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PubMed1980

Effects of intratesticular aflatoxin B1 on rat testes and blood estrogens.

An investigation of the effects of aflatoxin B1 on rat testes and plasma estrogens is reported. A normal saline-suspended aflatoxin B1 was injected into right testes of mature Sprague-Dawley rats at doses of 0, 5, 10, 25 or 50 micrograms. Effects were evaluated by histopathological alterations of the testes and by levels of plasma estrogens estimated by a modified Dextron-Charcoal radioimmune assay. Significant gross lesions were present in testes injected with the 50 microgram dose. There was a 50% reduction in size and weight as compared to the left testis. Histological changes were dose-dependent, with minimal or no changes at 5 micrograms and maximal effects at 50 micrograms. The lesions varied from mild testicular degeneration to complete disappearance of cellular components. Interstitial cell proliferation, occasional calcification of seminiferous tubules, and absence of spermatogenesis and spermatozoa were extreme toxic effects. Estrogen concentrations in injected rats were reduced compared to those of control and normal rats. This study suggested that following intratesticular aflatoxin B1 exerts a direct toxic effect on testes with a reduction in plasma estrogen levels.

Aflatoxins↗

PubMed1978

Distribution of [14C]-labelled aflatoxin B1 in mice.

The distribution of [14C]-labelled aflatoxin B1 has been studied in mice with the aid of whole-body autoradiography. In addition to the localisation of labelled aflatoxin B1 and/or its metabolities in the liver, bile, kidney, lung and urine an uptake of 14C in the pigment of the Harderian gland and the eye was observed. Uptake of radioactivity was also found in the eyes of the foetuses although their livers did not accumulate radioactivity.

Aflatoxins↗

PubMed1983

Extraction and thin layer chromatography of aflatoxin B1 in mixed feeds.

A method was developed for the determination of aflatoxin B1 in commercially prepared feeds. The method incorporates methylene chloride and citric acid solution extraction, cleanup on a small silica gel column, and thin layer chromatography for quantitation. Commercial turkey starter, catfish chow, medicated pig starter, broiler finisher, rabbit chow, horse feed, rat chow, and dog chow were investigated. The feeds were spiked with naturally contaminated corn at 4 different levels of aflatoxin B1 (16-130 microgram/kg). Three assays were run on each of the 32 combinations of feed and levels of aflatoxin. Mean recoveries were 85.9-92.8% at levels of 16.5, 32.9, 65.8, and 131.6 micrograms/kg. The relative standard deviation per assay was 18.6%. This method is more rapid and less involved than most previously published methods for mixed feeds.

Aflatoxin B1↗

PubMedDate not supplied

Use of polyethylene glycol in the radioimmunoassay of aflatoxin B1.

Polyethylene glycol (PEG) is used to separate the antibody-bound ligand from the free ligand in the radioimmunoassay of aflatoxin B1. Conditions affecting precipitation of the bound ligand are described. Maximal precipitation of antibody-bound aflatoxin B1 requires an aqueous PEG concentration of 15-20% and 0.4 mg of carrier gamma-globulin. Precipitation is unaffected by pH variations from 6 to 9, by NaCl concentrations below 0.28 M, and by Tris-HCl concentrations below 0.2 M. The radioimmunoassay procedure is simple, rapid, and sensitive and could be used to assay aflatoxin B1 in unextracted sera or in peanut butter after solvent extraction.

Aflatoxin B1↗

PubMed1988

The induction of neoplastic lesions by aflatoxin-B1 in the Egyptian toad (Bufo regularis).

The carcinogenic activity of aflatoxin-B1, the metabolic product of the mold Aspergillus flavus (a commonly occurring contaminant of groundnuts and other foodstuffs), was tested using the Egyptian toad (Bufo regularis). Injecting the toads with aflatoxin-B1 at a dose level of 0.01 mg/50 g body wt in 1 ml corn oil once a week for 15 weeks induced hepatocellular carcinomas in 19% of the experimental toads. Four toads developed tumors in the kidney due to metastases from the primary hepatocellular carcinomas.

Aflatoxin B1↗

PubMedDate not supplied

Determination of aflatoxin B1 in medical herbs: interlaboratory study.

A method was developed for the determination of aflatoxin B1 in medical herbs (senna pods, botanical name Cassia angustifolia; devil's claw, botanical name Harpagophytum procumbens; and ginger roots, botanical name Zingiber officinale). The method, which was tested in a mini-collaborative study by 4 laboratories, is based on an immunoaffinity cleanup followed by reversed-phase high-performance liquid chromatography separation and fluorescence detection after post-column derivatization. It allows the quantitation of aflatoxin B1 at levels lower than 2 ng/g. A second extractant (acetone-water) was tested and compared to the proposed methanol-water extractant. Several post-column derivatization options (electrochemically generated bromine, photochemical reaction, and chemical bromination) as well as different integration modes (height versus area) were also investigated. No differences were found depending on the choice of derivatization system or the signal integration mode used. The method was tested for 3 different matrixes: senna pods, ginger root, and devil's claw. Performance characteristics were established from the results of the study and resulted in HorRat values ranging from 0.12 to 0.75 with mean recoveries from 78 to 91% for the extraction with methanol-water and HorRat values ranging from 0.10-1.03 with mean recoveries from 98 to 103% for the extraction with acetone-water. As a result, the method, with all tested variations, was found to be fit-for-purpose for the determination of aflatoxin B1 in medical herbs at levels of 1 microg/kg and above.

Aflatoxin B1↗

PubMed1980

In vitro effects of aflatoxin B1 on the activities of three hydrolases.

The in vitro effects of aflatoxin B1 on the activities of trypsin, amylase and lipase in the pancreatic extract of male albino Wistar rats have been studied. Activities of the 3 hydrolases were inhibited at 1 microgram/ml, 200 microgram/ml and 400 microgram/ml concentrations of aflatoxin B1, with the exception that at the 1 microgram/ml concentration the activity of lipase was stimulated. Lineweaver-Burk reciprocal plots indicate non-competitive inhibition of the 3 hydrolases.

Aflatoxin B1↗

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 in common Egyptian foods.

Samples of common Egyptian foods (17 nuts and seeds, 10 spices, 31 herbs and medicinal plants, 12 dried vegetables, and 28 cereal grains) were collected from markets in Cairo and Giza. A portion of each sample was extracted with chloroform, and the concentrated extract was cleaned by passing through a silica gel column. Aflatoxin B1 was determined by reversed-phase liquid chromatography with UV detection. The highest prevalence of aflatoxin B1 was in nuts and seeds (82%), followed by spices (40%), herbs and medicinal plants (29%), dried vegetables (25%), and cereal grains (21%). The highest mean concentration of aflatoxin B1 was in herb and medicinal plants (49 ppb), followed by cereals (36 ppb), spices (25 ppb), nuts and seeds (24 ppb), and dried vegetables (20 ppb). Among nuts and seeds, the prevalence of aflatoxin B1 was highest (100%) in watermelon seeds, inshell peanuts, and unshelled peanuts. The lowest prevalence and concentrations were in hommos (garbanzo beans). The highest concentrations of aflatoxin B1 were detected in foods that had no potential for field contamination but required drying during processing and storage, such as pomegranate peel, watermelon seeds, and molokhia.

Aflatoxin B1↗

PubMed1982

Binding of aflatoxin B1, G1 and M to plasma albumin.

The aflatoxins B1, G1 and their metabolites exist in the systemic blood as protein conjugate. This conjugation is specific to plasma albumin and proceeds enzymatically by liver and kidney cells. The aflatoxin-albumin conjugate is permanent and the conjugation is an irreversible one. This may interpret the acute liver damage of animal ingested a single dose of aflatoxin (3,4). The existence of bound aflatoxin-albumin in the systematic blood could be considered as one factor of low excretions of aflatoxins and their metabolites in urine (5,6,7).

Aflatoxin B1↗

PubMed1993

A comparison of the effects of aflatoxin B1 on the livers of rats and duck hepatitis B virus-infected and noninfected ducks.

A need exists for an appropriate animal model for the involvement of both hepatitis B virus infection and ingestion of aflatoxins in the etiology of liver cancer. Duck hepatitis B virus-infected ducks, on the basis of hepatoma development in the wild in China, appear to offer this possibility. The duck has been reexamined as a model system, and key metabolic processes have been assayed in comparison with the rat model for hepatocarcinogenesis. Aflatoxin B1 was found to be more actively metabolized by hepatic microsomes isolated from Pekin ducks in vitro to the aflatoxin B1-8,9-epoxide than corresponding fractions from the rat, and in vivo, higher levels of aflatoxin B1-guanine adduct were formed in hepatic DNA than in the livers of the aflatoxin B1-sensitive F344 rat. Repair of this DNA lesion in the duck and the subsequent formation of the ring-opened aflatoxin B1-FAPy adduct paralleled that in the rat. No effect of duck hepatitis B virus infection was found on any of these biochemical processes. The formation of hepatic lesions was also studied, and lesions were compared with those seen in the aflatoxin B1-treated rat. Histological analysis of necropsy specimens from ducks, 20 mo after the ducks received doses of aflatoxin B1 (25 and 50 micrograms/kg body wt), showed almost complete regression of the early acute lesions, with no evidence of neoplasia. Male F344 rats treated with aflatoxin B1 150 micrograms/kg 5 days/wk for 4 wk had extensive bile duct hyperplasia at the end of the treatment period and 100% incidence of hepatocellular carcinoma after 52 wk. The possible basis for the relative sensitivity of ducks and rats to the carcinogenic action of aflatoxin B1 is discussed.

Aflatoxin B1↗

PubMed1988

In vitro effect of aflatoxin B1 on the transcriptional activity of DNA template, chromatin and soluble DNA-dependent RNA polymerases in buffalo liver.

The effect of aflatoxin B1 on the DNA template and DNA-dependent RNA polymerases in buffalo liver was studied. Aflatoxin B1 inhibited both Mg2+- and Mn2+-activated RNA polymerases in a dose-dependent manner. At 10 micrograms the inhibition of both enzymes was almost complete. The inhibitory effect on the solubilized enzymes was higher than the chromatin-bound, suggesting a direct effect at the enzyme level. On the other hand, incubating DNA or deoxyribonucleoprotein (DNP) with 2 micrograms aflatoxin reduces its transcriptional capacity with a greater effect on the Mg2+-activated RNA polymerase than the Mn2+-activated enzyme. These results suggest that aflatoxin B1 inhibits in vitro transcription in buffalo liver at both enzyme and template levels.

Aflatoxin B1↗

PubMed1988

Differences in response of glucuronide and glutathione conjugating enzymes to aflatoxin B1 and N-acetylaminofluorene in underfed rats.

Changes in the hepatic drug/xenobiotic-metabolizing enzymes in underfed rats exposed to aflatoxin B1 and N-acetylaminofluorene were investigated. Neither carcinogen, fed at the level of 10 micrograms and 0.667 mg per 100 g body weight, respectively, over a period of 3 wk, had any significant influence on cytochrome P-450 and aryl hydrocarbon hydroxylase in the undernourished rats. Significantly low activities of UDP-glucuronyltransferase and glutathione S-transferase were observed in food-restricted animals fed on aflatoxin B1. N-acetylaminofluorene, on the other hand stimulated both the enzyme activities in the underfed group, to as much observed in the respective well-fed treated group. UDP-Glucuronyltransferase and glutathione S-transferase in undernutrition seem to respond differently to aflatoxin B1 and N-acetylaminofluorene. Further studies are needed to assess the possible consequences of such alterations.

2-Acetylaminofluorene↗

PubMed1983

Hematological toxicology following embryonic exposure to aflatoxin-B1.

The influence of embryonic exposure to aflatoxin-B1 (AF-B1) upon the erythroid system of the maturing chicken was examined using a variety of assays. Since the chick embryo is known to possess mixed-function oxidase activity, this animal serves as an excellent model system for studies of human fetal toxicology. AF-B1 (0.1 microgram) was administered to either 6- or 12-day embryos by the air sac method. This level of AF-B1 was highly mutagenic and was found to induce an average of 10.6 sister chromatid exchanges (SCEs) per cell compared with 1.8 SCEs per cell for the acetone control solvent. Despite selection against treated embryos through acute and chronic embryonic toxicity, hatched chicks from AF-B1 treatment groups exhibited erythroid anemia when compared to the acetone controls. Cell count, hematocrit, and hemoglobin concentration were all significantly reduced in the 12-day AF-B1 treatment groups compared with controls. Both sexes were equally affected. While the number of peripheral erythrocytes was reduced following exposure to AF-B1, the differentiation status of erythrocytes was apparently unaltered. Mean cell volume, percentage of circulating reticulocytes, and incidence of an erythroid differentiation marker, chicken fetal antigen, were parameters in which no treatment effects were observed. An apparent maturation effect was noted since adult hematocrits were similar between control and treatment groups. Possible explanations for this age effect are discussed. The ability to detect significant posthatch erythroid toxicity following embryonic exposure to mutagenic levels of AF-B1 suggests the importance of this general approach to perinatal carcinogenic evaluation.

Aflatoxin B1↗

PubMed1984

Effect of aflatoxin B1 on brain serotonin and catecholamines in chickens.

A single oral dose of aflatoxin B1 at 3 mg/kg body weight caused a significant increase in brain serotonin (5-HT) in 5-week-old chickens. Norepinephrine (NE) brain concentration significantly decreased, whereas the dopamine (DA) concentration remained unchanged. These results suggest that in modifying the concentrations of biogenic amines in the brain, aflatoxin B1 may affect brain function.

Aflatoxin B1↗

PubMed1990

Linear dose-response relationship for DNA adducts in rat liver from chronic exposure to aflatoxin B1.

Male F-344 rats were given [3H]aflatoxin B1 (AFB1) in the drinking water at three exposure levels (0.02, 0.6, 20 micrograms/l, resulting in average dose levels of 2.2, 73, 2110 ng/kg per day). After 4, 6 and 8 weeks, DNA was isolated from the livers and analyzed for aflatoxin-DNA adducts. The level of DNA adducts did not increase significantly after 4 weeks, indicating that a steady-state for adduct formation and removal had nearly been reached. At 8 weeks, the adduct levels were 0.91, 32 and 850 nucleotide-aflatoxin adducts per 10(9) nucleotides, i.e. clearly proportional to the dose. At the high dose level, a near 50% tumor incidence would be expected in a 2-year bioassay with F-344 rats while the low dose used is within the range of estimated human dietary exposures to aflatoxin in Western countries. The proportionality seen between exposure and steady-state DNA adduct level is discussed with respect to a linear extrapolation of the tumor risk to low dose.

Administration, Oral↗

PubMed2000

[Study on the combined toxicity of aflatoxin B1 and deoxynivalenol].

The toxicity of aflatoxin B1(AFB1) and deoxynivalenol(DON) on the injury and repair of DNA was studied. Replicative DNA synthesis was used to detect the change of DNA synthesis in the primary rat hepatocytes at the S phase of cell cycle. The results showed that both AFB1 and DON could induce DNA synthesis in primary rat hepatocytes at the S phase of cell cycle, and an interaction between them was found. It suggested that AFB1 and DON produced marked effects on engendering tumor as genetoxic and nongenotoxic carcinogens complementarily.

Aflatoxin B1↗

PubMed1982

Rise of hepatic glutathione concentration induced in rats by chronic lead nitrate treatment. Its role in aflatoxin B1 intoxication.

Liver concentration of the reduced form of glutathione is increased by chronic lead nitrate administration. Hepatic glutathione content is lowered by acute aflatoxin B1 intoxication while in lead-pretreated rats this decrement is not evident. The administration of lead nitrate which increases liver glutathione also decreases acute aflatoxin B1 toxicity. This provides additional evidence that, in the liver, glutathione concentration plays a role in controlling acute aflatoxin B1 toxicity.

Aflatoxin B1↗