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PubMed1993

[Reconsideration of the role of aflatoxins in public health].

The pathogenicity of aflatoxins for human has been largely demonstrated. Although aflatoxin contamination of some foodstuffs has been unquestionably established, stress should be laid upon a certain lack of information: some of the affected foodstuffs have been "forgotten" in the enumeration of contaminated products (especially soybeans); relations between mycotoxins and food balance have not yet been taken into account: for instance, the influence of some vitamins, of various compounds (carotenoids, methionine, ...), influence of deficiency in proteins (often very important in Africa) etc... aflatoxin bioavailability has not sufficiently been examined (particularly that of milk aflatoxin M1.); concerning aflatoxin evaluation in contaminated products, it should be known that their distribution is very irregular. Sampling and following analysis should thus be carried out most carefully; for these motives, some conditions and likewise regulations would can again scrutinized.

Aflatoxins↗
PubMed1980

[Contamination of cow's milk during ingestion of small quantities of aflatoxin].

Sixteen cows, some in the early and the rest in the late lactation period, were given daily, during a eight day period a ration of peanut meal naturally contaminated by aflatoxin. The analysis for aflatoxin M1 of the milk obtained from these cows indicates the following points: --the level of aflatoxin M1 is not influenced by the volume of the daily milk secretion; --the quantity of this hydroxy-derivative expressed as a percentage of the parent toxin varies from 0.14 to 0.34 in the animals in the late lactation period, and from 0.66 to 0.95 in the cows producing some twenty litres of milk per day; --in order to achieve a tolerance limit of 20 ng/kg of aflatoxin M1, in the milk, the daily ingestion of the mycotoxin by cows should not exceed 90--100 micrograms per animal.

Aflatoxin B1↗
PubMed1977

Aflatoxicol M1, a new metabolite of aflatoxicol.

1. Using dog liver microsomal preparations, we have isolated and identified a new metabolite of aflatoxicol, aflatoxicol M1; this metabolic transformation is analogous to the conversion of aflatoxin B1 to aflatoxin M1. 2. Aflatoxicol M1 can also be produced from aflatoxin M1 by a reductase present in rabbit liver cytosol, a reaction analogous to the reduction of aflatoxin B1 to aflatoxicol. 3. In addition, aflatoxicol M1 can be oxidized to aflatoxin M1 by a carbon monoxide-insensitive dehydrogenase activity associated with human liver microsomes, a reaction analogous to the production of aflatoxin B1 from aflatoxicol by this fraction. 4. Ultra-violet, fluorescence, and mass spectral characteristics of aflatoxicol M1 are described. 5. The significance of this new aflatoxin metabolite and the possibility that it may be biologically active are discussed.

Aflatoxins↗
PubMedDate not supplied

The effect of indole-3-carbinol, an aflatoxin B1 hepatocarcinoma inhibitor, and other indole analogs on the rainbow trout hepatic mixed function oxidase system.

Rainbow trout were fed diets containing 3.4 mmol of indole-3-carbinol, indole-3-ethanol, indole-3-aldehyde, or indole-3-acetic acid in 100 g salmon oil/kg diet for 3 weeks. The indoles did not increase hepatic microsomal cytochrome(s) P-450 or P-448 nor induce the associated mixed function oxidase enzyme activities as measured by ethoxyresorufin-O-deethylase (EROD) and benzphetamine-N-demethylase activities. Indole-3-carbinol did not alter the in vitro metabolism of aflatoxin B1 to aflatoxicol and aflatoxin M1; but the other indoles did suppress the formation of aflatoxin M1 from aflatoxin B1. The results suggest that the mechanism by which indole-3-carbinol protected rainbow trout from aflatoxin B1 (AFB1) hepatocarcinogenesis was not via the alteration of the mixed function oxidase system.

Aflatoxin B1↗
PubMedDate not supplied

Aflatoxin B1 and aflatoxicol metabolism in rainbow trout (Salmo gairdneri) and the effects of dietary cyclopropene.

Aflatoxin M1 was identified as a minor metabolite formed by the in vitro incubation of aflatoxin B1 with the postmitochondrial fraction or microsomes from rainbow trout (Salmo gairdneri) liver. Fresh, whole trout liver converted perfused aflatoxin B1 to aflatoxicol and aflatoxin M1, and converted perfused aflatoxicol to aflatoxin B1 and aflatoxin M1. AFB1 reductive activity was found in the 105,000 xg supernatant, while activity converting AFL to AFB1 was distributed about equally in the 105,000 xg supernatant and in the microsomal pellet. Transformation of AFL to AFB1 was not inhibited by CO, but formation of AFM1 was completely blocked. Cyclopropene fatty acids (CPFA)-fed fish produced only one-half to one-third as much AFL from AFB1 as controls, and they produced no detectable AFM1. Most of the unreacted AFB1 was recovered by extraction of the incubation medium by organic solvent whereas, in controls, much of it remained bound to the protein. There was no difference in conversion of AFL to AFB1 when results were expressed in terms of postmitochondrial protein levels. CPFA-fed fish had lower microsomal protein and cytochrome P-450 levels and NADPH-cytochrome c reductase and aldrin epoxidation activities than did controls.

Aflatoxins↗
PubMedDate not supplied

Comparative mutagenicity of palmotoxin Bo and aflatoxins B1 and M1.

The mutagenicity of palmotoxin Bo and of aflatoxin M1 relative to that of aflatoxin B1, the potent mutagen, was studied in five Ames' Tester Strains of Salmonella typhimurium (TA-98, TA-100, TA-1535, TA-1537, TA-1538). Aflatoxins B1 and M1 are both highly mutagenic in a microsome-mediated system in TA-100. The prediction of the relative carcinogenicity of aflatoxin M1 to aflatoxin B1 posed by the mutation of TA-100 is probably more authentic than TA-87. The mutagenic potency of palmotoxin Bo is less than that of either aflatoxin B1 or M1.

Aflatoxins↗
PubMed1979

The reduced mutagenicity of aflatoxin B1 due to hydroxylation: observations on five Salmonella typhimurium tester strains.

The mutagenicity of aflatoxin M1 relative to that of aflatoxin B1, the parent compound, was studied in 5 Ames' tester strains of Salmonella typhimurium (TA 98, TA 100, TA 1535, TA 1537, TA 1538). Aflatoxins B1 and M1 are both highly mutagenic in microsome-mediated system in TA 100. The prediction of the relative carcinogenicity of aflatoxin M1 to aflatoxin B1 posed by the mutation of TA 100 is probably more authentic than by TA 98.

Aflatoxins↗
PubMed1979

[Determination of aflatoxins in cheeses].

To investigate cheeses for the presence of aflatoxins we chose the very sensitive method of Tuinstra and Bronsgeest (1975) used for the determination of aflatoxin M1 in milk. The method was slightly modified and the presence of aflatoxins was determined in 54 samples of different cheeses. Aflatoxin M1 was found out in 24% of the investigated samples. Most of positive samples were found among the soft cheeses (53.8 3/4), then in processed cheeses (13.6%) and in hard cheeses (12.5%). Aflatoxin M1 was not found in the group of mouldy cheeses and Olomouc cake cheeses, which were investigated in a smaller range. Positive findings did not exceed concentrations of 10 ng per kg, i.e. they did not even reach the value of permissible concentration as proposed in the Czech Socialist Republic for foods (5 microgram per kg).

Aflatoxins↗
PubMed1983

Aflatoxicol and aflatoxins B1 and M1 in eggs and tissues of laying hens consuming aflatoxin-contaminated feed.

This study was undertaken to relate quantitatively the aflatoxin residue found in eggs and tissues to the aflatoxin intake via feed. Eighteen hens were fed an aflatoxin B1 (B1)-contaminated feed (8 micrograms/g) for 7 days, after which half the group was sacrificed; the remainder were sacrificed after an additional 7 days on an aflatoxin-free diet. Eggs were collected over the entire 14-day period. Aflatoxicol (R0), B1, or both were found in eggs and tissues (kidneys, liver, muscle, blood, and ova). Aflatoxin M1 (M1) (.04 to .1 ng/g) was found only in the kidneys. Levels of R0 and B1 were approximately the same in eggs, ova, kidneys, and liver. In eggs, the levels of R0 and B1 (.02 to .2 ng/g) increased steadily for 4 or 5 days, after which time the levels plateaued and then decreased after B1 withdrawal at the same rate as they had increased. At 7 days after withdrawal, only trace amounts of R0 (.01 ng/g) remained in eggs. All tissues, except blood, from hens sacrificed immediately before aflatoxin withdrawal contained R0 (.04 to .4 ng/g) or R0 and B1 (.04 to .8 ng/g). The R0 (.03 to .11 ng/g) was the only aflatoxin detected in muscle, and B1 (.05 to .07 ng/g) was the only aflatoxin in blood. Seven days after aflatoxin withdrawal, B1 (.08 ng/g) was found in one of nine livers and R0 (.01 to .04 ng/g) in eight of nine muscles analyzed, but no aflatoxins were found in any other tissues.

Aflatoxin B1↗
PubMed2005

Fecal and urinary excretion of aflatoxin B1 metabolites (AFQ1, AFM1 and AFB-N7-guanine) in young Chinese males.

Our study was designed to assess the fecal and urinary excretion of 3 aflatoxin B1 (AFB1) metabolites, aflatoxins M1 (AFM1) and Q1 (AFQ1) and aflatoxin B1-N7-guanine (AFB-N7-guanine) that are produced by the predominant forms of cytochrome P450 enzymes responsible for the biotransformation of AFB1. Fecal and urinary AFM1, AFQ1 and urinary AFB-N7-guanine were assessed in 83 young Chinese males selected from a larger population (n = 300) based on detectable urinary AFM1. The concentration of fecal AFQ1 (median 137 ng/g fresh weight, IQR 9.1 to 450) was approximately 60 times higher than that of AFM1 (2.3 ng/g, IQR 0.0 to 7.3). In urine, the median AFQ1 was 10.4 ng/ml (IQR 3.4 to 23.3), and the median AFM1 and AFB-N7-guanine 0.04 ng/ml (IQR 0.01 to 0.33) and 0.38 ng/ml (IQR 0.0 to 2.15), respectively. A subgroup (n = 14) with hepatitis B virus (HBV) infection had significantly higher fecal concentrations of AFQ1 (p = 0.043) and AFM1 (p = 0.001) than those who were hepatitis B-virus antigen (HBsAg) negative, and the respective differences in urinary AFQ1 and AFM1 concentrations approached statistical significance (p = 0.054, p = 0.138). Our study demonstrates that AFQ1 is excreted in urine and feces at higher levels than AFM1, and feces are an important route of excretion of these AFB1 metabolites. AFQ1 should be further assessed for its predictive value as a marker for exposure and risk of dietary aflatoxins.

Aflatoxin B1↗
PubMed1982

Responses of dairy cows to dietary aflatoxin: feed intake and yield, toxin content, and quality of milk of cows treated with pure and impure aflatoxin.

Ten fistulated Holstein cows in midlactation were given daily doses of 13 mg of aflatoxin B1 for 7 days. Six received pure aflatoxin B1; three received an impure preparation that contained aflatoxin B1 plus other aflatoxins and metabolites produced by Aspergillus parasiticus in culture. Toxin was administered to each animal twice daily, one-half of the total dose each time, via the rumen orifice. Morning and evening milks were collected and analyzed for aflatoxin M1. Milk production and feed intake were monitored for 5 days before, every day during, and for 8 days after treatment with aflatoxin B1. Milk contained from 1.05 ppb to 10.58 ppb of aflatoxin M1. None was in milk 4 days after administration of toxin had stopped. Somatic cell counts and standard plate counts from milks of two cows were not affected appreciably by administration of toxin. Fluctuations in feed intake and milk production occurred in all animals during the treatment period with a significant decrease in milk production of those cows receiving 13 mg of impure aflatoxin B1 per day. Differences in results when cows received equal amounts of aflatoxin B1 may be attributable to the type of toxin administered (pure versus impure).

Aflatoxin B1↗
PubMed1982

Effect of beta-naphthoflavone on calf liver metabolism of aflatoxin B1.

Eight male Holstein calves were raised to 6 wk of age on whole milk at 8% of body weight and calf starter ration (15% crude protein) free choice. For each of 2 days prior to sacrifice, four of the calves were selected at random and administered the mixed function oxidase inducer beta-napthoflavone by bolus in starch carrier at .005% of metabolic body weight. After sacrifice, 10,000 X g postmitochondrial supernatant preparations were made from the excised livers and incubated with a 50-micrograms challenge of aflatoxin B1. Although there was no significant difference in total percent of the challenge metabolized, there was a large increase in aflatoxin M1 production by liver preparations from calves administered the flavone inducer. If the flavone family of inducers could alter the metabolic profile for aflatoxin in the adult lactating bovine, aflatoxin M1 excretion rates could be increased and pathways for production of mutagenic metabolites could be enhanced.

Aflatoxin B1↗
PubMed1987

Odontogenic tumors in Fischer rats.

The formation of odontogenic tumors in rats is rare unless they are treated with known carcinogens. In this study, male Fischer rats were continuously fed aflatoxins M1, B1, or control diets, then killed at 1, 6, 10, 16, 17, 19 and 21 months. Of the 186 rats fed aflatoxin M1 at 3 concentrations, 12 developed odontogenic tumors; 7 of 63 rats fed an agar-based diet also developed odontogenic tumors in 17-21 months. The purpose of this study is to describe these tumors. All the tumors were located in the upper jaw associated with the incisor teeth. The tumors developed in the periodontal ligament area and were composed mainly of highly cellular fibrous connective tissue. The fibroblastic nuclei were clustered in poorly defined swirls in areas and were evenly scattered in a myxomatous stroma in other areas. Within this tissue were ovoid sometimes coalescing, calcified bodies resembling cementum. Occasional inclusions of solid epithelial cell nests were present. Scattered nests were composed of ovoid epithelial ghost cells. Acellular cementum-like material surrounded many of these nests. An inductive phenomenon was present around occasional epithelial nests. Rare structures composed of globular dentin with irregular tubules were also observed. These tumors caused distortion of the facial areas and disruption of incisor tooth development. No metastatic lesions were noted but other neoplastic lesions occurred in these animals.

Aflatoxin B1↗
PubMedDate not supplied

[The significance of mycotoxin assimilation for the contamination of milk and milk products].

The two possible pathways contaminating milk and milk products with mycotoxins are either the secretory or post-secretory route. The latter is of only little importance due to cooling conditions in production and storage. A secretory contamination can only occur with such mycotoxins, which undergo no complete degradation through their passage into the milk. From the mycotoxins, present in cow's feed; virtually only aflatoxin B1 yields a milkborne metabolite, the aflatoxin M1. The carry over rate is low (2 +/- 1%), but can be enhanced by polyhalogenated biphenyls, also present in the forage. Under normal conditions, however, this enhancement will not be measurable due to low equimolar concentrations of both reactants. The aflatoxin M1 content in herd's bulk milk depends exclusively on the content of the precursor aflatoxin B1 in the ration of the cow and is with less than 10 ng/kg fairly low at present in the Federal Republic of Germany. A careful supervision of the imported feed ingredients for mixed feed, however, will ensure to keep those batches out of dairy cow feeding which exceed a certain level of aflatoxin. The legal threshold is 10 micrograms/kg, being even too high to ensure a milk containing less than 10 ng/kg under high energy feeding conditions. The discussed thresholds for aflatoxin M1 in milk are 50 and 10 ng/kg resp., the latter value is scheduled for milk used in infant nutrition. To keep this low concentration the intake of aflatoxin B1 must be less than 2 micrograms/kg of the daily ration.

Animal Feed↗
PubMed1977

[On the presence and the content of aflatoxin M in commercial cheese samples (author's transl)].

Between May 10 and August 9 1976, a total of 197 commercial cheese samples were tested on their aflatoxin M1 content; 136 samples (69%) were positive. The highest value was at 0.23 mug/kg, the average value of all positive samples was at 0.09 mug/kg. In more than half of the positive samples (54%), only traces of aflatoxin M1 could be detected, 21% contained up to 0.1 mug/kg and 14% more than 0.1 mug/kg. In soft cheese definitely less aflatoxin was found (57% positive samples) than in other cheese varieties (83--85% positive samples). Supplemental feeding of concentrates during spring season and pasture grazing of dairy cows resulted in more respectively less aflatoxin-positive cheese samples. This was especially true in soft cheese. The other cheeses with longer ripening periods showed the same effect, however, less pronounced with a clear lag phase. Inspite of many positive identity reactions on aflatoxin M1, a routine control of cheeses so far cannot be recommended because of the negative results on mass spectrometry.

Aflatoxins↗
PubMed1985

Metabolism of aflatoxin B1 by rat hepatic microsomes induced by polyhalogenated biphenyl congeners.

The metabolism of aflatoxin B1 to aflatoxins M1 and Q1 by rat liver microsomes from animals pretreated with polychlorinated or polybrominated biphenyl congeners depended on the structure of the halogenated biphenyl inducers. Microsomes from rats treated with phenobarbital (PB) or halogenated biphenyls that exhibit PB-type activity preferentially enhanced the conversion of aflatoxin B1 to aflatoxin Q1. In contrast, microsomes from rats treated with 3-methylcholanthrene (MC) or halogenated biphenyls that exhibit MC-type induction activity increased the metabolism of aflatoxin B1 to aflatoxin M1. The coadministration of PB and MC produced microsomes that exhibited both types of induction activity (mixed type) in catalyzing the oxidative metabolism of diverse xenobiotic agents. However, PB-plus-MC-induced hepatic microsomes from immature male Wistar rats preferentially increased the metabolism of aflatoxin B1 to aflatoxin M1 but did not enhance the conversion of aflatoxin B1 to aflatoxin Q1. Comparable results were observed with microsomes from rats pretreated with halogenated biphenyls classified as mixed-type inducers; moreover, in some cases there was a significant decrease in the conversion of aflatoxin B1 to aflatoxin Q1 (compared with that of controls treated with corn oil).

Aflatoxins↗
PubMed1982

Aflatoxins in the livers of children with kwashiorkor.

Autopsy liver specimens from Nigeria and South Africa obtained from three kwashiorkors, three marasmic-kwashiorkors and one marasmic child were analysed for the presence of aflatoxins using both high performance liquid chromatography and thin layer chromatography. Significant levels of aflatoxin B1 were found in the livers of the three kwashiorkor children. Aflatoxicol was detected in the liver of one marasmic-kwashiorkor and a small quantity of aflatoxin M1 in the liver of another. No aflatoxins were found in the livers of the third marasmic-kwashiorkor or the marasmic child. These findings extend recent clinical observations that indicate an association between aflatoxins and kwashiorkor.

Aflatoxin B1↗
PubMedDate not supplied

Variations in the levels of aflatoxin in cows milk consumed in the city of São Paulo, Brazil.

One hundred samples of commercially available cows milk, collected in the state of São Paulo, from July 1979 to September 1981, were analysed to determine the levels of aflatoxins M1 and M2 by the method of the AOAC. This investigation was also undertaken in 50 samples of cows milk from two farms located in the Médio Vale do Paraiba, from animals which had ingested stored feed. Aflatoxin M1 was detected in only one sample of commercially available cows milk, while those from the farms were found to contain a minimum of 0.1 microgram/l and a maximum of 1.68 microgram/l.

Aflatoxin M1↗