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PubMed1979

The effect of exercise on the toxicity of aflatoxin B1 in chickens.

Three trials were conducted to study the effects of exercise on aflatoxicosis in young broiler and layer chicks. Aflatoxin B1 was fed at levels of 0 or 5 ppm in a corn-based diet. Exercise was conducted on a motorized treadmill. In one trial, the growth rate of aflatoxin-fed birds was found to be increased significantly (P less than .05) by exercise, but it was not equal to that of the control birds. In other trials, growth rates were increased by exercise in birds receiving aflatoxin, but not significantly. Feed consumption measurements indicated that the decreased growth rates in the aflatoxin-fed birds were due to decreased feed consumption. Glucose-6-phosphate dehydrogenase levels were decreased significantly in the unexercised broiler chicks fed aflatoxin (P less than .025). In one trial, liver weights of broiler chicks were increased significantly by aflatoxin (P less than .005). In the birds fed aflatoxin and exercised, liver weights also were increased but to a lesser degree (P less than .01).

Aflatoxins↗

PubMed1981

Synergism between aflatoxin and ochratoxin A in broiler chickens.

A 2 X 2 factorial experimental design consisting of four treatments (0, 2.5 microgram/g aflatoxin, 2.0 microgram/g ochratoxin A, and 2.5 microgram/g aflatoxin + 2.0 microgram/g ochratoxin A) with six replicates of 10 birds each was used to evaluate the synergism between aflatoxin and ochratoxin A. The chicks (Hubbard X Hubbard) were maintained on these dietary treatments from hatching until they reached 3 weeks of age, when the experiment was terminated. The size of the liver, spleen, pancreas, and proventriculus was significantly (P less than .05) altered by the individual toxins; however, a synergistic effect on the size of these organs was not observed. The kidney and gizzard were sensitive to the coincident exposure to these mycotoxins and were significantly (P less than .05) enlarged. The kidney was the most sensitive organ to the combined toxicity of aflatoxin and ochratoxin A, and nephropathy was the most important characteristic of this interaction. The synergism between aflatoxin and ochratoxin A significantly (P less than .05) decreased growth rate and numerically increased mortality, demonstrating the enhanced toxicity of cocontaminated feed. Liver lipid levels were significantly (P less than .05) increased by aflatoxin and decreased by ochratoxin A. The interaction of both mycotoxins on this parameter was significant (P less than .05) and the combined effect demonstrates that ochratoxin A inhibited lipid accumulation normally induced by aflatoxin. The data show that toxicity-enhancing synergisms exist between mycotoxins and that symptom patterns are altered during multiple mycotoxicoses. The data also demonstrate that nephropathy is the primary effect of this interaction and, thus, is of diagnostic importance.

Aflatoxins↗

PubMed1985

Effect of dietary aflatoxin on the uptake and elimination of chlortetracycline in broiler chicks.

Day-old broiler chicks were fed 0, 1.25, 2.5, and 5.0 micrograms aflatoxin/g of feed for 3 weeks. Chlortetracycline (CTC) was administered in the drinking water at a concentration of 50 mg/liter for 27 hr starting on Day 21. Three hours after initiation of the CTC treatment, birds receiving 2.5 and 5.0 micrograms/g dietary aflatoxin had significantly lower CTC in blood compared with the controls. At 12 and 27 hr after the initiation of CTC treatment, birds receiving any level of aflatoxin had significantly decreased blood levels of CTC compared with the controls. Intravenous injection of CTC of control birds and birds receiving 2.5 micrograms/g aflatoxin revealed a significant decrease in the elimination half-life of CTC and a significant increase in the total systemic clearance of CTC in the birds receiving dietary aflatoxin. Birds receiving 2.5 micrograms/g dietary aflatoxin also had a significant increase in the volume of gall bladder bile; however, this did not result in a greater amount of CTC being eliminated via bile. Studies on protein binding of CTC in the plasma of control birds and the plasma of birds receiving 2.5 micrograms/g dietary aflatoxin demonstrated that 60% more CTC is "free", or unbound, in the plasma of birds receiving no aflatoxin. These results suggest that aflatoxicosis lowers the plasma concentrations of CTC as a result of a decreased binding of CTC to plasma protein. This allows more unbound CTC to be available for elimination from the plasma by a means other than the liver, most likely via the kidney.

Aflatoxins↗

PubMed1986

The relationship of certain blood parameters to aflatoxin resistance in Japanese quail.

Blood chemistry profiles were obtained for two lines of Japanese quail selected for resistance to aflatoxin, and for a nonselected control line. Nine of the 18 plasma components measured in samples taken at 4 weeks of age changed as a result of selection. Plasma concentrations of total protein, albumin, cholesterol, and potassium, and the activities of lactic dehydrogenase, glutamic-oxalacetic transaminase, and cholinesterase were significantly elevated in aflatoxin-resistant quail compared with the nonselected line. The activities of beta-glucuronidase and alpha-amylase changed most dramatically; both activities were much lower in the resistant lines than in the control line. In another experiment, serum total protein, albumin, alpha-amylase, and beta-glucuronidase were tested as identifiers of aflatoxin-resistant individuals within a nonselected population of quail. Serum samples obtained from 150 nonselected quail immediately before and 24 hr after administration of an oral dose of aflatoxin were analyzed for each of the four components. The acute toxicosis decreased body weight, serum alpha-amylase activity, total protein, and albumin; whereas, serum beta-glucuronidase activity and the coefficients of variation for each parameter were increased. Correlations between measurements made prior to dosing and parameters reflecting aflatoxin susceptibility were not significant. However, postdose determinations of albumin, protein, and beta-glucuronidase were significantly related to susceptibility parameters. These data indicate that the four blood components tested cannot be utilized to identify resistant birds within a nonselected population of quail without an aflatoxin challenge; but albumin, protein, and beta-glucuronidase are correlated with resistance when measured during an aflatoxin stress.

Aflatoxins↗

PubMed1986

Relative importance of dietary aflatoxin and feed restriction on reproductive changes associated with aflatoxicosis in the maturing White Leghorn male.

A study was conducted to investigate the relative contribution of dietary aflatoxin and feed restriction on reproductive and endocrine changes associated with aflatoxicosis. Pair-feeding was used to factor out nutritional and toxicological effects of aflatoxin on reproduction in the maturing White Leghorn male. Birds were randomly assigned to treatment groups at 9 weeks and fed experimental diets for 3 weeks. Experiment 1 involved the partitioning of toxicological and nutritional effects of aflatoxin on both physiological and reproductive parameters. Aflatoxin-fed males had significantly greater relative liver weights and liver lipid content than control or pair-fed males; no differences in testicular weights were found among treatments. Plasma testosterone levels in controls were significantly higher than in pair-fed birds; aflatoxin-treated males exhibited the lowest concentrations. Pituitary and testicular responsiveness to synthetic luteinizing hormone-releasing hormone (LHRH) were monitored in Experiment 2. Plasma luteinizing hormone (LH) levels in aflatoxin-fed males were significantly higher than in control or pair-fed males prior to LHRH administration. Additionally, the LH response of pair-fed birds to exogenous LHRH was qualitatively different from that observed in the other two treatments; this indicates that hormonal changes observed during aflatoxicosis and feed restriction are a result of different physiological mechanisms. Plasma testosterone also increased after LHRH injection. This response was significantly greater in controls than in pair-fed males, and nonexistent in aflatoxin-treated birds.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1996

Degradation of aflatoxin by poultry litter.

Two trials were conducted to determine whether deep stacking of contaminated corn with poultry litter destroys aflatoxin. Contaminated corn was ground and mixed with litter to carbon:nitrogen ratios of 30:1. Moistures were adjusted by adding tap water just prior to incubation or stacking. The initial laboratory trial included only broiler litter at 40% moisture, whereas the subsequent field trial involved a 2 x 2 factorial design with litter type (turkey or broiler) and moisture (20 or 40%) as main effects. Aflatoxin assays were reduced in the laboratory trial from 433 and 402 to 54 and 8 ppb in Containers 1 and 2, respectively, after 35 d of incubation at 28 C. In the field trial, aflatoxin disappeared from broiler and turkey litter mixtures with projected moistures of 20% after 10 and 6 wk of storage, respectively, whereas disappearance in mixtures containing projected moistures of 40% required 5 and 3 wk, respectively. Differences in moisture appear to account for differences in the ability of turkey and broiler litter to detoxify aflatoxin. Hence, turkey and broiler litter would appear equal with respect to the ability to detoxify aflatoxin-contaminated corn. Disappearance of aflatoxin during storage with litter could have occurred as a result of ammonia release during storage or microbial detoxification mechanisms. However, nitrogen values suggest that microbial action was responsible for much of the detoxification, as aflatoxin disappeared from mixtures with little apparent ammonia release.

Aflatoxins↗

PubMedDate not supplied

Characterization of aflatoxin-producing fungi outside of Aspergillus section Flavi.

Most aspergilli that produce aflatoxin are members of Aspergillus section Flavi, however isolates of several Aspergillus species not closely related to section Flavi also have been found to produce aflatoxin. Two of the species, Aspergillus ochraceoroseus and an undescribed Aspergillus species SRRC 1468, are morphologically similar to members of Aspergillus section Circumdati. The other species have Emericella teleomorphs (Em. astellata and an undescribed Emericella species SRRC 2520) and are morphologically distinctive in having ascospores with large flanges. All these aflatoxin-producing isolates were from tropical zones near oceans, and none of them grew on artificial media at 37 C. Aflatoxins and sterigmatocystin production were quantified by high-pressure liquid chromatography (HPLC) and confirmed by HPLC-mass spectrometry (LC-MS) detection. Phylogenetic analyses were conducted on these four species using A. parasiticus and Em. nidulans, (which produce aflatoxin and the aflatoxin precursor sterigmatocystin, respectively) for comparison. Two aflatoxin/sterigmatocystin biosynthesis genes and the beta tubulin gene were used in the analyses. Results showed that of the new aflatoxin-producers, Aspergillus SRRC 1468 forms a strongly supported clade with A. ochraceoroseus as does Emericella SRRC 2520 with Em. astellata SRRC 503 and 512.

Aflatoxins↗

PubMed1997

Growth of an Aspergillus flavus transformant expressing Escherichia coli beta-glucuronidase in maize kernels resistant to aflatoxin production.

Kernels of a maize inbred that demonstrated resistance to aflatoxin production in previous studies were inoculated with an Aspergillus flavus strain containing the Escherichia coli beta-D-glucuronidase reporter gene linked to a beta-tubulin gene promoter and assessed for both fungal growth and aflatoxin accumulation. Prior to inoculation, kernels were pin-wounded through the pericarp to the endosperm, pin-wounded in the embryo region, or left unwounded. After 7 days incubation with the fungus, beta-glucuronidase activity (fungal growth) in the kernels was quantified using a fluorogenic assay and aflatoxin B content of the same kernels was analyzed. Kernels of a susceptible inbred, similarly treated, served as controls. Results indicate a positive relationship between aflatoxin levels and the amount of fungal growth. However, resistant kernels wounded through the pericarp to the endosperm before inoculation supported an increase in aflatoxin B over levels observed in nonwounded kernels, without an increase in fungal growth. Wounding kernels of the resistant inbred through the embryo resulted in both the greatest fungal growth and the highest levels of aflatoxin B1 for this genotype. Maintenance of resistance to aflatoxin B1 in endosperm-wounded kernels may be due to the action of a mechanism which limits fungal access to the kernel embryo.

Aflatoxin B1↗

PubMed2005

Survey for co-occurrence of ochratoxin A and aflatoxin B1 in dried figs in Turkey by using a single laboratory-validated alkaline extraction method for ochratoxin A.

A survey was carried out to determine the co-occurrence of ochratoxin A and aflatoxin B1 in dried figs from Turkey. Samples from two seasons of crops (2003 and 2004) intended for export to the European Union and the 2004 crop obtained from the domestic Turkish market were analyzed. Affinity column cleanup methods were employed for determining separately ochratoxin A and aflatoxin B1, but for ochratoxin A an alkaline extraction procedure was employed (in contrast to the conventionally employed acidic extraction), which gave consistently higher toxin recovery. In-house validation of the ochratoxin A method gave a limit of detection of 0.15 ng/g and a limit of quantification of 0.5 ng/g with a repeatability of 5.8% in the range 5 to 10 ng/g (with a mean recovery of 94% for spiked samples). Positive results for ochratoxin A were confirmed by liquid chromatography-mass spectrometry. For the 2003 export figs (58 samples), 7 samples contained only aflatoxin B1, 2 samples contained only ochratoxin A, and 2 samples contained both toxins (with maximum concentrations of 35.1 ng/g for aflatoxin B1 and 13.0 ng/g for ochratoxin A). Similarly for the 2004 export figs (41 samples), 16 samples contained only aflatoxin B1, 4 samples contained only ochratoxin A, and 2 samples contained both toxins (with maximum concentrations of 20.6 ng/g for aflatoxin B1 and 26.3 ng/g for ochratoxin A). Of 20 retail samples of dried figs from Turkey, only one sample contained ochratoxin A (2.0 ng/g) and none were contaminated with aflatoxin B1. This survey revealed a 14 to 15% incidence of occurrence of ochratoxin A for 2 years, which is higher than previously reported.

Aflatoxin B1↗

PubMedDate not supplied

Short-term exposure to subacute doses of aflatoxin-induced depressed mitogen responses in young mallard ducks.

Mallard ducklings were fed diets containing corn naturally contaminated with mixed aflatoxins, purified T-2 toxin, or no detectable mycotoxin in two trials. The aflatoxin level used was 12 ppb in the first trial and 33 ppb in the second. T-2 was added at 2 ppm in both trials. No pathology was associated with the aflatoxin used in this study, and T-2--induced lesions were described in a previous publication. The weights of primary (thymus and bursa of Fabricius) and secondary (spleen) lymphoid organs were significantly reduced in the T-2--treated birds. The total number of viable cells recovered from the thymus was significantly reduced in aflatoxin-treated birds. The numbers of viable cells recovered from thymus, bursa of Fabricius, and spleen were all significantly reduced after treatment with T-2. In each trial, significantly lower mitogenic responses were seen to pokeweed mitogen and concanavalin A in birds fed aflatoxin or T-2, representing reduction in both B-cell and T-cell mitogenesis. Birds fed aflatoxin also had significantly reduced Escherichia coli O55 lipopolysaccharide-induced mitogenic responses. These studies indicate that subacute oral exposure to aflatoxin caused a loss of normal lymphocyte reactivity in mallard ducklings. This finding supports the hypothesis that waterfowl that ingest even small quantities of mycotoxin-contaminated waste grain are likely to be more susceptible to bacterial or viral infections.

Aflatoxins↗

PubMed2000

Toxicity of aflatoxin: effects on spermatozoa, oocytes, and in vitro fertilization.

Aflatoxin B1 has been reported to have a deleterious effect on the reproductive capacity of laboratory and domestic animals. We wanted to elucidate the mechanistic aspect of this phenomenon by determining the toxic potential of aflatoxin B1 on the in vitro fertilizing ability of oocytes and epididymal sperm in albino rats. In vitro fertilization medium (IVFM) containing aflatoxin B1 at concentrations of 2.0, 4.0, 8.0, and 16.0 ppb was cultured with oocytes obtained from superovulated healthy fertile female rats and exposed to sperm cells. Epididymal sperm capacitated in IVFM, with or without aflatoxin B1, were exposed to oocytes, and the rates of fertilization in the two experiments were assessed. Aflatoxin B1 significantly reduced the mean number of ova fertilized, even at the lowest concentration. Exposure to aflatoxin caused a significant reduction in the motility of sperm cells. These results demonstrate the adverse effects of aflatoxin B1 on oocytes, spermatozoa, and in vitro fertilization.

Aflatoxin B1↗

PubMedDate not supplied

Immunoaffinity column cleanup with liquid chromatography for determination of aflatoxin M1 in liquid milk: collaborative study.

A collaborative study was conducted to evaluate the effectiveness of an immunoaffinity column cleanup liquid chromatographic method for determination of aflatoxin M1 in milk at proposed European regulatory limits. The test portion of liquid milk was centrifuged, filtered, and applied to an immunoaffinity column. The column was washed with water, and aflatoxin was eluted with pure acetonitrile. Aflatoxin M1 was separated by reversed-phase liquid chromatography (LC) with fluorescence detection. Frozen liquid milk samples both naturally contaminated with aflatoxin M1 and blank samples for spiking, were sent to 12 collaborators in 12 different European countries. Test portions of samples were spiked at 0.05 ng aflatoxin M1 per mL. After removal of 2 noncompliant sets of results, the mean recovery of aflatoxin M1 was 74%. Based on results for spiked samples (blind pairs at 1 level) and naturally contaminated samples (blind pairs at 3 levels) the relative standard deviation for repeatability (RSDr) ranged from 8 to 18%. The relative standard deviation for reproducibility (RSDR) ranged from 21 to 31%. The method showed acceptable within- and between-laboratory precision data for liquid milk, as evidenced by HORRAT values at the low level of aflatoxin M1 contamination.

Aflatoxin M1↗

PubMed2001

Hepatitis B, aflatoxin B(1), and p53 codon 249 mutation in hepatocellular carcinomas from Guangxi, People's Republic of China, and a meta-analysis of existing studies.

The incidence of hepatocellular carcinomas (HCC) varies widely worldwide, with some of the highest incidence rates found in China. Chronic infection with the hepatitis B virus (HBV) and exposure to aflatoxins in foodstuffs are the main risk factors. A G to T transversion at codon 249 of the p53 gene (249(ser)) is commonly found in HCCs from patients in regions with dietary aflatoxin exposure. Because HBV infection is often endemic in high aflatoxin exposure areas, it is still unclear whether HBV acts as a confounder or as a synergistic partner in the development of the 249(ser) p53 mutation. Our report has two aims. First, we contribute data on HCCs from southern Guangxi, a high aflatoxin exposure area. Using DNA sequencing, we found that 36% (18 of 50) of tumors had a 249(ser) mutation. Also, 50% (30 of 60) were positive for p53 protein accumulation and 78% (28 of 36) were positive for HBV surface antigen, as detected by immunohistochemistry. Second, we present a meta-analysis, using our results along with those from 48 published studies, that examines the interrelationships among aflatoxin exposure, HBV infection, and p53 mutations in HCCs. We used a method that takes into account both within-study and study-to-study variability and found that the mean proportion of HCCs with the 249(ser) mutation was positively correlated with aflatoxin exposure (P = 0.0001). We found little evidence for an HBV-aflatoxin interaction modulating the presence of the p53 249(ser) mutation or any type of p53 mutation.

Aflatoxin B1↗

PubMed1975

Excretion of carbon-14-labeled aflatoxin B1 via bile, urine, and intestinal contents of the chicken.

Carbon-14-labeled aflatoxin B1 was prepared by growing Aspergillus parasiticus in medium containing sucrose-14-C as the sole carbon source. The 14-C-labeled aflatoxin B1 was extracted with chloroform and purified by thin-layer chromatography (TLC) followed by precipitation from solution and washing. The 14-C-labeled aflatoxin B1 was intravenously given to anesthetized dwarf White Leghorn or Rhode Island Red hens with cannulated ureters and bile ducts. The 14-C had a calculated plasma half-life of 1.5 minutes and rapidly appeared in the bile. The 14-C concentration in the bile reached values approximately 7 times maximum for plasma, and most could no longer be extracted with chloroform. This finding indicated that metabolites of the 14-C-labeled aflatoxin B1 had been excreted against a concentration gradient into the bile. The quantities of 14-C excreted via bile, urine, and intestinal contents remained at a fairly constant ratio of 70:15:15, respectively, over the 315-minute experimental period. Six major chloroform-soluble compounds containing 14-C were isolated. Three of these were tentatively identified as aflatoxin B1, B2, and M1. A 4th was believed to be aflatoxin B2a. None of the early chloroform-soluble metabolites were as cytotoxic as aflatoxin B1.

Aflatoxins↗

PubMed2001

Ameliorative effect of vitamin E on aflatoxin-induced lipid peroxidation in the testis of mice.

AIM: To evaluate the ameliorative effect of vitamin E on aflatoxin-induced lipid peroxidation in the testis. METHODS: Adult male albino mice were orally administered 25 or 50 microg of aflatoxin in 0.2 mL olive oil per d for 45 d. The testis was isolated, blotted free of blood and processed for biochemical analysis. RESULTS: There was a dose-dependent significantly higher lipid peroxidation in the testis of aflatoxin treated mice than in the controls. The levels of non-enzymatic antioxidants such as glutathione, total and reduced ascorbic acid, as well as the activities of enzymatic antioxidants, such as superoxide dismutase, glutathione peroxidase and catalase were significantly lower in the testis of aflatoxin treated mice. Vitamin E (2 mg/d per animal; orally) pretreatment significantly ameliorates the aflatoxin-induced lipid peroxidation which could be due to higher enzymatic and non-enzymatic antioxidants in the testis of mice as compared with those given aflatoxin alone. CONCLUSION: Vitamin E pretreatment significantly ameliorates aflatoxin-induced lipid peroxidation in the testis of mice.

Aflatoxins↗

PubMed1999

Parasitological effects of simultaneous infections induced by Schistosoma mansoni and aflatoxin B1 in Syrian golden hamsters.

To determine the effect of S. mansoni and aflatoxin B1, 120 hamsters were divided into six groups of 20 each as follows: group I, S. mansoni only, group II, aflatoxin B1 only, group III, S. mansoni then aflatoxin B1 eight week, group IV, aflatoxin B1 then infected with S. mansoni six weeks, later, group V, aflatoxin B1 and S. mansoni simultaneously, group VI control. Loss of body, liver, and spleen weight was more prominent in groups IV and V than in other four groups. The higher mortality rate was in group III. Animals treated with aflatoxin followed by S. mansoni infection appeared to have a less deteriorating effect on the liver (group IV) than group III treated with by S. mansoni first followed by aflatoxin treatment. No morphological abnormalities were detected in the worms including testicular changes in males but a significant number of females was immature even in copula (P < 0.01) in groups III, IV, and V. The average number of S. mansoni eggs was less in groups III, IV, and V in comparison to group I. No abnormalities were detected in the eggs for groups infected with S. mansoni. The diameters of granulomas around eggs, were large on an average in groups III, IV and V as compared with groups I and II.

Aflatoxin B1↗

PubMed1976

Acute and protracted changes in the liver of Syrian hamsters induced by a single dose of aflatoxin B1. Observations on pathological effects of the solvent (dimethylformamide).

Male Syrian hamsters, 8-10 weeks of age, were treated with a single intraperitoneal injection of crystalline aflatoxin B1 in solution of N -N -Dimethylformamide (DMF). The concentrations of aflatoxin were adjusted to the smallest controllable amount of solvent in relation to the size of the animal (0-5 or 1-0 ml/kg). Treatment with, respectively, 5-0 or 2-5 mg/kg aflatoxin in 1-0 ml/kg DMF was lethal to most animals within one week. However, reduction of the solvent to 0-5 ml/kg, while not eliminating the mortality entirely during the first week, made possible observation of the survivors up to 28 days. Hamsters appear to be more susceptible to DMF poisoning than other species, like rat, guinea-pig and rabbit in which this solvent was used by investigators on the biological effects of aflatoxin. Either dose given of DMF alone was lethal for several animals during the first week of observation and sufficient to produce histological lesions in the liver which were characteristic and clearly different from those induced by aflatoxin during the same period. DMF alone caused centrilobular necrosis which was accompanied by haemosiderosis of liver structures. With a aflatoxin, in addition, periportal and midzonal necrosis of the liver was present. Aflatoxin B1 and B1 and DMF both induce haemorrhagic tendency probably involvement in the coagulation process of the blood. It cannot be decided, however, at present whether this is the result of an indentical mechanism.

Aflatoxins↗

PubMedDate not supplied

Chemical inactivation of aflatoxins in peanut protein ingredients.

Aflatoxin contamination of peanuts has posed a threat to the peanut industry in utilizing peanuts as a source of a low-cost protein ingredient for food and feed. Although the best approach to containing the aflatoxin problem in peanuts is prevention, it appears that chemical inactivation of aflatoxin in contaminated raw material provides the best means to salvaging the contaminated material. Several chemical reagents have been investigated for their efficacy in destroying aflatoxins present in raw peanuts and defatted peanut meal. Using certain oxidizing agents such as NaOCl, H2O2, and benzoyl peroxide; bases such as ammonia, methylamine, and calcium hydroxide; and aldehydes such as formaldehyde, contaminated raw peanuts or defatted peanut meal have been demonstrated to yield peanut meals, protein isolates, and concentrates having trace amounts or nondetectable levels of aflatoxins. Processing conditions for inactivating aflatoxins using these chemicals were investigated. The chemical treatments had little effect on the physiochemical properties of the detoxified protein product. The advantages and disadvantages of using these chemicals for inactivation of aflatoxins are discussed.

Aflatoxins↗