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PubMed1978

Modification of DNA by aflatoxin B1 creates alkali-labile lesions in DNA at positions of guanine and adenine.

The damage to DNA by the hepatocarcinogen aflatoxin B1 was investigated. A DNA fragment of known sequence of the lactose promoter-operator region was used as a substrate for modification by aflatoxin B1. The DNA was incubated with aflatoxin B1 in crude mammalian liver extracts or with purified microsomes. Treatment of the DNA incubated in the complete system with either 1 M piperidine or 0.1 M NaOH at 90 degrees revealed alkali-labile lesions in the DNA. The exact location of the cleavage site was determined by comparison of the length of the cleavage products with the known sequence on polyacrylamide gels. The lengths of the cleavage products were the same as those produced by alkali-induced breakage of the same sequence of DNA that had been modified with dimethyl sulfate. The major cleavage products of the aflatoxin B1-modified DNA were at positions of guanine and the minor cleavage products were at positions of adenine. These studies show that modification of DNA by aflatoxin B1 creates alkali-labile sites at positions of guanine and, to a lesser extent, adenine.

Aflatoxins↗

PubMedDate not supplied

Characterization of iodine derivatives of aflatoxin B1 and G1 by thermospray mass spectrometry.

Thermospray mass spectrometry (TSMS) was used to identify the derivatives formed when iodine is reacted with aflatoxins B1 and G1 at approximately 70 degrees C to enhance fluorescence. It was found that stable derivatives were formed by addition of an iodine atom and a methoxy group across the double bond located on the furan ring of the aflatoxin B1 and G1 molecules. TSMS and TSMS/MS daughter spectra of the reaction products of aflatoxin B1 and G1 with iodine provide evidence of the addition of each moiety to produce the iodo-methoxy derivative. The addition of an iodine atom to one carbon and a methoxy group to the other carbon of the furan ring provided molecular weights of 470 and 486 for the products of aflatoxin B1 and G1, respectively.

Aflatoxin B1↗

PubMed1986

Effect of ethanol on the in vivo covalent binding and in vitro metabolism of aflatoxin B1 in rats.

The binding of [3H]aflatoxin B1 (AFB1) to the DNA, RNA and protein of liver after i.p. administration to rats with and without ethanol pretreatment was studied. The quantities of AFB1 binding to DNA and RNA were significantly increased by ethanol pretreatment but the formation of protein adducts was not affected. AFB1 metabolism by hepatic microsomes from ethanol-treated rats to aflatoxins M1 (AFM1) and Q1 (AFQ1) was increased when compared to those of control microsomes. These results suggest that an increase in AFB1 binding to liver nucleic acids and AFB1 metabolism after pretreatment of ethanol resulted from an increase in hepatic mixed-function oxidases and a possible decrease in hepatic glutathione (GSH) content which subsequently lead to an increase in hepatotoxicity of AFB1.

Administration, Oral↗

PubMed1986

Aflatoxin B1 toxicosis in dairy calves pretreated with selenium-vitamin E.

Effects of a single IM injection of selenium-vitamin E (Se-E; 5 mg of Se + 68 IU of alpha-tocopherol/60 kg of body weight) as a pretreatment 14 days before an oral dose of aflatoxin B1 (1.0 mg/kg) were studied in 24 dairy calves. Treatment groups were designated as follows: group 1 = no Se-E or aflatoxin B1 (control); group 2 = Se-E supplementation only; group 3 = aflatoxin B1 dose only; and group 4 = Se-E supplementation before aflatoxin B1 dose. Clinical signs of toxicosis in aflatoxin B1-treated calves included anorexia, ataxia, rough haircoats, increased respiration rates, dyspnea, dehydration, and nasal discharge. Packed-cell volume, RBC, WBC, and hemoglobin were increased in aflatoxin-treated calves. Significant increases in serum aspartate aminotransferase (P less than 0.05) and gamma-glutamyl-transferase (P less than 0.001) activities and prothrombin times (P less than 0.001) were observed in aflatoxin-treated calves, indicating that there was hepatic involvement. Although aflatoxin exposure caused a significant decrease in body weight (P less than 0.01) and feed intake (P less than 0.001) in treatment groups 3 and 4, Se was demonstrated to interact significantly (P less than 0.001) with aflatoxin B1 for feed intake, causing an improved feed intake in treatment group 4 calves.

Aflatoxin B1↗

PubMed1983

Errors in DNA synthesis induced by aflatoxin B1 modification of poly(dC-dG).

Aflatoxin B1 reacts with poly(dC-dG) to form guanine adducts and apurinic sites. Such modification strongly inhibits the template capacity of the polynucleotide and leads to an increase in non-complementary nucleotide incorporation. The template inhibition and induced errors are reduced by mild heat depurination which removes all 7-substituted modifications.

Aflatoxin B1↗

PubMed1976

Induction of liver tumors by aflatoxin B1 in the tree shrew (Tupaia glis), a nonhuman primate.

The epidemiological studies suggest that aflatoxins, the toxic metabolites of the ubiquitous mold Aspergillus flavus, may play a significant role in the evolution of hepatocellular carcinoma in man in certain geographic areas of the world. To ascertain their carcinogenicity in nonhuman primates, we have administered highly purified aflatoxin B1, intermittently in the diet at 2 ppm, to 10 female and 8 male tree shrews. The tree shrew (Tupaia glis) is a nonhuman primate occurring throughout Southeast Asia which can be reared easily in captivity. Of 12 animals that survived, 6 of 6 female (100%) and 3 of 6 male (50%) tree shrews developed hepatocellular carcinomas between 74 and 172 weeks after the beginning of the experiment. None of the 8 control animals developed liver cancers. The estimated total amount of aflatoxin B1 consumed by these animals ranged from 24 to 66 mg. The development of liver tumors did not follow a specific pattern; considerable variation in hepatocellular responses to aflatoxin B1 was noted in these animals. In 2 tree shrews, the liver tumors were associated with severe post necrotic scarring; in the other 7 tumor-bearing livers, only mild to moderate portal fibrosis was encountered. This individual variation in hepatocellular response and in the amount of aflatoxin B1 required to induce hepatocellular carcinomas is attributed to inherent differences in the susceptibility within a given species of outbred animals and suggests extreme caution in proposing the "permissible" or "safe" levels of contamination of carcinogens in the food-stuffs.

Aflatoxins↗

PubMedDate not supplied

Enzyme-linked immunosorbent assay for screening aflatoxin B1 in cottonseed products and mixed feed: collaborative study.

A joint AOAC/IUPAC (International Union of Pure and Applied Chemistry) interlaboratory study of an enzyme-linked immunosorbent screening assay (ELISA) for aflatoxins was conducted in laboratories in Canada, France, Japan, South Africa, Switzerland, The Netherlands, Tunisia, and the United States. Twenty-eight samples of raw and roasted peanuts, corn, whole cottonseed, cottonseed meal, ammoniated cottonseed meal, and poultry feed containing various quantities of natural aflatoxins and supplemented when appropriate with aflatoxin B1 were distributed to participating laboratories for testing. The assay is based on conjugation of pure aflatoxin B1 to an enzyme and the competition between this conjugate and (free) aflatoxins in the product for aflatoxin-specific antibodies coated onto microtiter well walls. After a wash step to remove all unbound aflatoxins, a substrate, added to each well, is catalyzed from a colorless to a green solution by any bound enzyme-conjugated aflatoxin B1 present. The intensity of the color decreases as the amount of free aflatoxin B1 in the product increases. Overall correlation was good between ELISA and thin-layer chromatographic (TLC) results for cottonseed products and mixed feed. Variable results were reported for corn and peanut product samples. Although some positive samples (greater than 15 ng/g) of cottonseed products and mixed feed were reported to contain less than 15 ng/g by visual determination, a review of data for absorbance measurements showed that the contamination level was close to the greater than or equal to 15 ng/g standard and would not have been reported as negative under routine screening.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxin B1↗

PubMed1992

Aflatoxin B1 and DNA adducts. Proposed model for surface noncovalent and covalent complexes with N(7) of guanine. II.

An alternate model for surface noncovalent and surface covalent binding of aflatoxin B1 to N(7) of guanine in DNA is proposed. This model considers the out-of-plane motions of C(8) of aflatoxin B1 in those interactions. The covalent intercalated fit of aflatoxin B1 into DNA arises from steric adjustments made by DNA at the covalent intercalation site as well as local strain in the bond angles about N(7) of guanine and C(8) of aflatoxin B1. The bond angle about N(7) deviates modestly from the sp2 value toward the sp3 value. This study suggests that the surface covalent aflatoxin B1-DNA complex serves only a minor role in aflatoxin's precarcinogenic interaction with DNA and is a likely correctable error.

Aflatoxin B1↗

PubMed1997

Aflatoxin B1 and reproduction. II. Gametoxicity in female rats.

It has been reported that aflatoxin B1 impairs the reproductive performance of female animals. The mechanism of action of this toxin on the reproductive system was investigated. Female Druckery Strain rats were administered aflatoxin B1 at doses of 7.5 and 15.0 mg/kg body weight through oral intubation for 21 days. The ovary was examined by counting superovulated oocytes and the follicles in 6 mm thick sections. Estradiol and progesterone blood levels were determined. The body and sex organ weights of rats were recorded. There were significant reductions in the number of oocytes and large follicles in a dose dependent response. The blood hormone level and body and sex organ weight were significantly disturbed. We propose that aflatoxin B1 is gametotoxic and deranges hormonal balance in affected animals.

Aflatoxin B1↗

PubMed1982

Impairment of bile secretion induced by aflatoxin B1 in the rat.

The influence of Aflatoxin B1 on bile secretion was examined in rats. The toxin was given i.p. at a dose of 100 micrograms/kg body wt. It was observed 48 h after the injection a decrease in bile acid-independent and bile acid-dependent flow. Bile acid secretion was also decreased, whereas the outputs of cholesterol and phospholipids and the cholesterol saturation index of bile were unchanged. (14C) erythritol and (14C) sucrose biliary clearances decreased in parallel to bile flow, suggesting that the decrease in bile flow was of canalicular origin and that there was not alteration in the permeability of the biliary system.

Aflatoxin B1↗

PubMed1989

[A study on primary liver cancer in tree shrews induced by human hepatitis B virus and aflatoxin B1].

Among 41 tree shrews exposed to aflatoxin B1(AFB1), 17 were experimental infected by human hepatitis B virus (HHBV) and 24 were uninfected. After 158 weeks, 9 cases (52.94%) of primary liver cancer (PLC) were found out of the 17 tree shrews infected by HHBV and only 3 cases (12.5%) developed PLC in the 24 uninfected animals. Significant difference of PLC incidence was seen between the HHBV-infected and uninfected groups (P less than 0.05). Moreover, 1/9 of the tree shrews that had been infected by HHBV but without exposure to AFB1 developed PLC at the 83rd week. No PLC was found in 6 tree shrews that had neither been infected with HHBV nor been exposed to AFB1. These results demonstrate the possible etiologic relationship between HHBV infection and PLC, and the synergistic effects of HHBV and AFB1 during PLC development.

Aflatoxin B1↗

PubMed1983

Alterations in renal function induced by aflatoxin B1 in the rat.

The effects of aflatoxin B1 (AFB1) on renal function were determined in adult male Wistar rats by in vivo and in vitro studies. In vivo studies demonstrated that AFB1 decreased glomerular filtration rate, tubular reabsorption of glucose, and tubular transport for p-amino-hippurate. Furthermore, AFB1 pretreatment increased urinary excretion of sodium and potassium and urinary gamma-glutamyl transferase content. In vitro studies showed that slices of renal cortical tissue obtained from AFB1-treated rats (100 microgram/kg) exhibited a diminished capacity to accumulate p-aminohippurate. On the other hand, total water content of tissue, amount of extracellular water, and intracellular sodium were increased. Intracellular potassium was diminished by treatment with AFB1. Although the molecular species responsible for the effects is not known, these results indicated that AFB1 is nephrotoxic in the rat following a single low dose (100 microgram/kg body wt, ip).

Aflatoxin B1↗

PubMedDate not supplied

Improved enzyme-linked immunosorbent assay for aflatoxin B1 in agricultural commodities.

An improved enzyme-linked immunosorbent assay (ELISA) for aflatoxin B1 in cornmeal and peanut butter was developed. Aflatoxin B1 in cornmeal and peanut butter samples was extracted with 70% methanol in water containing 1% dimethylformamide diluted with assay buffer to a final concentration of 7.0% methanol, and directly subjected to an ELISA procedure that took less than 1 h for quantitative analysis and less than 30 min for screening tests. Analytical recoveries for 5-100 ppb B1 added to the cornmeal and peanut butter were 91 and 95.4%, respectively. The interwell and interassay coefficient of variation was 10% or less at the 20 ppb level and above. Agreement for B1 levels in more than 30 naturally contaminated corn, mixed feed, and peanut butter samples was excellent between the ELISA data and the data obtained from different independent laboratories using TLC or other analytical methods.

Aflatoxin B1↗

PubMed1982

Cholangiocellular carcinomas induced in Syrian golden hamsters administered aflatoxin B1 in large doses.

The hepatocarcinogenicity of aflatoxin B1 (AFB1) was compared in male Syrian golden hamsters and inbred F344 rats. AFB1 was administered by gavage 5 days/week for 6 weeks at doses of 1 and 2 mg/kg body weight/day to rats and hamsters, respectively; rate did not survive beyond 3 weeks with doses of 2 mg/kg/day. After 6 weeks the animals either received no further treatment or were given 0.1% phenobarbital sodium in the drinking water. ATPase-deficient foci of hepatic parenchymal cells, neoplastic nodules, and hepatocellular carcinomas were observed in liver sections from AFB1-treated rats killed at 6, 14, or 23 weeks; they were not seen in sections from AFB1-treated hamsters killed at 6, 14, or 46 weeks. Each of the 50 AFB1-treated rats developed hepatocellular carcinomas by 46 weeks; many also had cholangiocarcinomas and mixed hepatocellular-cholangiocellular carcinomas. Hepatocellular carcinomas were found in only 2 of 49 AFB1-treated hamsters by 78 weeks. At this time cholangiocarcinomas were found in 15 hamsters, and microscopic cholangiomas were seen in all of the livers. Compared to the rat, the hamster was resistant to the hepatotoxic and hepatocellular carcinogenic effects of AFB1.

Adenoma, Bile Duct↗

PubMed1991

The in vivo disposition of aflatoxin B1 in rat liver.

The disposition of a non-toxic i.p. dose of [3H]-aflatoxin B1 (0.70 micrograms/kg) in the blood, plasma, and liver was studied in male Wistar rats. Uptake into the blood, plasma, and liver was biphasic; there was an initial rapid rise (0-2 hr) followed by a second phase (2-12 hr) of a gradual increase. Most of the radioactivity in the blood was bound noncovalently to albumin. Distribution of radioactivity in the subcellular fractions of liver showed that the microsomes exhibited the highest labeling which increased over the time course; labeling of the cytosol reached a maximum at 2 hr then decreased to a new steady state, whereas the mitochondria and nuclei reached a plateau. When the content of aflatoxin B1 in the nuclear subfractions was examined, greater than 92% of the total radioactivity was found in the deoxyribonucleoprotein fraction, and 84% of this was bound noncovalently. These results suggest that aflatoxin B1 is transported from the site of injection through the blood to the liver and its subcellular and subnuclear fractions primarily in a noncovalent form.

Aflatoxin B1↗

PubMed1984

An enzyme-linked immunosorbent procedure for assaying aflatoxin B1.

A polyclonal rabbit antibody preparation against aflatoxin B1 (AFB1), produced by immunization with a bovine serum albumin-AFB1 conjugate, has been used to develop an enzyme-linked immunosorbent assay (ELISA). AFB1-ovalbumin, obtained by reacting either AFB1-8,9-dichloride or -8,9-dibromide with ovalbumin, was used to coat each well of a polyvinyl microtitre dish. Rabbit antibody, diluted 1:100 000, was added to each well and left to attach for 90 min, then the excess was washed off with phosphate-buffered saline/Tween. Anti-rabbit IgG coupled to peroxidase was then added, left for 90 min and the excess washed away. Residual peroxidase activity was assayed using tetramethylbenzidine as substrate; the reaction was quenched at the end of the 15-min incubation period with 2 N sulfuric acid. Inhibitor studies to assay AFB1 and related compounds in urine involved prior incubation of the diluted anti-AFB1 antibody with inhibitor for 60 min at 37 degrees C, prior to dispensing into the multi-well plates. Inhibitor studies with AFB1 showed inhibition over a concentration range of 10(-1) to 10(-5) micrograms/ml. The minimum detectable concentration was approximately 10(-5) micrograms/ml (0.032 pmol/ml). Anti-AFB1 antibody was also inhibited by iro-AFB1-DNA, one of the forms of AFB1-DNA, as well as by AFB1-guanine. Undiluted urine from normal subjects inhibited antibody binding to plates; this inhibition could be prevented by either dilution or extraction procedures.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxin B1↗

PubMed2006

The protective effect of hydrated sodium calcium aluminosilicate against the adverse effects of aflatoxin B1 on D. melanogaster.

The main aim of this study was to investigate the effects of Aflatoxin B1 (AFB1) and Aflatoxin B1 + hydrated sodium calcium aluminosilicate (HSCAS) on various developmental stages of Drosophila melanogaster. Different concentrations of AFB1 and HSCAS + AFB1 were administered during the developmental periods of the fly (egg, larvae and pupae). When the F1 progeny of control and application groups were compared, AFB1 was found to extend the process of metamorphosis and decrease the total number of offspring. However, these negative effects were inhibited with HSCAS treatment at different concentrations (5.0 and 10.0 ppm). These results suggest that HSCAS could effectively inhibit AFB1-induced abnormalities in the developmental stages of D. melanogaster.

Aflatoxin B1↗

PubMed1983

Base substitution mutations induced by metabolically activated aflatoxin B1.

We have determined the base substitutions generated by metabolically activated aflatoxin B1 in the lacI gene of a uvrB- strain of Escherichia coli. By monitoring over 70 different nonsense mutation sites, we show that activated aflatoxin B1 specifically induced GxC leads to TxA transversions. One possible pathway leading to this base change involves depurination at guanine residues. We consider this mechanism of mutagenesis in the light of our other findings that the carcinogens benzo[a]pyrene diol epoxide and N-acetoxyacetylaminofluorene also specifically induce GxC leads to TxA transversions.

Aflatoxin B1↗