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PubMed2005

[Fungal spoilage of foods and its risk assessment].

From the second half of the 1990s, an increased regard has been given to the fungal spoilage of foods as follows: 1) post-harvest diseases and losses of fruits and vegetables, 2) deterioration of low water activity foods by xerophilic fungi, 3) contamination of psychrotolerant or psychrophilic fungi on foodstuffs and processed foods during storage and distribution at low temperature, and 4) spoilage of heat processed foods and soft drinks by heat-resistant fungi. In accordance with an international concern about food safety, mycotoxin contamination of foods has gained much global attention in recent times owing to its potential health hazards. The evaluation of mycotoxin hazards is principally based on the determination of a no-observed effect level (NOEL) in long-term toxicological studies, and the application of a safety factor (usually 100). In addition to hazard assessment, data on the natural occurrence of mycotoxins in various commodities and food intake data are needed to enable exposure assessment. Thus risk assessment of mycotoxins is, in fact, the product of hazard assessment and exposure assessment. In 1997, the FAO/WHO Joint Expert Committee on Food Additives (JECFA) considered estimates of the carcinogenic potency of aflatoxins and the potential risks associated with their intake. Recently the Codex Alimentarius Commission (Codex) has established standards for aflatoxin M1 in milk and for patulin in apple juice. The Codex is an international organization, supported by FAO/WHO, aiming at facilitating world trade and protecting the health of the consumer by developing international standards for food and feeds. Apart from aflatoxins, the JECFA has measured a provisional tolerable daily intake (TDI) for ochratoxin A, patulin, deoxynivalenol, T-2/HT-2 toxins, zearalenone and fumonisins. In 2001, the mycotoxins evaluated or re-evaluated at the JECFA meeting included ochratoxin A, deoxynivalenol, T-2/HT-2 toxins, fumonisins, and aflatoxin M1. In Japan, specific regulations now exist for deoxynivalenol (1.1 ppm) in wheat grains and for patulin (50 ppb) in apple juice and its products.

Aflatoxin B1↗
PubMed1984

Effect of aflatoxin B1 and major metabolites on phytohemeagglutinin-stimulated lymphoblastogenesis of bovine lymphocytes.

Effects of aflatoxin B1 and three of its metabolites on cellular immune response were assessed with an assay based on inhibition of tritiated thymidine uptake by phytohemeagglutinin stimulated lymphocytes. In this in vitro system aflatoxin B1 and aflatoxin Q1 were strongly inhibitory (more than 50% inhibition) at concentrations of 10 mu/ml, whereas aflatoxicol and aflatoxin B2 alpha exhibited little inhibition at 10 micrograms/ml and only 45 to 50% inhibition at 25 micrograms/ml. Contrasts with single degrees of freedom and orthogonal polynomial analysis revealed that the pair of aflatoxin B1 and aflatoxin Q1 differed linearly and quadratically from the pair of aflatoxin B2 alpha and aflatoxicol, but within each pair there were no differences. Limited data with aflatoxin M1 revealed that it was slightly more active than aflatoxicol in the assay, but minimal replication prevented rigorous statistical testing. It may be theorized that the moderate to strong inhibition of blastogenesis by aflatoxin B1 and its metabolites could inhibit T lymphocyte functions, such as killer, helper, effector, or other immune processes, and thus compromise the immunological surveillance mechanism.

Aflatoxin B1↗
PubMedDate not supplied

Robotic automated analysis of foods for aflatoxin.

Immunoaffinity column-based sample preparation procedures for determination of aflatoxins B1, B2, G1, and G2 in several food matrixes and aflatoxin M1 in milk have been automated by using flexible automation, or robotics. Components used to assemble the system were purchased commercially or developed and built in-house. A liquid-level sensor developed in-house to assist elution of the immunoaffinity column is described. After immunoaffinity column cleanup, aflatoxins are separated by reversed-phase liquid chromatography and determined by fluorescence without derivatization. Mean recoveries of aflatoxins B1, B2, and G1 added to corn and nuts at 9-36 ng/g total aflatoxins were > 85% (coefficient of variation [CV] = 16%). Recoveries of aflatoxin G2 averaged 50% (CV = 28%). Recoveries of aflatoxin M1 added to milk at 0.12-0.50 ng/mL averaged 78% (CV = 19%). The ability of the automated system to reproduce its results is demonstrated by the fact that the CV of replicate assays is generally better than 10%. Comparability between the automated procedure and the AOAC official method is demonstrated.

Aflatoxins↗
PubMed1981

High performance liquid chromatographic determination of aflatoxins in animal tissues and products.

A method was developed for the determination of aflatoxins, M1, B1, G1, B2, and G2 in animal tissues, meat, eggs, and dairy products by high performance liquid chromatography (HPLC). Previous extraction procedures were modified to optimize the precision and recovery of the method. HPLC is performed isocratically with a 5 micrometer microparticulate octadecylsilica column and fluorometric detection. The analysis is based on treatment of the purified sample extract or standard with trifluoroacetic acid (TFA) to catalyze the hydration of aflatoxins M1, B1, and G1 to the highly fluorescent M2a, B2a, and G2a derivatives. Analysis by HPLC with and without TFA treatment of the extract provides quantitative and qualitative data. The recovery of added aflatoxins and the precision of the recovery depend on the type of sample; mean coefficient of variation for all recovery values was 19.7 +/- 11.0% for the analysis of liver, ground beef, dairy products, and eggs. The method was sensitive, with a detection limit of 0.05 + 0.10 ng/g for each aflatoxin. This procedure provides an alternative to existing thin layer chromatographic methods for determining aflatoxins in animal tissues and products

Aflatoxins↗
PubMed2006

A simple steady-state model for carry-over of aflatoxins from feed to cow's milk.

A simple steady-state model is derived from two kinetic one-compartment models for the disposition of aflatoxin B1 (AFB1) and aflatoxin M1 (AFM1) in the lactating cow. The model relates daily intake of AFB1 in feed of dairy cattle and the cow's lactation status to resulting concentrations of AFM1 in milk. Moreover, assuming a linear relationship between the cow's lactation status and feed intake, the model relates daily milk production and AFB1 concentration in total feed to AFM1 levels in milk. The model explains similar experimental outcomes from different investigations into carry-over of aflatoxins from feed to milk. Although it is difficult to set a permanent limit for AFB1 in feed, the European Union (EU) limit of 5 microg AFB1 kg(-1) concentrate has proved, thus far, to be an appropriate level in preventing the EU limit of 0.05 microg AFM1 kg(-1) milk being exceeded.

Aflatoxin B1↗
PubMed2000

In vitro metabolism of aflatoxin B1 by larvae of navel orangeworm, Amyelois transitella (Walker) (Insecta, Lepidoptera, Pyralidae) and codling moth, Cydia pomonella (L.) (Insecta, Lepidoptera, Tortricidae).

Larvae of the navel orangeworm (NOW), Amyelois transitella (Walker), a major pest of almonds and pistachios, and the codling moth (CM), Cydia pomonella (L.), the principal pest of walnuts and pome fruits, are commonly found in tree nut kernels that can be contaminated with aflatoxin, a potent carcinogen. The ability of larvae of these insects to metabolize aflatoxin B1 (AFB1) was examined. A field strain of NOW produced three AFB1 biotransformation products, chiefly aflatoxicol (AFL), and minor amounts of aflatoxin B2a (AFB2a) and aflatoxin M1 (AFM1). With AFL as a substrate, NOW larvae produced AFB1 and aflatoxicol M1 (AFLM1). A lab strain of CM larvae produced no detectable levels of AFB1 biotransformation products in comparison to a field strain which produced trace amounts of only AFL. Neither NOW nor CM produced AFB1-8,9-epoxide (AFBO), the principal carcinogenic metabolite of AFB1. In comparison, metabolism of AFB1 by chicken liver yielded mainly AFL, whereas mouse liver produced mostly AFM1 at a rate eightfold greater than AFL. Mouse liver also produced AFBO. The relatively high production of AFL by NOW compared to CM may reflect an adaptation to detoxify AFB1. NOW larvae frequently inhabit environments highly contaminated with fungi and, hence, aflatoxin. Only low amounts, if any, of this mycotoxin occur in the chief CM hosts, walnuts, and pome fruits. Characterizations of enzymes and co-factors involved in biotransformation of AFB1 are discussed.

Aflatoxin B1↗
PubMed2005

Determination of mycotoxins in bovine milk by liquid chromatography tandem mass spectrometry.

Liquid chromatographic/tandem mass spectrometric methods using pneumatically assisted electrospray ionisation (LC-ESI-MS/MS) was developed for determination of 18 mycotoxins and metabolites-ochratoxin A, zearalenone, alpha-zearalenol, beta-zearalenol, alpha-zearalanol (zeranol), beta-zearalanol (taleranol), fumonisin B1, fumonisin B2, T-2 toxin, HT-2 toxin, T-2 triol, diacetoxyscirpenol (DAS), 15-monoacetoxyscirpenol (MAS), deoxynivalenol (DON), 3-acetyldeoxynivalenol (3-AcDON), 15-acetyldeoxynivalenol (15-AcDON), deepoxy-deoxynivalenol (DOM-1) and aflatoxin M1--in milk. The mycotoxins were extracted and cleaned up simultaneously. Extraction and removal of lipophilic compounds was performed at pH 2 using a two-phase mixture of acetonitrile and hexane. The acetonitrile concentration of the aqueous phase was reduced and the pH was adjusted to 8.5 before clean up by solid phase extraction (SPE) on Oasis HLB. The toxins DON, DOM-1, 3-AcDON, 15-AcDON, ochratoxin A, zearalenone, alpha-zearalenol, beta-zearalenol, alpha-zearalanol and beta-zearalanol were detected in negative ion mode after separation on a Hypersil ENV analytical column, while the toxins T-2 toxin, HT-2 toxin, T-2 triol, DAS, MAS, fumonisin B1, fumonisin B2 and aflatoxin M1 were detected in positive ion mode after separation on a Luna C18 column. Two transition products were monitored for each compound. The extraction and SPE conditions were optimised to obtain maximum recovery and minimum signal suppression/enhancement. The detection capabilities related to the transition products of lowest abundance were in the range 0.020-0.15 microg/l. The mean true recoveries were in the range 76-108% at levels of 0.2-10 microg/l.

Animals↗
PubMed1984

Effect of butylated hydroxytoluene on the disposition of [14C]aflatoxin B1 in the lactating rat.

The distribution and metabolism of an ip dose of [14C]aflatoxin B1 (AFB1) were studied in lactating Sprague-Dawley rats fed for the previous 13 days on a diet containing 0.5% butylated hydroxytoluene (BHT). Compared with ingestion of a BHT-free diet, treatment with BHT increased the biotransmission of AFB1 metabolites, predominantly aflatoxin M1 (AFM1), into the mammary gland and its content of milk, decreased AFB1 binding to liver nuclear DNA and enhanced the excretion of water-soluble metabolites of AFB1, all measured 6 hr after an oral dose of [14C]AFB1. These changes are related to the induction by BHT of hepatic enzymes involved in the transformation and detoxification of AFB1. The results suggest that exposure to BHT may protect the lactating animal from the carcinogenic effect of AFB1 but may increase the risk of exposure of the newborn infant to the carcinogenic metabolite AFM1.

Aflatoxin B1↗
PubMed1982

Aflatoxin B1 metabolism and DNA binding in isolated hepatocytes from rainbow trout (Salmo gairdneri).

The metabolism of aflatoxin B1 (AFB1) was examined in freshly isolated hepatocytes from rainbow trout. Intracellular DNA adduct formation was linearly related to AFB1 dose, and qualitatively similar to adducts formed in vivo. The rate of adduct accumulation was constant during the first hour following completion of the preparation, after which an increase and gradual decrease in rate routinely occurred. The relative rates of production of the major unbound AFB1 metabolites aflatoxicol, aflatoxin M1, and polar conjugates, also remained constant over the first hour of preparation age, but subsequently changed in a manner consistent with the changes in DNA binding. The common solvent vehicles ethanol and dimethyl sulfoxide were shown to seriously perturb AFB1 metabolism and DNA binding even at levels less than 1%. A simple method is reported for removal of ethanol prior to introduction of hepatocytes for incubation with AFB1. The influence of cell concentration was also examined. DNA binding and relative distribution of AFB1 metabolites showed little or no dependence in the range 1-6 x 10(6) cell/ml, but were substantially altered above 10(7) cells/ml. Under defined conditions, studies in isolated hepatocytes appear to reflect in vivo cell capabilities for AFB1 metabolism.

Aflatoxin B1↗
PubMed1988

Cytochrome P3-450 cDNA encodes aflatoxin B1-4-hydroxylase.

Aflatoxin B1 (AFB1), a potent hepatocarcinogen and ubiquitous dietary contaminant in some countries, is detoxified to aflatoxin M1 (AFM1) via cytochrome P-450-mediated AFB1-4-hydroxylase. Genetic studies in mice have demonstrated that the expression of AFB1-4-hydroxylase is regulated by the aryl hydrocarbon locus and suggested that different cytochrome P-450 isozymes catalyze AFB1-4-hydroxylase and aryl hydrocarbon hydroxylase activities. We have now examined lysates from mammalian cells infected with recombinant vaccinia viruses containing expressible cytochrome P1-450 or P3-450 cDNAs for their ability to metabolize AFB1 to AFM1. Our results show that cytochrome P3-450 cDNA specifies AFB1-4-hydroxylase. This is the first direct assignment of a specific cytochrome P-450 to an AFB1 detoxification pathway. This finding may have relevance to the dietary modulation of AFB1 hepatocarcinogenesis.

Aflatoxin B1↗
PubMed1989

Replication blocks and sequence interaction specificities in the codon 12 region of the c-Ha-ras proto-oncogene induced by four carcinogens in vitro.

We have examined the region surrounding codon 12 in the human c-Ha-ras proto-oncogene in vitro to determine the reaction intensities at the guanine nucleotides after exposure to the mycotoxin aflatoxin B1, to one of its human metabolites aflatoxin M1, to dimethyl sulfate, and to the major ultimate carcinogen of benzo(a)pyrene, benzo(a)pyrene diol-epoxide. Among the adducts produced, those at N-7-guanyl sites are alkali-labile and can be identified using a variation of the Maxam-Gilbert sequencing procedure. Data indicate that the guanine nucleotides of codon 12 have above average potential for adduct formation by the genotoxins when compared to other guanine sites, but were not the strongest sites. This codon 12 region has been inserted into single-stranded M13 phage, exposed to several of the genotoxins, and used as a template for DNA synthesis in vitro. There is a sequence-specific variation in polymerase inhibition at various adducted nucleotide sites, but replication blocks are not preferentially seen at the carcinogen-adducted guanines of codon 12. These results indicate that the predominance of point mutations which are detected in vivo at codon 12 do not reflect sequence-mediated preferential susceptibility of these sites to initial DNA adduction or to replication errors. The mechanisms controlling these sequence effects are not currently understood, and attempts to predict relative alkylation or termination frequencies based solely on local DNA sequence are not reliable.

Aflatoxin B1↗
PubMed1986

Mechanisms of anti-carcinogenesis: the distribution and metabolism of aflatoxin B1 in rainbow trout fed aroclor 1254.

Polychlorinated biphenyls (PCBs) have previously been shown to be inhibitors of carcinogenesis in trout. The mechanism of this inhibition was investigated by studying the effects of PCBs on aflatoxin B1 (AFB1) distribution, metabolism and DNA adduct formation, both in vivo and in vitro. A 24 h distribution study of injected tritiated AFB1 showed more radioactivity in blood, liver and bile in fish fed PCBs, but less in residual carcass. The metabolites of AFB1 found in vivo in blood plasma and liver homogenates were shifted by PCB pretreatment towards greater production of the polar metabolite aflatoxin M1 (AFM1) and glucuronide conjugates. The major metabolite in bile of PCB fish was the glucuronide of aflatoxicol M1 (AFL-M1), which was enhanced 15-fold over controls. Levels of aflatoxicol (AFL) glucuronide, the major conjugate in controls, were unaltered by PCBs. The pattern of AFB1 metabolism in isolated hepatocytes from PCB-prefed fish was consistent with in vivo metabolism. AFB1--DNA adduct formation in a 1 h assay was similar in hepatocytes from PCB-fed and control fish. However, the total rate of AFB1 metabolism was significantly elevated in hepatocytes from PCB-fed fish such that the degree of AFB1--DNA adduct formed per unit AFB1 metabolized was 42% lower than control. Similarly, adduct formation in vivo during the first 24 h post-AFB1 injection in PCB fish was not significantly different from controls. However, over a longer 21 day period, adduct levels in PCB fish were only 48-69% of controls (P less than 0.005, analysis of variance), once peak adduct formation was reached. Thus, initial rates of adduct formation may be misleading in the absence of further information on rates of carcinogen metabolism in vitro and/or pharmacokinetics of peak adduct formation in vivo. These results indicate that PCB inhibition of AFB1 carcinogenesis in trout involves dramatic initial changes in carcinogen distribution, metabolism and elimination which, over time, results in a net reduction of DNA adduct formation.

Aflatoxin B1↗
PubMed1988

The genetics of aflatoxin B1 metabolism. Association of the induction of aflatoxin B1-4-hydroxylase with the transcriptional activation of cytochrome P3-450 gene.

The association between murine cytochrome P3-450 and hepatic aflatoxin B1-4-hydroxylase, a cytochrome P-450-dependent enzyme which converts aflatoxin B1 (AFB1) to aflatoxin M1 (AFM1), was examined by (a) purification of the cytochrome P-450 which preferentially metabolizes AFB1 to AFM1; (b) isolation of the specific cDNA clone; and (c) correlating induction of transcriptional activation of the specific message with the enzyme activity in the hepatic microsomes. Isolation of cytochromes P-450 from C57BL/6 mice, an Ah-responsive strain, pretreated with a 150 mg/kg dose of beta-naphthoflavone resulted in the partial purification of the cytochrome P-450 with preference for the metabolism of AFB1 to AFM1. Antibodies raised against this cytochrome P-450 were used to enrich hepatic mRNA for cDNA cloning. A cDNA library screened with a rat cytochrome P-450c gene probe yielded only two types of cDNA clones that contained inserts corresponding to cytochrome P1-450 and cytochrome P3-450. Specific restriction fragments of near full-length P1-450 cDNA and full-length P3-450 cDNA, hybridizing only with their respective messages, were isolated and used to assess transcriptional activation of these messages in liver and extrahepatic tissues from C57BL/6 mice treated with 3-methylcholanthrene, beta-naphthoflavone, indolylacetonitrile, and Aroclor-1254. Dose-dependent induction of the two messenger RNAs, when compared with the induction of specific enzyme activities, demonstrated the association of cytochrome P1-450 with aryl hydrocarbon hydroxylase activity and the association of cytochrome P3-450 with AFB1-4-hydroxylase activity. This supports our earlier hypothesis that AFB1-4-hydroxylase and aryl hydrocarbon hydroxylase, although regulated by the Ah locus, are the products of two separate genes (Gurtoo, H.L., Dahms, R.P., Kanter, P., and Vaught, J.B. (1978) J. Biol. Chem. 253, 3952-3961).

Aflatoxin B1↗
PubMed1979

In vivo covalent binding of organic chemicals to DNA as a quantitative indicator in the process of chemical carcinogenesis.

The covalent binding of chemical carcinogens to DNA of mammalian organs is expressed per unit dose, and a 'Covalent-Binding Index', CBI, is defined. CBI for various carcinogens span over 6 orders of magnitude. A similar range is observed for the carcinogenic potency in long-term bioassays on carcinogenicity. For the assessment of a risk from exposure to a carcinogen, the total DNA dmaage can be estimated if the actual dose is also accounted for. A detailed description is given for planning and performing a DNA-binding assay. A complete literature survey on DNA binding in vivo (83 compounds) is given with a calculation of CBI, where possible, 153 compounds are listed where a covalent binding to any biological macromolecule has been shown in vivo or in vitro. Recent, so far unpublished findings with aflatoxin M1, macromolecule-bound aflatoxin B1, diethylstilbestrol, and 1,2-epithiobutyronitrile are included. A comparison of CBI for rat-liver DNA with hepatocarcinogenic potency reveals a surprisingly good quantitative correlation. Refinements for a DNA-binding assay are proposed. Possibilites and limitations in the use of DNA binding in chemical carcinogenesis are discussed extensively.

Aerosols↗
PubMedDate not supplied

Current situation on regulations for mycotoxins. Overview of tolerances and status of standard methods of sampling and analysis.

A worldwide enquiry was undertaken in 1986-1987 to obtain up-to-date information about mycotoxin legislation in as many countries of the world as possible. Together with some additional data collected in 1981, information is now available about planned, proposed, existing or absence of legislation in 66 countries. Details about tolerances, legal bases, responsible authorities, prescribed methods of sampling and analysis and disposition of commodities containing inadmissible amounts of mycotoxins, are given. The information concerns aflatoxins in foodstuffs, aflatoxin M1 in dairy products, aflatoxins in animal feedstuffs, and other mycotoxins in food- and feedstuffs. In comparison with the situation in 1981, limits and regulations for mycotoxins have been expanded in 1987 with more countries having legislation (proposed or passed) on the subject, more products, and more mycotoxins covered by this legislation. The differences between tolerances in the various countries are sometimes quite large, which makes harmonization of mycotoxin regulations highly desirable.

Global Health↗
PubMedDate not supplied

Mycotoxins: regulations, quality assurance and reference materials.

Some 60 countries have currently enacted or proposed regulations for control of mycotoxins (primarily the aflatoxins) in food and animal feed. Various factors influence the establishment of limits for certain mycotoxins, but there is no consistent rationale for setting limits or for enforcement control. The enforcement of the regulations requires monitoring of suspected commodities. Many laboratories perform large numbers of determinations of mycotoxins, in particular aflatoxins, and consider their results to be reliable. Nevertheless, it often happens that laboratories find quite different analytical results on samples that have been especially homogenized for interlaboratory studies. The application of Quality Assurance principles contributes to the reliability of mycotoxin measurements. Quality Assurance is focused on the organizational process and the conditions under which laboratory studies are planned, performed, monitored, recorded, reported and archived. This is, in itself, an important contribution to the scientific value of a study. A Quality Assurance programme should include various elements, including (certified) reference materials, if available. Certified reference materials are stable, homogeneous products with certified values of the analyte(s) of interest. Various certified reference materials for mycotoxins have been prepared by the European Commission's Community Bureau of Reference, in co-operation with several European laboratories (aflatoxin M1 in milk powder, aflatoxins B1 B2, G1, and G2 in peanut butter, aflatoxin B1 in peanut meal and compound feed, deoxynivalenol in wheat and maize flour). Other reference materials are in a well-advanced development stage (ochratoxin A in wheat flour and pig kidney, fumonisins B1 and B2 in maize).

Food Contamination↗
PubMed2005

Immunoaffinity clean-up and direct fluorescence measurement of aflatoxins B1 and M1 in pig liver: comparison with high-performance liquid chromatography determination.

An improved analytical method for aflatoxin B1 (AFB1) and aflatoxin M1 (AFM1) determination in pig liver is described, using an aqueous methanol extraction, an immunoaffinity column clean-up step and a direct fluorometric measurement for toxin detection and quantification. A detection limit of 1.0 microg kg-1 was achieved for AFB1 and AFM1. Mean recoveries of 80.7+/-9.0% for AFB1 spiked at 1.0-9.7 microg kg-1 levels and of 76.7+/-6.6% for AFM1 spiked at 1.0-5.5 microg kg-1 levels were obtained. Recovery data for spiked samples were statistically compared with those obtained by the same extract using classical reversed-phase high-performance liquid chromatography (RP-HPLC) with fluorescence detection, showing a significant correlation (p<or=0.05) for both aflatoxins. Both procedures were applied to the analysis of 50 pig livers, collected from 10 farms in the north of Italy. All the samples showed a contamination level lower than 1.0 microg kg-1 for AFB1 and one liver sample has shown an AFM1 contamination greater than 1.0 microg kg-1. The direct fluorometric procedure is particularly suitable for food manufacturers and control laboratories where quick procedures are mainly required for food quality control as well as for diagnostic and research purposes.

Aflatoxin B1↗
PubMed1981

Effects of dietary aflatoxin on existing bacterial intramammary infections of dairy cows.

Aflatoxin, a naturally occurring mycotoxin with immunosuppressive properties, was given to 4 lactating dairy cows that had experimentally induced or naturally occurring mammary infections in 2 of their 4 mammary quarters. Aflatoxin was given orally in daily doses approximating 0.3 mg of B1 activity/kg of body weight for periods of 12 to 14 days. Infecting organisms were Streptococcus agalactiae, Staphylococcus aureus, and Staphylococcus hyicus. The 4 cows were monitored for clinical signs of disease and signs of mastitis for periods before, during, and after aflatoxin consumption. The cows developed inappetence, lost body weight, and had variable reductions in daily milk yield. Serum ornithine-carbamoyl transferase and sorbitol dehydrogenase activities were elevated during and 1 to 3 weeks after aflatoxin consumption. Exacerbations of acute clinical mastitis did not occur in any of the infected quarters; however, bacterial populations in the milk increased in 3 of the 4 cows during aflatoxin consumption. Mean California mastitis test scores were generally highest in the infected quarters in the period after the last dose of aflatoxin was given. Aflatoxin M1 appeared in milk 3 to 6 hours after aflatoxin consumption began, and persisted for 72 hours or longer after the last dose of aflatoxin was given. Aflatoxin B1 and M1 were present in urine samples taken at 6 hours after aflatoxin consumption began and persisted for 72 through 120 hours after the last dose of aflatoxin was given.

Aflatoxins↗