SEARCH · PubMed Health

Results for “Aflatoxin”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 289 records · Page 16Linked to original sources

PubMed1987

Characterization of the aflatoxin B1-binding site of rat albumin.

A fluorescence-enhancement method was used to investigate the non-covalent interaction between aflatoxin B1 and rat albumin. Solvent-induced shifts in the emission spectrum of aflatoxin B1 provided evidence that the aflatoxin B1-binding site of rat albumin is a highly nonpolar environment. A dissociation constant of 20 microM was determined at 20 degrees C. The possibility that aflatoxin B1 binds one of the three major drug sites of albumin was investigated by ligand-displacement experiments. Mechanisms whereby marker ligands displace aflatoxin B1 were further investigated by comparing the experimental binding parameters with those derived theoretically, assuming competitive binding. The results indicate that: aflatoxin B1 and phenylbutazone compete for a common high-affinity site on rat albumin; high-affinity binding of aflatoxin B1 and site-II marker ligands takes place independently; aflatoxin B1 does not compete with either cholate or warfarin for the same high-affinity site, but the simultaneous binding of warfarin or cholate negatively modulates the binding of aflatoxin B1 to albumin. Fluorescence energy-transfer studies show that the lone tryptophan residue, Trp-214, is not associated with the aflatoxin B1-binding site.

Aflatoxin B1↗

PubMed1984

Effect of dietary selenium on the metabolism of aflatoxin B1 in turkeys.

To investigate the biochemical mechanism of the previously reported protective effect of dietary selenium against aflatoxin toxicity, the hepatic metabolism of aflatoxin B1 in turkey poults was examined at various dietary selenium concentrations. Diets were supplemented with 0.2, 2.0 or 4.0 ppm selenium (as sodium selenite) and 500 ng aflatoxin B1/g diet in an 18-day trial. Free and conjugated aflatoxin and metabolites were quantified using high-performance liquid chromatography. The proportion of liver aflatoxins in conjugated forms increased and the ratio of free aflatoxin B1/M1 decreased with increasing dietary selenium concentrations. These in vivo results provide evidence of selenium-induced enhancement of aflatoxin detoxification processes. In a similar experiment using 2.0 ppm selenium and 750 ng aflatoxin B1/g diet, the concentration of hepatic reduced glutathione, cytochrome P-450 and the activity of enzymes involved in the metabolism of aflatoxin B1 and glutathione were determined. Although the selenium supplement increased glutathione peroxidase activity, dietary selenium had no effect on reduced glutathione or cytochrome P-450 concentrations or on the activities of glutathione transferase E, glucuronyl transferase and cytochrome c reductase. These data indicate that the protective action of selenium is not mediated by an increase in glutathione availability for aflatoxin conjugation or by effects on the activities of these enzymes as measured in vitro.

Aflatoxin B1↗

PubMed2002

Aflatoxin and fumonisin contamination of commercial corn (Zea mays) hybrids in Mississippi.

Resistance to mycotoxin contamination was compared in field samples harvested from 45 commercial corn (maize) hybrids and 5 single-cross aflatoxin-resistant germplasm lines in years with high and moderate heat stress. In high heat stress, mycotoxin levels were (4.34 +/- 0.32) x 10(3) microg/kg [(0.95-10.5 x 10(3) microg/kg] aflatoxins and 11.2 +/- 1.2 mg/kg (0-35 mg/kg) fumonisins in commercial hybrids and 370 +/- 88 microg/kg (140-609 microg/kg) aflatoxins and 4.0 +/- 1.3 mg/kg (1.7-7.8 mg/kg) fumonisins in aflatoxin-resistant germplasm lines. Deoxynivalenol was detected (one-fourth of the samples, 0-1.5 mg/kg), but not zearalenone. In moderate heat stress, mycotoxin levels were 6.2 +/- 1.6 microg/kg (0-30.4 microg/kg) aflatoxins and 2.5 +/- 0.2 mg/kg (0.5-4.8 mg/kg) fumonisins in commercial hybrids and 1.6 +/- 0.7 microg/kg (0-7 microg/kg) aflatoxins and 1.2 +/- 0.2 mg/kg (0.5-3.0 mg/kg) fumonisins in aflatoxin-resistant germplasm lines. The results are consistent with heat stress playing an important role in the susceptibility of corn to both aflatoxin and fumonisin contamination, with significant reductions of both aflatoxins and fumonisins in aflatoxin-resistant germplasm lines.

Aflatoxin B1↗

PubMed1981

Monoclonal antibody to aflatoxin B1-modified DNA detected by enzyme immunoassay.

Monoclonal antibodies were obtained after fusion of mouse P3 X 63 myeloma cells with spleen cells isolated from BALB/c mice that had been immunized with aflatoxin B1-adducted DNA complexed with methylated bovine serum albumin. Selected hybridomas were found to produce monoclonal antibodies specific for aflatoxin B1-modified DNA containing both the 2,3-dihydro-2-(N7-guanyl)-3-hydroxyaflatoxin B1 and the putative 2,3-dihydro-2-(N5-formyl-2',5',6'-triamino-4'oxo-N5-pyrimidyl) -3-hydroxyaflatoxin B1, suggesting that these DNA adducts share a common antigenic determinant. The monoclonal antibody was not reactive towards the free aflatoxin B1-guanine adducts in solution, seven other aflatoxin derivatives, or benzo[a]pyrene-adducted DNA. A noncompetitive ultrasensitive enzyme radioimmunoassay could measure 15 fmol of aflatoxin B1-DNA adducts in 10 ng of DNA and was at least 100-fold more sensitive than the standard enzyme-linked immunosorbent assay. Competitive enzyme-linked immunosorbent assay with these monoclonal antibodies reliably quantitated aflatoxin B1 adducted in vivo to rat liver DNA at adduct levels of one aflatoxin B1 residue per 250,000 nucleotides. The competitive ultrasensitive enzyme radioimmunoassay was determined to be at least 6-fold more sensitive than the competitive enzyme-linked immunosorbent assay in analysis of aflatoxin B1-adducted DNA. Therefore, enzyme immunoassay using monoclonal antibodies will be useful analytical tools for studying both the molecular interactions of aflatoxin B1 with DNA and the occurrence of aflatoxin B1-DNA adducts in biological specimens from people exposed to this environmental carcinogen.

Aflatoxin B1↗

PubMed1985

Aflatoxin metabolism in humans: detection of metabolites and nucleic acid adducts in urine by affinity chromatography.

A high-affinity IgM monoclonal antibody specific for aflatoxins was covalently bound to Sepharose 4B and used as a preparative column to isolate aflatoxin derivatives from the urine of people and experimental animals who had been exposed to the carcinogen environmentally or under laboratory conditions. Aflatoxin levels were quantified by radioimmunoassay and high-performance liquid chromatography after elution from the affinity column. In studies on rats injected with [14C]aflatoxin B1, we identified the major aflatoxin-DNA adduct, 2,3-dihydro-2-(N7-guanyl)-3-hydroxy-aflatoxin B1 (AFB1-N7-Gua), and the oxidative metabolites M1 and P1 as the major aflatoxin species present in the urine. When this methodology was applied to human urine samples obtained from people from the Guangxi Province of China exposed to aflatoxin B1 through dietary contamination, the aflatoxin metabolites detected were also AFB1-N7-Gua and aflatoxins M1 and P1. Therefore, affinity chromatography using a monoclonal antibody represents a useful and rapid technique with which to isolate this carcinogen and its metabolites in biochemical epidemiology and for subsequent quantitative measurements, providing exposure information that can be used for risk assessment.

Aflatoxin B1↗

PubMed2002

Occurrence of aflatoxins B1, B2, G1 and G2 in some Brazilian pet foods.

The presence of cereals and grains in the formulation of pet foods suggests the need to control aflatoxin contamination in these foods. The objective of the study was to analyse domestic pet food to determine the occurrence of aflatoxins as well as their risk to animal health. One hundred food samples (45 for dogs, 25 for cats, 30 for birds) were collected at random from pet shops in Alfenas city, south-east Brazil. Thin-layer chromatography was used for separation, identification and quantification of the compounds after validation of the method. Aflatoxins were detected in 12.0% of the samples. Levels of aflatoxins (B(1) + B(2) + G(1) + G(2)) above the maximum limit established in Brazil (50 microg kg(-1)) for animal food were detected in five of the 12 positive samples (41.7%). The concentration of total aflatoxins was 15-374 microg kg(-1) (mean 131 microg kg(-1)). All samples containing peanuts were positive for aflatoxin B(1). Aflatoxins are carcinogenic and their consumption might be a risk for domestic animal health. The high prevalence of aflatoxin B(1) in foods prepared for birds, species highly susceptible to aflatoxins, shows the need for the re-evaluation of the use of peanuts (present in seven of the eight samples positives for aflatoxin) and/or the addition of fungicides to the food.

Aflatoxin B1↗

PubMed1995

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↗

PubMed1980

Influence of temperature cycling on the production of aflatoxins B1 and G1 by Aspergillus parasiticus.

The effect of temperature cycling on the relative productions of aflatoxins B1 and G1 by Aspergillus parasiticus NRRL 2999 was studied. The cycling of temperature between 33 and 15 degrees C favored aflatoxin B1 accumulation, whereas cycling between 35 and 15 degrees C favored aflatoxin G1 production. Cultures subjected to temperature cycling between 33 and 25 degrees C at various time intervals changed the relative productions of aflatoxins B1 and G1 drastically. Results obtained with temperature cycling and yeast extract-sucrose medium with ethoxyquin to decrease aflatoxin G1 production suggest that the enzyme system responsible for the conversion of aflatoxin B1 to G1 might be more efficient at 25 degrees C than at 33 degrees C. The possible explanation of the effect of both constant and cycling temperatures on the relative accumulations of aflatoxins B1 and G2 might be through the control of the above enzyme system. The study also showed that greater than 57% of aflatoxin B1, greater than 47% of aflatoxin G1, and greater than 50% of total aflatoxins (B1 plus G1) were in the mycelium by day 10 under both constant and cyclic temperature conditions.

Aflatoxin B1↗

PubMed1983

Effect of feeding corn naturally contaminated with aflatoxin on feed efficiency, on physiologic, immunologic, and pathologic changes, and on tissue residues in steers.

Two of 3 groups of Holstein-Friesian steers (groups II and III; n = 5 each) were fed a ration containing corn naturally contaminated with 800 ng of aflatoxin/g. The other group of steers (group I; n = 5) was fed a ration containing noncontaminated corn. The respective rations were fed for 17.5 weeks, except the ration given to group III; the latter's first diet (contaminated with aflatoxin) was changed to a noncontaminated diet after 15 weeks, continuing for the remaining 2.5 weeks. All steers were killed and tissues and fluids were obtained for aflatoxin analysis. Although aflatoxin B1 and M1 could be detected in blood and urine at several sampling times during the experimental period in groups II and III steers (given the diets containing aflatoxin), there appeared to be no effects on body weight gains and immune phenomena, such as lymphoblastogenesis and antibody production, but there was a waning of the delayed cutaneous hypersensitivity in steers given aflatoxin-contaminated diets. In group III animals (diet was changed to noncontaminated ration at 15 weeks), aflatoxin B1 and M1 disappeared from urine before they were slaughtered. All tissues and fluids, except the rumen contents from these group III steers, were void of detectable aflatoxins B1 and M1 at necropsy. The concentrations of aflatoxin B1 in the rumen content of the latter steers were low. All tissues collected at necropsy from the group II steers fed the aflatoxin diet throughout the 17.5 weeks had detectable aflatoxins B1 or M1 present.

Aflatoxin B1↗

PubMed1982

Inhibition by specific antibodies of the mutagenicity of aflatoxin B1 in bacteria.

Two anti-aflatoxin B1 antisera, antiserum 'O' and antiserum 'C', were raised against conjugates in which the bovine serum albumin protein carrier was coupled to aflatoxin B1 derivatives at carbon 1 or 8. Their action was investigated in Salmonella thyphimurium assays using a fortified 9000 x g supernatant (S9) of rat liver homogenate or using rat hepatocytes as the metabolic activation system. In all cases, a substantial reduction in mutagenicity was observed: the mutagenicity caused by 12.5 ng aflatoxin B1 was inhibited by 50% with 2 microliters of antiserum 'O' and with 12 microliters of antiserum 'C' when activation was catalysed by rat liver supernatant; the mutagenicity of 3.31 micrograms aflatoxin B1 was inhibited by 50% with 25 microliters of antiserum 'O' in experiments using hepatocytes as the metabolic activation system. Several lines of evidence indicate that the inhibition is caused by specific antibodies. The molar ratios of aflatoxin B2 or aflatoxin G2 to aflatoxin B1 required to reduce by 50% the effect of antisera on aflatoxin B1 mutagenicity were 2.9-76-fold higher than those required to reduce by 50% the tracer antibody binding in radioimmunoassay. Possible mechanisms by which anti-aflatoxin B1 antisera inhibit aflatoxin B1 mutagenicity are discussed.

Aflatoxin B1↗

PubMed1995

Selective chemisorption and detoxification of aflatoxins by phyllosilicate clay.

Practical and effective strategies for the detoxification of aflatoxins are critically needed. We have shown that a phyllosilicate clay (HSCAS): i) tightly binds aflatoxins in aqueous solutions, including milk; ii) markedly decreases the bioavailability of radiolabeled aflatoxins; iii) greatly diminishes aflatoxicosis in young animals, i.e., rats, chickens, turkeys, lambs, and pigs; and iv) reduces the level of aflatoxin M1 in the milk from lactating dairy cattle and goats. In further studies, ligands with one or more of the functional groups in common with aflatoxin were reacted with HSCAS in vitro in an attempt to elucidate the specificity and mechanism of tight binding (or chemisorption). A chemisorption index (C alpha) was developed, allowing for direct comparison of various clay and zeolitic minerals with HSCAS. Chemisorption indices were determined by HPLC analysis of extracts of the supernatants and sorbed pellets (exhaustively extracted with methanol and chloroform). The beta-dicarbonyl system of aflatoxin was found to be essential for tight binding by HSCAS. Comparison of the chemisorption indices from various classes of compounds with spectral data (DRIFTS) indicated that the molecular mechanism of aflatoxin binding may involve the chelation of metal ions in HSCAS with the beta-dicarbonyl moiety in aflatoxin. Computer modeling was utilized to provide additional information. Preliminary evidence suggests that aflatoxin B1 may react at surfaces and within the interlayers of HSCAS particles. With knowledge of the mechanism involved, it has been possible to further enhance the propensity of HSCAS for aflatoxins.

Aflatoxins↗

PubMed1984

The influence of aflatoxins on child health in the tropics with particular reference to kwashiorkor.

Aflatoxins are common environmental hazards in all the underdeveloped countries of the tropics where they commonly contaminate food. They are toxic to most species of animals and are among the most powerful carcinogenic agents known. The liver is the principal target for toxicity. Metabolic derangements caused by aflatoxins include depression of protein and enzyme synthesis, disorder of lipid metabolism and immunological suppression. The aetiology and pathogenesis of kwashiorkor remains somewhat obscure. Similarities in the geographical and climatic prevalence of kwashiorkor and aflatoxins and similarities in the metabolic derangements caused by aflatoxins and those observed in kwashiorkor, prompted investigation of the relationship between aflatoxin and kwashiorkor in the Sudan and elsewhere in Africa. Analysis of foods from markets and in homes revealed widespread aflatoxin contamination. Aflatoxins were found more frequently and at higher concentrations in the serum of children with kwashiorkor than in those with other types of malnutrition or in normal children. Aflatoxicol, a metabolite of aflatoxin B1 was detected in serum in kwashiorkor and marasmic kwashiorkor but not in normally nourished children and only once in marasmus. Autopsy liver samples from West and Southern Africa have shown aflatoxins in all cases of kwashiorkor but not in marasmus. These findings establish relationships between aflatoxin and kwashiorkor the nature of which remains obscure but includes the possibility of a causal association.

Aflatoxins↗

PubMedDate not supplied

Aflatoxin exposure, malaria and hepatitis B infection in rural Gambian children.

Aflatoxin-albumin adduct levels were measured in serum samples obtained from a group of Gambian children. The relationships between exposure to aflatoxin and the prevalence of malaria, between exposure and humoral and cellular responses in vitro to defined malaria antigens and, amongst children with evidence of exposure to hepatitis B infection, between aflatoxin and carriage of the hepatitis B surface antigen (HBsAg), were assessed. Aflatoxin-albumin adduct was found in nearly all serum samples collected during a survey performed at the end of the dry season and levels of adduct were generally high (up to 720 pg aflatoxin-lysine equivalent/mg albumin). Higher levels of aflatoxin-albumin adduct were detected in Wollof children than in children of other ethnic groups and marked variation in mean adduct levels between villages was observed. Aflatoxin-albumin adduct levels were higher in children who were HbsAg positive and in children with Plasmodium falciparum parasitaemia than in controls. However, levels of adduct had no consistent effect on either malaria-specific antibody responses, lymphoproliferative responses in vitro, or morbidity from malaria during the subsequent rainy season. Much lower levels of aflatoxin-albumin adduct were detected in repeat samples obtained at the end of the rainy season. There was poor correlation between dry and rainy season levels of adduct in individual children. We have shown that Gambian children are exposed to high levels of aflatoxin. The seasonal variation of aflatoxin-albumin adduct and marked fluctuation of adduct with time in individual children need to be considered in the future planning of epidemiological studies using this marker of exposure.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗

PubMedDate not supplied

Reduction in exposure to carcinogenic aflatoxins by postharvest intervention measures in west Africa: a community-based intervention study.

BACKGROUND: Aflatoxins are fungal metabolites that frequently contaminate staple foods in much of sub-Saharan Africa, and are associated with increased risk of liver cancer and impaired growth in young children. We aimed to assess whether postharvest measures to restrict aflatoxin contamination of groundnut crops could reduce exposure in west African villages. METHODS: We undertook an intervention study at subsistence farms in the lower Kindia region of Guinea. Farms from 20 villages were included, ten of which implemented a package of postharvest measures to restrict aflatoxin contamination of the groundnut crop; ten controls followed usual postharvest practices. We measured the concentrations of blood aflatoxin-albumin adducts from 600 people immediately after harvest and at 3 months and 5 months postharvest to monitor the effectiveness of the intervention. FINDINGS: In control villages mean aflatoxin-albumin concentration increased postharvest (from 5.5 pg/mg [95% CI 4.7-6.1] immediately after harvest to 18.7 pg/mg [17.0-20.6] 5 months later). By contrast, mean aflatoxin-albumin concentration in intervention villages after 5 months of groundnut storage was much the same as that immediately postharvest (7.2 pg/mg [6.2-8.4] vs 8.0 pg/mg [7.0-9.2]). At 5 months, mean adduct concentration in intervention villages was less than 50% of that in control villages (8.0 pg/mg [7.2-9.2] vs 18.7 pg/mg [17.0-20.6], p<0.0001). About a third of the number of people had non-detectable aflatoxin-albumin concentrations at harvest. At 5 months, five (2%) people in the control villages had non-detectable adduct concentrations compared with 47 (20%) of those in the intervention group (p<0.0001). Mean concentrations of aflatoxin B1 in groundnuts in household stores in intervention and control villages were consistent with measurements of aflatoxin-albumin adducts. INTERPRETATION: Use of low-technology approaches at the subsistence-farm level in sub-Saharan Africa could substantially reduce the disease burden caused by aflatoxin exposure.

Aflatoxin B1↗

PubMed2001

Detection of moulds producing aflatoxins in maize and peanuts by an immunoassay.

An enzyme-linked immunosorbent assay (ELISA) was developed to detect moulds producing aflatoxins in maize and peanuts by an antibody produced to extracellular antigen from Aspergillus parasiticus. This antibody recognized species with phenotypic similarities to A. parasiticus, A. flavus and the domesticated species A. sojae and A. oryzae. For maize samples that were naturally contaminated with aflatoxins, low and high levels of aflatoxin corresponded with low and high ELISA readings for mould antigens, respectively. Maize and peanuts inoculated with 10(2) spores ml(-1) of A. parasiticus and incubated at 15 degrees C for 18 days or 21 degrees C for 7 days were analyzed for mould antigens and aflatoxin levels. At 15 degrees C, mould antigens were detected by day 4 in maize when 0.16 ng g(-1) of aflatoxin was detected by ELISA but not by thin layer chromatography (TLC). Antigens were detected in peanuts by day 4 before aflatoxin was found. Likewise, at 21 degrees C, antigens were detected by day 4 in maize when less than 1 ng g(-1) of aflatoxin was detected by ELISA but not by TLC, but by day 2 in peanuts when no aflatoxin was detected. A. parasiticus could be detected before it could produce aflatoxins. Therefore, this ELISA shows potential as an early detection method for moulds that produce aflatoxins.

Aflatoxins↗

PubMed1998

Survey of fungal counts and natural occurrence of aflatoxins in Malaysian starch-based foods.

In a survey of starch-based foods sampled from retail outlets in Malaysia, fungal colonies were mostly detected in wheat flour (100%), followed by rice flour (74%), glutinous rice grains (72%), ordinary rice grains (60%), glutinous rice flour (48%) and corn flour (26%). All positive samples of ordinary rice and glutinous rice grains had total fungal counts below 10(3) cfu/g sample, while among the positive rice flour, glutinous rice flour and corn flour samples, the highest total fungal count was more than 10(3) but less than 10(4) cfu/g sample respectively. However, in wheat flour samples total fungal count ranged from 10(2) cfu/g sample to slightly more than 10(4) cfu/g sample. Aflatoxigenic colonies were mostly detected in wheat flour (20%), followed by ordinary rice grains (4%), glutinous rice grains (4%) and glutinous rice flour (2%). No aflatoxigenic colonies were isolated from rice flour and corn flour samples. Screening of aflatoxin B1, aflatoxin B2, aflatoxin G1 and aflatoxin G2 using reversed-phase HPLC were carried out on 84 samples of ordinary rice grains and 83 samples of wheat flour. Two point four percent (2.4%) of ordinary rice grains were positive for aflatoxin G1 and 3.6% were positive for aflatoxin G2. All the positive samples were collected from private homes at concentrations ranging from 3.69-77.50 micrograms/kg. One point two percent (1.2%) of wheat flour samples were positive for aflatoxin B1 at a concentration of 25.62 micrograms/kg, 4.8% were positive for aflatoxin B2 at concentrations ranging from 11.25-252.50 micrograms/kg, 3.6% were positive for aflatoxin G1 at concentrations ranging from 25.00-289.38 micrograms/kg and 13.25% were positive for aflatoxin G2 at concentrations ranging from 16.25-436.25 micrograms/kg. Similarly, positive wheat flour samples were mostly collected from private homes.

Aflatoxins↗

PubMed1995

Neonatal jaundice with reference to aflatoxins: an aetiological study in Zaria, northern Nigeria.

Two prospective studies were undertaken to determine a possible relationship between perinatal aflatoxin exposure and neonatal jaundice. First, cord blood samples from 37 neonates who subsequently developed jaundice and from 40 non-jaundiced (control) babies were analysed for six major aflatoxins and aflatoxicol. Peripheral blood samples of both groups were also analysed postnatally for aflatoxins. In a second study, serum aflatoxin levels of 64 jaundiced neonates admitted from outside the hospital were compared with levels in 60 non-jaundiced control babies. Aflatoxins were detected in 14 (37.8%) cord blood samples of jaundiced neonates and in nine (22.5%) of the controls. The mean cord aflatoxin concentration was highest in jaundiced neonates with septicaemia, but the difference was not statistically significant. The frequency of detection of aflatoxins in peripheral blood was not significantly different in jaundiced and non-jaundiced babies. Aflatoxins were detected in the blood of over 50% of neonates with jaundice of 'unknown' aetiology. There was no correlation between severity of hyperbilirubinaemia and serum aflatoxin levels. Further studies are needed to determine the extent of pre- and postnatal exposure to aflatoxin in Nigerian infants and the effects of such exposure on fetal and neonatal health.

Aflatoxins↗

PubMed1995

Effects of maize weevils (Coleoptera: Curculionidae) on production of aflatoxin B1 by Aspergillus flavus in stored corn.

Insects play an important role as facilitators of the aflatoxin-producing fungus, Aspergillus flavus Link, in both preharvest and postharvest corn. The current study investigated the role of maize weevils, Sitophilus zeamais Motschulsky, in enhancing aflatoxin B1 content in stored corn. In laboratory experiments, aflatoxin B1 was quantified with an indirect enzyme-linked immunosorbent assay (ELISA) on corn following artificial infestation with adult weevils that had each been topically treated with 100 spores of A. flavus. Corn kernels infested with A. flavus-contaminated weevils had significantly higher levels of aflatoxin B1 than A. flavus-inoculated corn without weevils. The presence of maize weevils resulted in increased kernel moisture content during incubation, and grain moisture was positively correlated with aflatoxin content across treatments receiving spores. Aflatoxin B1 levels were higher in corn treated with fungus-contaminated weevils compared with corn that was mechanically damaged and inoculated with spores, which in turn had more aflatoxin than undamaged corn treated with spores. Aflatoxin B1 content in corn increased with time of weevil exposure from 7 to 21 d, but decreased after 28 d of exposure. Aflatoxin levels in infested corn increased significantly with increased numbers of A. flavus-contaminated weevils. Maize weevils carried spores both internally and externally; however, substantial numbers of spores were intimately associated with the exoskeleton of adult weevils. These findings indicate that maize weevils facilitate the growth of A. flavus and aflatoxin production in corn by increasing surface area susceptible to fungal infection and increasing moisture content as a result of weevil metabolic activity.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxin B1↗