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PubMed1987

Simple method for screening aflatoxin-producing molds by UV photography.

UV absorption by aflatoxins was monitored in GY agar medium by UV photography. In the UV photographs, aflatoxin-producing molds were identified as gray or black colonies, whereas aflatoxin-nonproducing molds appeared as white colonies. By cellophane transplantation experiments and silica gel thin-layer chromatography, the products absorbing UV light substantially were found to be mainly aflatoxins B1 and G1 excreted from the mold mycelium into the agar medium. UV absorption did not occur when the agar medium contained aflatoxin-noninducible carbon sources instead of glucose. Various inhibitors of aflatoxin production, such as dichlorovos and dimethyl sulfoxide, also decreased the intensity of UV absorption. These results indicate that this technique can be used as a simple, safe, and rapid method of screening aflatoxin-producing molds.

Aflatoxins↗

PubMed1966

Production of aflatoxin on rice.

A method has been developed for the production of aflatoxin by growing Aspergillus flavus strain NRRL 2999 on the solid substrate rice. Optimal yields, more than 1 mg of aflatoxin B(1) per g of starting material, were obtained in 5 days at 28 C. A crude product containing aflatoxins was isolated by chloroform extraction and precipitation with hexane from concentrated solutions. The crude product consisted of 50% aflatoxin in the following ratio: B(1)-B(2)-G(1)-G(2), 100:0.15:0.22:0.02. Aflatoxin B(1) was separated from almost all the impurities and from the other aflatoxins by chromatography on silica gel with 1% ethyl alcohol in chloroform. Analytically pure aflatoxin B(1) was recrystallized from chloroform-hexane mixtures.

Aflatoxins↗

PubMed1967

Production of aflatoxin on wheat and oats: measurement with a recording densitometer.

A method has been developed for the production of aflatoxin by growing Aspergillus flavus NRRL 3145 on solid substrate wheat. Optimal yields of 900 mug of aflatoxin G(1) and 900 mug of aflatoxin B(1) per g of substrate were obtained in 4 to 5 days at 28 C. A study of aflatoxin production on hulls and groats of oats and on whole oats by A. flavus strains NRRL 2999, NRRL 3000, and NRRL 3145 revealed that aflatoxin was produced on all three substrates, although production was very slight on hulls. Strain NRRL 3145 grown on solid substrate groats produced the largest amounts of aflatoxin: 580 mug of B(1) and 450 mug of G(1) per g of substrate. A densitometric method for reading thin-layer chromatographic plates is described; this is more objective and more accurate than the visual methods previously used for the determination of all four aflatoxins.

Aflatoxins↗

PubMed1968

Factors influencing aflatoxin accumulation in peanut kernels and the associated mycoflora.

Accumulation of aflatoxin in Spanish peanut kernel samples from different geographical areas in Texas during 1966, as detected by the thin-layer chromatographic method, was relatively low. Analysis of samples obtained from growers using artificial drying equipment (forced air and supplemental heat), when windrow conditions were unfavorable for rapid drying, suggests that this practice reduces the possibility of aflatoxin accumulation. In general, peanuts harvested from land planted to peanuts the previous year were more highly infested with fungi and contained more aflatoxin than peanuts grown on land planted with rye, oats, melons, or potatoes the previous year. Aflatoxin incidence tended to decrease from south to north Texas. These findings verify previous research observations that moist tropical climates are conducive to fungal infestation and aflatoxin accumulation. Detection of aflatoxin in sound mature kernels (kernels screened for minimal size) indicates that the practice of screening for removal of small immature kernels and removal of obviously damaged kernels does not completely eliminate aflatoxin contamination.

Aflatoxins↗

PubMed1995

Characterization of the polyketide synthase gene (pksL1) required for aflatoxin biosynthesis in Aspergillus parasiticus.

Aflatoxins are potent toxic and carcinogenic compounds, produced by Aspergillus parasiticus and A. flavus as secondary metabolites. In this research, a polyketide synthase gene (pksL1), the key gene for aflatoxin biosynthesis initiation in A. parasiticus, has been functionally identified and molecularly characterized. PCR-derived DNA probes were used to find the pksL1 gene from subtracted, aflatoxin-related clones. Gene knockout experiments generated four pksL1 disruptants which lost both the ability to produce aflatoxins B1, B2, and G1 and the ability to accumulate norsolorinic acid and all other intermediates of the aflatoxin biosynthetic pathway. A pksL1 DNA probe detected a 6.6-kb poly(A)+ RNA transcript in Northern (RNA) hybridizations. This transcript, associated with aflatoxin production, exhibited a regulated expression that was influenced by growth phase, medium composition, and culture temperature. DNA sequencing of pksL1 revealed an open reading frame for a polypeptide (PKSL1) of 2,109 amino acids. Sequence analysis further recognized four functional domains in PKSL1, acyl carrier protein, beta-ketoacyl-acyl carrier protein synthase, acyltransferase, and thioesterase, all of which are usually present in polyketide synthases and fatty acid synthases. On the basis of these results, we propose that pksL1 encodes the polyketide synthase which synthesizes the backbone polyketide and initiates aflatoxin biosynthesis. In addition, the transcript of pksL1 exhibited heterogeneity at the polyadenylation site similar to that of plant genes.

Aflatoxins↗

PubMed1982

Aflatoxins and kwashiorkor: a study in Sudanese children.

Blood and urine samples from 252 Sudanese children were investigated for their aflatoxin content by high-performance liquid chromatography. The children comprised 44 with kwashiorkor, 32 with marasmic kwashiorkor, 70 with marasmus, and 106 age-matched, normally nourished controls. Aflatoxins were detected more often and at higher concentrations in sera from children with kwashiorkor than in the other malnourished and control groups. Aflatoxicol, a metabolite of aflatoxins B1 and B2, was detected in the sera of children with kwashiorkor and marasmic kwashiorkor but not in the controls and only once in a marasmic child. The difference between children with kwashiorkor or marasmic kwashiorkor and those in the control or marasmus groups was significant. Urinary aflatoxin was most often detected in children with kwashiorkor but their mean concentration was lower than in the other groups. Aflatoxicol was not detected in urine in any group. These findings suggest either that the children with kwashiorkor have a greater exposure to aflatoxins or that their ability to transport and excrete aflatoxins is impaired by the metabolic derangements associated with kwashiorkor. The presence of aflatoxicol in the sera of children with kwashiorkor but not in the others suggests a difference in metabolism between the two groups. Further studies are needed, and measurement of aflatoxins in the food eaten by these children is already underway.

Aflatoxins↗

PubMed1997

Immunotoxicological effects on piglets of feeding sows diets containing aflatoxins.

Three groups of four Large White sows were fed diets containing either 800 ppb purified aflatoxin B1 (group 1), 800 ppb purified aflatoxin G1 (group 2) or 400 ppb B1 and 400 ppb G1 (group 3) throughout gestation and lactation. A control group of four sows was fed a diet free of aflatoxins. Aflatoxins B1 and M1 were found in milk samples taken five and 25 days after parturition from the sows of group 1, aflatoxin G1 was present in the milk of the sows of group 2 and all three aflatoxins were present in samples from the sows of group 3. The concentration of aflatoxin in the milk was about 1000-fold lower than that in the feed, but increased over the 25 days after parturition. The piglet suckling on a central teat was selected from each sow, given sow milk until the fourth day of age, and was then free to eat prepared feed while suckling. At the 25th day of age the selected piglets were removed from the sow and sacrificed. Blood samples were collected from each piglet and cellular populations were separated for immunological measurements: an in vitro lymphocyte proliferation test, and tests to derive the phagocytic activity, phagocytic index and superoxide anion production of monocyte-derived macrophages were carried out along with studies on the motility, differential chemotaxis and chemotactic index of circulating granulocytes. The lymphoproliferative response to mitogens was reduced and monocyte-derived macrophages failed to efficiently produce superoxide anions after oxidative burst stimulation in vitro, while their ability to phagocytose red blood cells was not compromised. Granulocytic cells showed a reduction of chemotactic response in vitro to chemoattractant bacteria factor and casein.

Aflatoxins↗

PubMed2004

Comparison of cultural and analytical methods for determination of aflatoxin production by Mississippi Delta Aspergillus isolates.

This study compared cultural and analytical methods for detecting aflatoxin production by Aspergillus species. Aspergillus isolates were obtained from various Mississippi Delta crops (corn, peanut, rice, cotton) and soils. Most of the isolates (99%) were A. flavus and the remainder comprised A. parasiticus and A. nomius. The following three cultural methods were evaluated on potato dextrose agar: fluorescence (FL) on beta-cyclodextrin-containing media (CD), yellow pigment (YP) formation in mycelium and medium, and color change after ammonium hydroxide vapor exposure (AV). Aflatoxins in culture extracts were confirmed by thin-layer chromatography (TLC) and quantified by enzyme-linked immunosorbent assay (ELISA). Of the 517 isolates, 314 produced greater than 20 ng/g of total aflatoxin based on ELISA, and 180 produced greater than 10 000 ng/g of aflatoxin in the medium. Almost all the toxigenic isolates (97%) were confirmed by TLC as producers. Of the toxigenic isolates, as determined by ELISA, 93%, 73%, and 70% gave positive FL, YP, and AV responses, respectively. Of the 203 isolates producing less than 20 ng/g of aflatoxin, 20%, 6%, and 0% of respective FL, YP, and AV methods gave false-positive responses. The 9% false-positive results from TLC fall within this range. This study showed good agreement among all tested cultural methods. However, these cultural techniques did not detect aflatoxin in all cultures that were found to produce aflatoxins by ELISA, LC/MS, and TLC. The best results were obtained when the AV color change and CD fluorescence methods were used together, yielding an overall success rate comparable to TLC but without the need for chemical extraction and the time and expense of TLC.

Aflatoxins↗

PubMed2002

Fetal exposure to aflatoxins in the United Arab Emirates.

This is a prospective study in which aflatoxin levels were measured in umbilical cord blood from 201 women delivered consecutively in Tawam and Al Ain hospitals in order to determine whether the fetuses had been significantly exposed to the toxin. Aflatoxin B1, M1 and M2 were measured using high performance liquid chromatography. Aflatoxins were detected in 110 (54.7%) samples, 27 of which were positive for B1, 106 for M1 and 31 for M2. There was a significant negative correlation (p < 0.001) between birthweight and levels of aflatoxin. The high rate of detection of aflatoxins confirms that a significant number of infants in the UAE are exposed to these toxins which reflects maternal ingestion of aflatoxin-containing food. The presence of aflatoxin resulted in lower birthweights.

Aflatoxins↗

PubMed2003

Aflatoxin M1 in breast-milk of UAE women.

A study was undertaken to determine whether breast-milk of mothers from the United Arab Emirates (UAE) contained aflatoxins. One hundred and forty lactating mothers, 55 who had delivered premature infants (<2500 g, </=37 wk gestational age) and 85 who had full-term infants, agreed to participate in the study. Breast-milk was collected during regular feeding of infants in the special care baby unit and postnatal wards using an electric breast pump and ten ml of milk was siphoned off into a zinc-free plastic container for analysis. Aflatoxin M(1) concentration in the breast-milk samples was measured by HPLC. Samples were collected between January 1999 and December 2000. Approximately 66% of the mothers were expatriates and 34% were UAE nationals. Babies' weight, postnatal age, sex, birthweight and gestational age, and mothers' nationality, age and parity were recorded. Overall, 92% of the breast-milk samples contained aflatoxin M(1). Both univariate and multivariate logistic regression analysis failed to show significant correlation between aflatoxin M(1) and gestational age, postnatal age, gender, nationality and clinical condition. Levels of lactose, protein and lipids did not correlate significantly with levels of aflatoxin M(1). The public should be educated about storing food and the hazards of aflatoxin ingestion to reduce the unacceptably frequent presence of aflatoxin in breast-milk.

Aflatoxin M1↗

PubMed2003

The effects of aflatoxin B1 on the development of kwashiorkor in mice.

Seventy Swiss albino mice (6-week-old male) were selected for the investigation into aflatoxin B1's role in the cause of kwashiorkor. The mice were divided randomly into four groups. They were grouped within each group by being fed either low or normal protein level diets supplemented with very small amounts of aflatoxin B1 (0.5 microg/day). The control groups were fed aflatoxin B1-free diets containing either normal or low protein levels. All groups were monitored for 7 weeks. The increase in body weight was found to be low in groups I and II, given diets contaminated with aflatoxin B1. Although groups II and IV, which were given low dietary protein, showed remarkable decreases in serum total protein and albumin levels (group II: total protein 4.1 +/- 0.1 g/dL, albumin 2.6 +/- 0.8 g/dL and group IV: total protein 4.6 +/- 1.3 g/dL, albumin 2.8 +/- 0.82 g/dL) when compared with the groups fed a normal dietary protein level (group I: total protein 5.9 +/- 1.3g/dL, albumin 3.4 +/- 0.7g/dL and group III: total protein 5.4 +/- 1.6g/dL, albumin 3.5 +/- 1.2g/dL; P < 0.05). The statistical difference between these two groups was found not to be significant (P > 0.05). However, decreases in total protein and albumin levels were a little more prominent in group II. In addition, histopatological changes of the liver was remarkable in the group fed a low protein diet and aflatoxin B1 when compared with the group fed only a low protein diet and no aflatoxin B1. More significantly, however, was the increase in liver weight in both groups fed a low protein diet (groups II and IV). Our conclusion is that aflatoxin B1 could not have contributed to the development of kwashiorkor.

Aflatoxin B1↗

PubMed1999

Inhibition by the bioflavonoid ternatin of aflatoxin B1-induced lipid peroxidation in rat liver.

Aflatoxin B1, a metabolite of Aspergillus flavus is a potent hepatotoxic and hepatocarcinogenic mycotoxin. Lipid peroxidation and oxidative DNA damage are the principal manifestations of aflatoxin B1-induced toxicity which could be mitigated by antioxidants. Many plant constituents, e.g. flavonoids, lignans and spice principles (capsaicin, curcumin, eugenol, etc.) have been reported to prevent liver damage associated with lipid peroxidation. In this study we investigated ternatin, a tetramethoxyflavone isolated from Egletes viscosa, for possible protection against liver injury induced by aflatoxin B1 in rats. Seventy two hours after a single intraperitoneal dose of aflatoxin B1 (1 mg kg(-1)), the concentration of malondialdehyde, the product of lipid peroxidation in liver homogenates, and serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were significantly elevated (P<0.001). Subcutaneous ternatin (25 mg kg(-1)) pretreatment greatly reduced aflatoxin B1-induced increases in the levels of serum enzymes (ALT from 5071+/-763 to 293+/-66 international units L(-1) and AST from 4241+/-471 to 449+/-108 international units L(-1)) and elevated malondialdehyde levels (from 11.37+/-1.27 to 0.79+/-0.22 nmol (mg wet tissue)(-1)) in a manner similar to oral vitamin E (300 mg kg(-1)), a standard antioxidant. Further, histological changes induced by aflatoxin B1 such as hepatocellular necrosis and bile-duct proliferation were markedly inhibited in animals pretreated with ternatin or vitamin E. These data provide evidence that ternatin inhibits lipid peroxidation and affords protection against liver damage induced by aflatoxin B1. Ternatin might, therefore, be a suitable candidate for the chemoprevention of aflatoxicosis associated liver cancer.

Aflatoxin B1↗

PubMed2004

Postweaning exposure to aflatoxin results in impaired child growth: a longitudinal study in Benin, West Africa.

Aflatoxins are dietary contaminants that are hepatocarcinogenic and immunotoxic and cause growth retardation in animals, but there is little evidence concerning the latter two parameters in exposed human populations. Aflatoxin exposure of West African children is known to be high, so we conducted a longitudinal study over an 8-month period in Benin to assess the effects of exposure on growth. Two hundred children 16-37 months of age were recruited from four villages, two with high and two with low aflatoxin exposure (50 children per village). Serum aflatoxin-albumin (AF-alb) adducts, anthropometric parameters, information on food consumption, and various demographic data were measured at recruitment (February) and at two subsequent time points (June and October). Plasma levels of vitamin A and zinc were also measured. AF-alb adducts increased markedly between February and October in three of the four villages, with the largest increases in the villages with higher exposures. Children who were fully weaned at recruitment had higher AF-alb than did those still partially breast-fed (p < 0.0001); the major weaning food was a maize-based porridge. There was no association between AF-alb and micronutrient levels, suggesting that aflatoxin exposure was not accompanied by a general nutritional deficiency. There was, however, a strong negative correlation (p < 0.0001) between AF-alb and height increase over the 8-month follow-up after adjustment for age, sex, height at recruitment, socioeconomic status, village, and weaning status; the highest quartile of AF-alb was associated with a mean 1.7 cm reduction in growth over 8 months compared with the lowest quartile. This study emphasizes the association between aflatoxin and stunting, although the underlying mechanisms remain unclear. Aflatoxin exposure during the weaning period may be critical in terms of adverse health effects in West African children, and intervention measures to reduce exposure merit investigation.

Benin↗

PubMed1997

Hepatocellular carcinoma p53 G > T transversions at codon 249: the fingerprint of aflatoxin exposure?

The molecular epidemiology of p53 mutations allows the possibility of correlating particular mutations with specific environmental carcinogens and establishing one step in the causal pathway between exposure to carcinogens and the development of cancer. A striking example is the G > T transversion at the third base pair of codon 249 observed in liver cancer patients possibly exposed to high levels of aflatoxins in their agricultural products. In this paper, we describe a systematic review of the literature and access the quality of the available data. We found methodologic limitations in the studies. In particular, the key independent variable, aflatoxin exposure, was not assessed in these studies, with the exception of one study that measured a marker of exposure. Instead, nationality, geographic residence, or geographic site of hospital were used as surrogate markers for exposure. Patients from areas with high aflatoxin levels were more likely to have p53 mutations than were patients from areas with low aflatoxin levels. In the group with p53 mutations, patients from areas with high aflatoxin levels had higher proportions of mutations with codon 249 G > T transversions. The differences in proportions with p53 mutations were significant, as were the differences in proportions of codon 249 G > T transversions among patients with p53 mutations. Aflatoxin may increase the proportion of p53 mutations by causing a single mutation, the codon 249 G > T transversion, thus explaining some of the excess liver cancer associated with aflatoxin exposure. However, it is premature to conclude that p53 mutations are established markers for environmental carcinogens.

Aflatoxins↗

PubMed2004

Determination of aflatoxins and zearalenone in different culture media.

Some molds produce desirable changes in food, but most are merely esthetically undesirable. There has also been an increasing awareness that certain metabolic products of some molds commonly found on foods and feed are dangerous to humans and animals. These toxin substances, mycotoxins, are secondary metabolites produced by different fungi, especially Aspergillus, Penicillium, Fusarium, and, to a lesser degree, Alternaria. The most important toxins for humans are aflatoxins, ochratoxin A, fumonisins, certain trichothecenes, and zearalenone. Aflatoxins are fungal metabolites produced by different Aspergillus species: A. flavus, A. parasiticus, and A. nomius. The most commonly encountered aflatoxins are B1, B2, G1, G2, M1, and M2, but aflatoxin B1 is the most frequently found in contaminated samples, and aflatoxins B2, G1, and G2 are generally not reported in the absence of AFB1. The International Agency for Research on Cancer (IARC) considers that aflatoxins are carcinogenic (hepatocarcinogenic) to humans (group 1) and animals. Zearalenone is an estrogenic mycotoxin produced by several species of Fusarium (F. acuminatum, F. culmorum, F. equiseti, F. graminearum, F. verticilliodes, F. oxysporum, F. poae, F. rosum, F. solani, F. semitectum, and F. sporotrichioides) that primarily colonize different cereal grains. Several reports were noted on the occurrence of ZEA along with various combinations of group B trichothecenes, fumonisins, aflatoxins, and ochratoxins. In most cases, the levels of ZEA were considered to be low; however, the toxicological significance is not known. This toxin is not classifiable as to carcinogenicity in humans (group 3) by the IARC, but ZEA was implied in precocious sexual development in children in Puerto Rico and a breast enlargement in young boys in Italy.

Aflatoxins↗

PubMed1997

[Aflatoxins: current concepts on mechanisms of toxicity and their involvement in the etiology of hepatocellular carcinoma].

Current concepts derived from intensive research over the last decade, on biotransformation, mechanisms of toxicity and evidences for the involvement of aflatoxins in the etiology of human liver cancer are summarily presented. Aflatoxin B1(AFB1), the main metabolite produced by moulds of genus Aspergillus, exerts its effects after conversion to the reactive compound AFB1-epoxide, by the action of cytochrome P450-dependent enzymes. This epoxide can form derivatives with cellular macromolecules, including proteins, RNA and DNA. The reaction with DNA occurs with guanines in the códon 249 of tumor suppressor gene p53. Primary biotransformation of AFB1 also produces hydroxylated and less toxic derivatives, such as aflatoxins Q1 and P1. Differences intra and interspecies in the pathways of activation/detoxification are directly related to the susceptibility of animals to aflatoxin effects. In humans, studies of individual biomonitoring of AFB1 metabolites such as AFB1-N7-guanine have demonstrated that aflatoxins constitute an important risk factor for hepatocellular carcinoma (HCC) in exposed populations. Some of these studies also show a synergistic action between aflatoxins and the hepatitis B virus in the development of human HCC. In view of these concepts, and taking into account the frequent detection of aflatoxins in Brazilian foodstuffs, the need for investigation into the level of exposure to these toxins and its impact on human health is stressed.

Aflatoxin B1↗

PubMed1996

Bioactivation of aflatoxin B1 in the nasal and tracheal mucosa in swine.

Whole-body autoradiography of 3H-labeled aflatoxin B1 in young pigs showed a localization of bound label in the nasal olfactory and respiratory mucosa, in the tracheo-laryngeal mucosa, and in the conjunctiva, in addition to the liver. Whole-body and microautoradiography also showed a labeling of pigmented tissues, which can be ascribed to a melanin binding of AFB1. In vitro experiments with microsomal preparations of various tissues from sows revealed that the nasal respiratory and olfactory mucosa had the highest capacity to form DNA-bound aflatoxin B1-metabolites. The tracheal mucosa and the liver, in order, had lesser binding capacity. The lung was found to be devoid of aflatoxin B1-bioactivating capacity. In vitro microautoradiography revealed bound label in specific cell types in the nose and trachea and in some cells of the conjunctiva. A drastic decrease in the aflatoxin B1-DNA binding was observed when microsomal preparations of the nasal respiratory and olfactory mucosa were incubated in the presence of reduced glutathione, but without any addition of cytosolic glutathione-S-transferases. In incubations of liver microsomes under these conditions a somewhat lower inhibition of the aflatoxin B1-DNA binding was seen. Our results demonstrate that the nasal olfactory and respiratory mucosa and the tracheal mucosa have a higher capacity than the liver to bioactivate aflatoxin B1 in swine. Our data further show that microsomal-associated glutathione-S-transferases with a high capacity to catalyze the conjugation of the reactive aflatoxin B1-epoxide to reduced glutathione are present in the nasal olfactory and respiratory mucosa of swine.

Aflatoxin B1↗

PubMed1986

Feedlot performance and tissue residues of cattle consuming diets containing aflatoxins.

A comparative slaughter feeding trial was conducted using crossbred Hereford-Angus steers. Cottonseed meal known to be contaminated with aflatoxins was fortified with long-grain rice cultures of Aspergillus flavus to produce complete rations that contained 0, 60, 300 and 600 ppb aflatoxin B1 (AFB1). Forty steers, weighing approximately 250 kg were randomly assigned to four equal treatment groups. Animals were housed in individual pens and fed the assigned contaminated ration ad libitum for 155 d. On d 156 all animals were placed on the control ration for 14 d. Animals were weighed and blood samples collected every month for clinical chemistry analysis. Liver, muscle and fat biopsies were collected at 6-wk intervals. These samples were stored in liquid N2 prior to analysis for aflatoxin M1 and B1 content. Separate liver samples were taken for histopathological examination. Aflatoxin was withdrawn from the diet 2 wk prior to slaughter. After 1 wk of withdrawal liver, muscle and fat samples were collected and assayed for AFB1 and aflatoxin M1 (AFM1). Liver samples also were taken for histopathological examination. Growth rates and feed intakes in the 60 and 300 ppb aflatoxin treatments were not significantly different from controls. The 600-ppb treatment group had a decrease in feed intake and rate of gain. Rations containing 60 and 300 ppb of aflatoxin had no significant influence on blood components and enzyme patterns. The 600-ppb treatment caused a slight, but consistent, increase in serum glutamic oxaloacetic transaminase and alkaline phosphatase.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxins↗