effects of aflatoxin exposure in children is merited.

Aflatoxins↗

PubMed1979

The detoxication of aflatoxin B1 with glutathione in the rat.

1. The deactivation of aflatoxin B1 by glutathione (GSH) has been investigated in rat. Binding of metabolites of aflatoxin B1 to [3H]glutathione in vitro with rat liver microsomes is insignificant. Incubation with rat liver 10 000 g supernatant results in increased binding. Under identical conditions, benzo(a)pyrene metabolites are bound to [3H]glutathione much more than is aflatoxin B1. 2. Pre-treatment of rats with aflatoxin 1 (2 mg/kg) caused depletion in GSH of rat liver with a minimum at 6 h but returning to above normal at 24 h. GSH S-transferase activity was marginally increased at 6 h also and returned to normal at 24 h. 3. Kidney GSH was not significantly decreased, but kidney GSH S-transferase activity showed a sudden increase in 6 h, returning to almost normal at 24 h. 4. Pre-treatment with benzo(a)pyrene (2 mg/kg) caused greater depletion of hepatic GSH than occurred with aflatoxin B1 but did not show any effect on kidney GSH. 5. Hepatic and kidney GSH S-transferase in benzo(a)pyrene-treated rats showed greatest activity at 2 h followed by a gradual fall through 24 h. 6. GSH was therefore a less efficient nucleophile for aflatoxin B1 metabolites than for benzo(a)pyrene metabolites.

Aflatoxins↗

PubMed1975

Stability of aflatoxin M in milk.

This three-part study was designed to determine aflatoxin M recovery from pasteurized and/or stored cow's milk. (a) Aflatoxin M was added to samples of raw Holstein milk at a concentration of 2.0 mug/liter. Half of each sample then was pasteurized at 63 C for 30 min, and both raw and pasteurized portions were stored at 4 C up to 17 days. (b) Samples of raw milk, pasteurized (77 C, 16 s) skim milk, dry cottage cheese curd, and cottage cheese whey were taken from a commercial operation in an area in which natural contamination had been encountered. (c) Milk from a cow dosed with aflatoxin B1 was stored frozen (-18 C) in bulk and in assay-size sample containers for 120 days. Aflatoxin M was recovered completely after either storage or pasteurization in (a) and (b). In (c), a recovery deficiency was detectable after 68 days of storage, which increased to 45% of the original value by 120 days. These observations differ from those of others in that loss of aflatoxin M was significant after pasteurization or storage of raw milk, totaling 87% loss after 120 days of frozen storage. Aflatoxin M partitioning between curd and whey in the preparation of cottage cheese agrees with more recent studies, but differs from previous reports. Three possible explanations for the differences are offered.

Aflatoxins↗

PubMed2005

Aflatoxin and hepatitis B virus biomarkers: a paradigm for complex environmental exposures and cancer risk.

The use of biomarkers in molecular epidemiology studies for identifying stages in the progression of development of the health effects of environmental agents has the potential for providing important information for critical regulatory, clinical and public health problems. Investigations of aflatoxins probably represents one of the most extensive data sets in the field and this work may serve as a template for future studies of other environmental agents. The aflatoxins are naturally occurring mycotoxins found on foods such as corn, peanuts, various other nuts and cottonseed and they have been demonstrated to be carcinogenic in many experimental models. As a result of nearly thirty years of study, experimental data and epidemiological studies in human populations, aflatoxin B(1) was classified as carcinogenic to humans by the International Agency for Research on Cancer. The long-term goal of the research described herein is the application of biomarkers to the development of preventative interventions for use in human populations at high-risk for cancer. Several of the aflatoxin specific biomarkers have been validated in epidemiological studies and are now being used as intermediate biomarkers in prevention studies. The development of these aflatoxin biomarkers has been based upon the knowledge of the biochemistry and toxicology of aflatoxins gleaned from both experimental and human studies. These biomarkers have subsequently been utilised in experimental models to provide data on the modulation of these markers under different situations of disease risk. This systematic approach provides encouragement for preventive interventions and should serve as a template for the development, validation and application of other chemical-specific biomarkers to cancer or other chronic diseases. This systematic approach provides encouragement for preventive interventions and should serve as a template for the development, validation and application of other chemical-specific biomarkers to cancer or other chronic diseases.

Aflatoxins↗

PubMed1978

Acquired resistance in turkey poults to Pasteurella multocida (P-1059 strain) during aflatoxin consumption.

The potential for impairment by aflatoxin of the development of acquired immunity to fowl cholera in 8 week old turkey poults from a commercial flock was investigated by challenge of vaccinated poults at 10, 12, and 16 weeks of age. Sixty poults were allotted to 4 groups: A) aflatoxin fed, nonvaccinated; B) aflatoxin fed, vaccinated; C) control fed, nonvaccinated; and D) control fed, vaccinated. Aflatoxin B-1 (.5 ppm) was added to the control ration of groups A and B from 49 to 70 days of age. The avirulent CU (Clemson University) strain of Pasteurella multocida drinking water vaccine was given for one day to groups B and C. Challenge (5 poults from each group) was by administration of the virulent (P-1059) strain of P. multocida in the drinking water for 4 consecutive days. The presence of aflatoxin B-1 (.5 ppm) in the feed during oral vaccination with the avirulent strain of P. multocida did not impair the development of acquired resistance to later challenge with the virulent strain. Results indicate that age of poults and method of vaccination may be important factors in the development of acquired resistance to fowl cholera when aflatoxin is present in the diet.

Administration, Oral↗

PubMed1985

Comparative responses of genetically resistant and nonselected Japanese quail to dietary aflatoxin.

Two lines of Japanese quail (AR2.5 and AR3) selected for resistance to aflatoxin and a nonselected control line (NS) were fed diets containing 0, 10, and 20 micrograms of aflatoxin/g of feed. Line-related reductions in mortality and growth inhibition clearly demonstrated the resistance of the AR lines to dietary aflatoxin. Two-week cumulative mortality percentages for the NS, AR2.5, and AR3 lines fed the 10 micrograms/g diet were 13.9, 7.7, and 2.6%, respectively, and 44.4, 17.9, and 12.8% at 20 micrograms/g. Average growth reduction percentages resulting from feeding the 10 and 20 micrograms/g diets to the NS, AR2.5, and AR3 lines were: 17.3 and 27.5%, 10.7 and 20.1%, and 4.3 and 10.5%, respectively. In addition, AR quail were resistant in varying degrees to the following aflatoxin-induced effects: liver lipid accumulation and enlargement, hepatic protein depletion, elevated hepatic beta-glucuronidase activity, bursal regression, and hypoproteinemia. Comparisons of the AR and NS lines fed the control diet revealed no detrimental physiological or biochemical response to selection for aflatoxin resistance. Genetic resistance to aflatoxin was associated with increased relative liver weight, higher liver protein content, and elevated plasma concentrations of protein and lipid compared with NS quail. One or more of these differences may be related to the mechanism of genetic resistance to aflatoxin in AR quail.

Aflatoxins↗

PubMed1987

Hepatic fatty acid profiles in aflatoxin-exposed broiler chickens.

This study was initiated to determine whether a specific fatty acid marker from hepatic lipids could be identified to confirm aflatoxin exposure in chickens. Male broiler chicks (240) were reared to 21 days of age on diets containing 0, 625, 1.25, 5.0, and 10.0 ppm aflatoxin. Live weights and organ weights differed significantly among the dietary groups. Total liver lipids increased significantly (P less than .001) with increasing aflatoxin levels. Separation of extracted lipids into neutral and polar fractions established that this increase in hepatic lipid was accounted for almost entirely by increases in neutral lipid fractions. A gain of 117% occurred in the weight of neutral lipids as aflatoxin increased from 0 to 10 ppm. In both neutral and polar lipid fractions subsequent chromatographic analysis of fatty acid methyl esters (FAME) showed linear increases in the monoenoic fatty acids with increasing aflatoxin. No single FAME from either lipid fraction was suitable for confirming aflatoxin exposure.

Aflatoxins↗

PubMed1987

Selection for resistance to aflatoxin in chickens.

Two populations of broiler chickens [Athens-Canadian (AC) and a commercial stock] were selected for resistance to aflatoxicosis by dosing chickens in each population with a single oral dose of aflatoxin, which resulted in 40 to 70% mortality. Chickens that did not receive aflatoxin served as the nonselected control groups. Birds surviving the aflatoxin challenge were used as breeders for subsequent generations. Rapid progress was made in the AC population for resistance to aflatoxin, but only moderate progress for this trait was attained in the commercial broiler stock. After five generations of selection in the AC population, LD50 values of 9.42 and 17.05 milligrams aflatoxin per kilogram body weight (BW) were determined for the nonselected and selected lines, respectively. After four generations of selection in the commercial broiler population, LD50 values of 6.05 and 8.02 mg aflatoxin/kg BW were determined for the nonselected and selected lines, respectively. These data demonstrate that genetic progress can be made in chickens, but the amount of progress for resistance to aflatoxin may be influenced by the population.

Animals↗

PubMed1988

Aflatoxin-impaired ability to accumulate oxycarotenoid pigments during restoration in young chickens.

The mechanism by which aflatoxin causes paling in chickens was investigated by measuring its effect on the restoration of pigments in 3-wk-old birds made pale by feeding a white corn-soy diet. Pigment restoration was accomplished by feeding the same diet supplemented with lutein (70 micrograms/g of diet), which is the major oxycarotenoid pigment in chicken diets and tissues. The oxycarotenoids (free, monoester, and diester forms of lutein) in the toe web, liver, serum, and jejunal mucosa of control and aflatoxin-fed (2 micrograms/g of diet) birds were measured by HPLC at 0, 1, 2, 3, 6, and 9 days of repletion. Aflatoxin caused a significant (P less than .05) depression of all forms of lutein in the toe web. In the liver, aflatoxin decreased lutein significantly (P less than .05) but increased lutein monoester and lutein diester. Lutein accumulation in serum and mucosa were inhibited significantly (P less than .05) starting on Days 2 and 3, respectively. These data imply that the normal accumulation of lutein from the diet proceeded into and through the mucosa to the serum to depot sites in the liver and integument, where lutein was acylated to its monoester, which was acylated to its diester. Further, aflatoxin inhibited, apparently independently, the accumulation of lutein by the mucosa, serum, liver, and integument. Pharmacokinetic analysis of the data indicated that both acylation steps in the integument were sensitive to aflatoxin, but the passage of lutein from serum into the integument was not affected.

Aflatoxins↗

PubMed1988

Chlortetracycline and aflatoxin interaction in two lines of chicks.

To determine if feed contaminants and feed additives interact, day-old chicks from lines bred for high and low antibody response to sheep erythrocytes were fed aflatoxin at a level of 3,000 ppb, chlortetracycline at a level of 550 ppm, or a combination of aflatoxin and chlortetracycline for a period of 6 wk. Weight gain in both lines of chicks was adversely affected by the aflatoxin treatment. There was a synergistic adverse effect in chicks of the low antibody response line when given chlortetracycline as well as aflatoxin, an effect not noted in chicks of the high antibody response line. Chlortetracycline alone had no effect on weight gain of low antibody response birds but increased the weight gain of chicks from the high antibody response line. Bursa to body weight ratios were adversely affected by aflatoxin in both lines of chicks, but chlortetracycline further adversely affected this parameter only in the low antibody response line. These results indicate that adverse effects of aflatoxin may be enhanced by addition of antibiotics to feed.

Aflatoxins↗