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PubMedDate not supplied

Oxidation of aflatoxins and sterigmatocystin by human liver microsomes: significance of aflatoxin Q1 as a detoxication product of aflatoxin B1.

Aflatoxin Q1 8,9-oxide was synthesized and found to yield lower levels of N7-guanyl adducts than obtained from aflatoxin B1 8,9-oxide when mixed with calf thymus DNA or Salmonella typhimurium TA 98 cells. However, when S. typhimurium TA 98 was treated with the (analogous) epoxides of aflatoxin B1, aflatoxin G1, aflatoxin Q1, or sterigmatocystin, the ratios of revertants to N7-guanyl DNA adducts were similar. Aflatoxin Q1 and aflatoxin B1 8,9-oxide (trapped here as the glutathione conjugate) are the major oxidative products formed from aflatoxin B1 at all substrate concentrations in human liver microsomes, and cytochrome P-450 (P-450) 3A4 appears to be the dominant enzyme involved in both oxidations, as judged by studies involving correlation of activities in different liver samples, chemical inhibition, immunoinhibition, and reconstitution with purified hepatic and yeast recombinant P-450 3A4. Aflatoxin Q1 is not appreciably oxidized in human liver microsomes and is not very genotoxic. The postulated formation of both aflatoxin Q1 and aflatoxin 8,9-oxide from aflatoxin B1 can be rationalized by a model in which P-450 3A4 binds the substrate in either of two different configurations. This is further demonstrated by the dichotomous effect of 7,8-benzoflavone--this flavone stimulates 8,9-epoxidation while inhibiting the 3 alpha-hydroxylation reaction to form aflatoxin Q1. Thus, the 3 alpha-hydroxylation of aflatoxin B1 to aflatoxin Q1 is viewed as a potentially significant detoxication pathway.

Aflatoxin B1↗

PubMed1992

Molecular dosimetry in rat urine of aflatoxin-N7-guanine and other aflatoxin metabolites by multiple monoclonal antibody affinity chromatography and immunoaffinity/high performance liquid chromatography.

The development of molecular dosimetry methods will simplify the identification of people at high risk for cancer. A combined monoclonal antibody immunoaffinity chromatography/high performance liquid chromatography method has been devised to isolate and quantify aflatoxin-DNA adducts and other metabolites in rat urine samples. We report the production of 11 different monoclonal antibodies recognizing aflatoxin B1, aflatoxin Q1, aflatoxin G1, aflatoxicol, and aflatoxin M1 and the application of these antibodies to a multiple monoclonal antibody affinity chromatography technique. Using the multiple monoclonal antibody affinity column with rat urines obtained from dosed animals, between 90 and 95% of total aflatoxin metabolites can be bound to the column and isolated. Analytical immunoaffinity chromatography/high performance liquid chromatography analysis of these isolated aflatoxins reveals that more than 55% of the aflatoxins in rat urine are aflatoxin-dihydrodiol, aflatoxin-N7-guanine, aflatoxin Q1, aflatoxin M1, aflatoxin P1, and aflatoxin B1, accounting for 1.5, 9.6, 1.8, 34.5, 8.0, and 1.0% of the total aflatoxins, respectively. Further, a perchloric acid digestion of the aflatoxin-N7-guanine peak was used to confirm its identity by its conversion to guanine. The measurement of aflatoxin-N7-guanine excretion in rat urine was examined to assess its utility as a marker of DNA adduct formation in the liver, and a dose-dependent excretion in urine was found with a correlation coefficient of 0.99. A comparison of the dose-dependent residual levels of aflatoxin binding to liver DNA with the amount of aflatoxin-N7-guanine excreted in urine showed a correlation coefficient of 0.98. Besides the nucleic acid adduct excretion data, aflatoxin M1 and aflatoxin P1 were evaluated as molecular dosimeters in the urine. Aflatoxin M1 was found to be an excellent marker, whereas no linear relationship between dose and aflatoxin P1 excretion in urine was found.

Aflatoxin B1↗

PubMedDate not supplied

Alteration of the aflatoxin cyclopentenone ring to a delta-lactone reduces intercalation with DNA and decreases formation of guanine N7 adducts by aflatoxin epoxides.

The regio- and stereospecificity exhibited by reaction of aflatoxin B1 8,9-epoxide with DNA as well as the efficiency of reaction are remarkable and suggests that a specific orientation of bound epoxide facilitates formation of the transition state leading to guanine N7 adducts. We have compared aflatoxins B1 and B2 with aflatoxins G1 and G2 as to their binding with calf thymus DNA, d(ATGCAT)2, d(GCATGC)2, and plasmid pBR322. Aflatoxins B1 and B2 contain a cyclopentenone ring fused to the lactone ring of the coumarin. They have similar DNA association constants and intercalate with B-DNA, as demonstrated by NMR analysis of association with d(ATGCAT)2 and d(GCATGC)2, alteration of pBR322 electrophoretic mobility, and flow dichroism using linearly oriented calf thymus DNA. The less planar delta-lactone ring of aflatoxins G1 and G2 reduces DNA binding affinity by approximately 1 order of magnitude. Nevertheless, binding studies with d(ATGCAT)2 and d(GCATGC)2 suggest that aflatoxins G1 and G2 also bind B-DNA by intercalation. To establish the existence of a relationship between the association of these aflatoxins with DNA and adduct formation induced by aflatoxin epoxides, we compared the yield of guanine N7 adduct from aflatoxin B1 8,9-epoxide and from aflatoxin G1 9,10-epoxide at three concentrations of calf thymus DNA. As DNA concentration is decreased, two observations are made: (1) the number of adducts formed by either aflatoxin B1 8,9-epoxide or aflatoxin G1 9,10-epoxide is reduced with a concomitant increase in formation of the respective dihydrodiols, and (2) the ratio of adducts formed by aflatoxin G1 9,10-epoxide to those formed by an equivalent concentration of aflatoxin B1 8,9-epoxide decreases.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxin B1↗

PubMedDate not supplied

Evidence for human antibodies that recognize an aflatoxin epitope in groups with high and low exposure to aflatoxins.

Antibody activity against an aflatoxin epitope has been detected in serum from individuals who live in Kenya and who experience high exposure to aflatoxin B1. The activity was higher than in Danish people. The highest antibody activity was found in individuals who were recently exposed to aflatoxin B1. The ratio between IgG and IgM activities was higher in individuals with a high antibody titer. The specificity of the antibody activity differed in the serums obtained from Danish and Kenyan persons ("Danish" and "Kenyan" serum, respectively). The activity in Danish serum was inhibited by an aflatoxin-like substance isolated from human urine, whereas aflatoxin B1 did not inhibit the activity. In contrast, the activity in Kenyan serum was not inhibited by the aflatoxin-like substances. Therefore, the presence of antibodies against aflatoxin in humans indicates exposure to aflatoxin or aflatoxin-antigenic material. However, the biological consequences of these antibodies remain unknown.

Aflatoxin B1↗

PubMed1992

Molecular dosimetry of urinary aflatoxin-N7-guanine and serum aflatoxin-albumin adducts predicts chemoprotection by 1,2-dithiole-3-thione in rats.

Hepatocellular carcinoma has one of the poorest 5 year survival rates of any human cancer. Preventive measures offer the best possibility of ameliorating this disease and chemoprotective agents are being developed for this purpose. The dithiolethiones, including oltipraz and the unsubstituted molecule 1,2-dithiole-3-thione, have been shown to be potent inhibitors of aflatoxin-induced hepatic tumorigenesis in rats. However, subsequent evaluation of dithiolethiones or other chemoprotective agents in human clinical trials will require the development of intermediate, non-invasive biomarkers to evaluate the efficacy of these interventions. In this study, levels of molecular dosimetry biomarkers for determining genotoxic damage caused by aflatoxin B1 have been measured in a chronic exposure model with male F344 rats wherein half the animals were fed a diet supplemented with 0.03% 1,2-dithiole-3-thione to lower their risk for tumors and the other half were fed unsupplemented AIN-76A diet and were at high risk for tumor development. Levels of hepatic aflatoxin-DNA adducts, serum aflatoxin-albumin adducts and excreted aflatoxin-N7-guanine adducts in urine were determined following multiple administrations of 250 micrograms aflatoxin B1/kg body wt on days 0-4 and 7-11 to assess the use of the serum and urinary biomarkers as indices of chemoprotective efficacy. In the rats fed 1,2-dithiole-3-thione, the overall diminutions in the levels of hepatic DNA adducts, urinary aflatoxin-N7-guanine and serum aflatoxin-albumin adducts over the 2 week exposure period were 76, 62 and 66% respectively. This parallelism in reductions of levels of biomarkers relative to target organ DNA adduct burden suggests that these biomarkers are predictive short-term, non-invasive measures for assessing the efficacy of chemoprotective interventions in experimental studies and can be applied to human clinical trials directed at populations at high risk for aflatoxin exposure and primary hepatocellular carcinoma.

Aflatoxin B1↗

PubMed1975

The reactivity and carcinogenicity of aflatoxin B1-2,3-dichloride, a model for the putative 2,3-oxide metabolite of aflatoxin B1.

Aflatoxin B1-2,3-dichloride (AFB1-Cl2) was synthesized as a model for the probable ultimate carcinogen, aflatoxin B1-2,3-oxide. As expected for aflatoxin B1-2,3-oxide, AFB1-Cl2 has an electrophilic carbon 2; it decomposed in water (half-life of 0.5 min in 10% dimethyl sulfoxide, pH 7.4) with the formation of 3-chloro-2,3-dihydro-2-hydroxyaflatoxin B1 and 2,3-dihydro-2,3-dihydroxyaflatoxin B1. AFB1-Cl2 formed covalent adducts with DNA and RNA with retention of one-half of the chlorine; the major products apparently contained glycosidic bonds between carbon 2 of the aflatoxin residues and nitrogen or oxygen atoms in the nucleic acids. Polyguanylic acid was the most reactive homopolymer toward AFB1-Cl2. AFB1-Cl2 was less reactive toward mononucleotides than toward polynucleotides. The major adducts formed on incubation of AFB1-Cl2 with protein contained little chlorine and could have resulted from alkylation of primary amino groups or from reactions with the hydrolysis products. Similarly, incubation of AFB1-Cl2 with amino acids apparently resulted in Schiff base formation between primary amino groups and the dialdehyde rearrangement forms of the hydrolysis products of AFB1-Cl2. AFB1-Cl2 was much more active than aflatoxin B1 in inducing sarcomas at the s.c. injection site in rats, in the initiation of papillomas on the skin of mice, and in the induction of lung tumors in mice. AFB1-Cl2 was also highly mutagenic for Salmonella typhimurium TA 98 and TA 100. Aflatoxin B1 and its 2,3,-dihydro- (aflatoxin B2), 2,3-dihydro-2-hydroxy- (aflatoxin B2a), 2,3-dihydro-2,3-dihydroxy-, and 3-chloro-2,3-dihydro-2-hydroxy- derivatives were inactive in the mutagenicity tests; and the latter four compounds were also inactive as initiators of papillomas of the skin in mice. The structures of the macromolecular adducts of AFB1-Cl2 formed in vitro, the carcinogenicity of this electrophile, and the lack of carcinogenicity of its hydrolysis products indicate that alkylation of nucleic acids is a critical reaction in tumor induction with this carcinogen and aflatoxin B1.

Aflatoxins↗

PubMedDate not supplied

Dietary intake of aflatoxins and the level of albumin-bound aflatoxin in peripheral blood in The Gambia, West Africa.

Aflatoxin is implicated as a risk factor for hepatocellular carcinoma in areas of the world with a high incidence of this tumor. The present study was designed to validate the use of aflatoxin-albumin adducts in peripheral blood as a measure of individual exposure to this carcinogen. Dietary intake of aflatoxin was measured at the individual level in 20 residents of Keneba, West Kiang, The Gambia, over a 7-day period and correlated with the level of aflatoxin bound to peripheral blood albumin at the beginning and end of the study. Complementary enzyme-linked immunosorbent assay and high-performance liquid chromatography-fluorescence techniques were used to assay the aflatoxin adducts. All subjects were exposed to aflatoxin originating from several food types, with an average daily intake of 1.4 micrograms/day. A significant correlation (r = 0.55; P = < 0.05) was observed between the dietary intake and the level of albumin-bound aflatoxin at the end of the study. In addition, a good agreement was obtained with the two analytical techniques. A comparison of matched chronic hepatitis B surface antigen carriers with noncarriers did not reveal any difference in adduct formation for a given dietary intake of aflatoxin. These studies demonstrate the validity of aflatoxin-albumin adducts as a marker of human exposure to this carcinogen.

Adolescent↗

PubMedDate not supplied

An analytical survey of aflatoxins in tissues from swine grown in regions reporting 1988 aflatoxin-contaminated corn.

A joint project was undertaken by the Food Safety and Inspection Service (FSIS) and the Agriculture Research Service branches of the U.S. Department of Agriculture to determine the presence of aflatoxins in the U.S. meat supply during a drought year. In 1988, high incidences of aflatoxins occurred in corn grown in regions of the Midwest, Southeast, and South. Six states were identified as having serious aflatoxin contamination in their corn crop: Virginia, North and South Carolina, Texas, Iowa, and Illinois. Swine liver and pillars of diaphragm (muscle) tissues were sampled by federal FSIS Inspectors in plants located in these states. A worstcase sampling plan was conducted. Samples were taken in January 1989 from hogs fed corn soon after harvest and in April 1989 from hogs fed corn originally stored and then fed in the spring. A modification of the official AOAC method for the thin-layer chromatography (TLC) determination of aflatoxins in animal tissue was used to permit quantitation by LC with fluorescence detection. The official AOAC TLC confirmation of identity method was used to confirm all positive samples with B1 concentrations greater than 0.04 ppb and M1 concentrations greater than 0.1 ppb. Sixty samples in the January group and 100 samples in the April group were assayed. Concentrations of aflatoxins B1 and M1 in the first group of pig livers ranged from 0.04 to 0.06 ppb. The identity of aflatoxin B1 was confirmed in all positive samples. Aflatoxin M1 could not be confirmed in any of the positive liver samples because the method was insufficiently sensitive for this aflatoxin.(ABSTRACT TRUNCATED AT 250 WORDS)

Aflatoxin B1↗

PubMed1990

Effects of dietary aflatoxin in aflatoxin-resistant and control lines of chickens.

The resistance to a single oral dose (12 mg of aflatoxin per kg of BW) and 4 wk of dietary aflatoxin (2.5 mg per kg of feed) were investigated in chicks selected for five generations for resistance to acute aflatoxicosis (AR) and unselected control (C) chicks. The AR chicks were more resistant to a single oral dose of aflatoxin and had significantly decreased sodium pentobarbital sleeping time compared to C chicks. Four-weeks exposure to dietary aflatoxin did not result in any significant change in BW or feed conversion ratios of chicks from either the C or AR line. However, more sensitive indicators of aflatoxicosis including plasma total protein, albumin, cholesterol concentrations, and gamma glutamyl transferase activity were significantly altered in C chicks but not in AR chicks fed aflatoxin. Percentages of liver lipid and liver hyperplasia score were also significantly altered as a result of dietary aflatoxin treatment in C but not AR chicks. These data indicate that selection-associated differences exist between the C and AR lines of chickens that convey resistance to not only a single oral dose of aflatoxin but also to a more chronic dietary exposure to aflatoxin.

Aflatoxins↗

PubMedDate not supplied

Two-dimensional chromatographic method for determination of aflatoxins in liver; occurrence of aflatoxins in animal liver.

A thin-layer chromatographic method is described for the analysis of aflatoxins in animal liver. Liver samples are extracted with chloroform and phosphoric acid. After filtration, an aliquot is evaporated and defatted by liquid-liquid partitioning. The extract is submitted to silica gel minicolumn cleanup and the final extract is concentrated and submitted to two-dimensional thin-layer chromatography (TLC). The identity of aflatoxins B1 and M1 is confirmed with trifluoroacetic acid (TFA) carried out on the thin-layer plate used for quantitation of these aflatoxins. The method permits the detection and confirmation of aflatoxins in liver in concentrations as low as 0.05 micrograms/kg. Average recoveries for aflatoxin M1 and aflatoxin B1 at spiking levels of 0.2 micrograms/kg were found to be 65% and 85%, respectively. With this method, 73 samples of bovine liver, 70 samples of porcine liver, and 56 samples of chicken liver taken from different slaughterhouses were investigated. In one sample of bovine liver, aflatoxins B1, B2, and M1 could be detected in concentrations of 0.10, 0.03, and 0.08 micrograms/kg, respectively.

Aflatoxin B1↗

PubMedDate not supplied

Occurrence of aflatoxins and aflatoxin-producing moulds in fresh and processed meat in Egypt.

A survey was carried out to detect aflatoxins and isolate aflatoxigenic moulds contaminating fresh and processed meat products. The fungal contamination was examined in 215 samples of fresh and processed meat products and 130 samples of spices used in the meat industry collected from different local companies in Cairo, Egypt. Processed meat products such as beefburger, hot-dog, kubeba, sausage, luncheon meat had the highest count of moulds as compared with fresh and canned meat. Out of 150 samples of meat products and 100 samples of spices, aflatoxin B1 was detected in five samples of beefburger, (8 micrograms/kg), four samples of black pepper (35 micrograms/kg), and four samples of white pepper (22 micrograms/kg). Aflatoxins B1 and B2 were detected in one sample of kubeba (150 micrograms B1/kg and 25 micrograms B2/kg); hot-dog (5 micrograms B1/kg and 2 micrograms B2/kg) sausage (7 micrograms B1/kg and 3 micrograms B2/kg) and luncheon meat (4 micrograms B1/kg and 2 micrograms B2/kg). Also, aflatoxins B1 and G1 were detected in two samples of turmeric (12 micrograms B1/kg and 8 micrograms G1/kg) and coriander (8 micrograms B1/kg and 2 micrograms G1/kg). Aspergillus flavus (24 isolates), and Aspergillus parasiticus (16 isolates) were the predominant aflatoxin-producing moulds isolated from both processed meat products and spices. Aflatoxins were absent in fresh meat, canned meat, salami, beefsteak and minced meat. The contamination of processed meat with aflatoxin was shown to correlate with the addition of spices to fresh meat.

Aflatoxin B1↗

PubMed1991

Determination of exposure to aflatoxins among Danish workers in animal-feed production through the analysis of aflatoxin B1 adducts to serum albumin.

Aflatoxin B1 is suspected as an etiologic factor in the increased risk for primary liver cancer among workers in animal-feed processing plants in Denmark. Aflatoxin bound to serum albumin was therefore measured for feed-processing workers. Blood samples were collected immediately after vacation and after four weeks of work, and aflatoxin was quantified by competitive enzyme-linked immunosorbant assay. Seven of 45 individuals with an estimated exposure of 64 ng aflatoxin B1.d-1.kg-1 body weight were positive. Three positive workers had been unloading a cargo with an aflatoxin B1 level of 26 micrograms.kg-1 raw material. The exposure level correlated well with the job titles. Dust samples collected at different sites showed considerable variation in the amount of aflatoxin B1 (nondetectable to 8 micrograms.kg-1 dust). The exposure to aflatoxin B1 may only partially explain the increased risk of liver cancer.

Adult↗

PubMed1975

Screening method for the detection of aflatoxins in mixed feeds and other agricultural commodities with subsequent confirmation and quantitative measurement of aflatoxins in positive samples.

The method described will detect total aflatoxins (B1, B2, G1, and G2) in mixed feeds, grains nuts, and fruit products in samples containing as little as 5-15 mug/kg. In addition, the presence of aflatoxins in the positive samples can be confirmed and the toxins can be quantitatively measured, using the same extract as that used for the screening method. In the screening method, aflatoxins are extracted with acetone-water (85+15), and interferences are removed by adding cupric carbonate and ferric chloride gel. The aflatoxins are extracted from the aqueous phase with chloroform and the chloroform extract is washed with a basic aqueous solution. A Velasco-type minicolumn is used to further purify the extract and capture the aflatoxins in a tight band. The screening method has been successfully applied to 24 different agricultural commodities. Quantitative thin layer chromatography was also performed with extracts of each of these commodities. An average recovery of 94% B1, 108% B2, 130% G1, and 103% G2 was obtained compared to the official final action AOAC method for cottonseed products, 26.048-26.056. Within-laboratory coefficients of variation of 10-15% were obtained for each of the aflatoxins and total aflatoxins in a sample of peanut meal naturally contaminated with 11 mug B1+3 mug B2+11 mug G1+5 mug G2/kg.

Aflatoxins↗

PubMed1992

Aflatoxins in cosmetics containing substrates for aflatoxin-producing fungi.

29 random samples of eight different products of skin cleansing creams or powders and skin peeling products (including practically all products of this type available on the German market), containing substrates for aflatoxin-producing fungi or plant parts directly connected with such substrates, such as almond bran, peach bran, apricot seeds, wheat bran, horse chestnut and cob were analysed for aflatoxin B1, B2, G1 and G2. In 11 (38%) of the samples aflatoxins were not detectable ( < 0.1 micrograms/kg); 18 (62%) of the samples contained from 0.4 to 78.5 micrograms aflatoxin/kg. The majority of the positive samples contained all four types of aflatoxin. Aflatoxins can be absorbed through the skin. To what extent this happens with these products and the resulting toxicological significance is difficult to estimate. Nevertheless, potent carcinogens such as aflatoxins should be completely absent from cosmetics; this can be achieved by careful quality control of the raw materials.

Aflatoxins↗

PubMed1990

Effects of phenobarbital and beta-naphthoflavone on the in vivo toxicity and in vitro metabolism of aflatoxin in an aflatoxin-resistant and control line of chickens.

The in vivo toxicity of aflatoxin and the in vitro microsomal metabolism of aflatoxin B1 (AFB1) were investigated in a population of chickens previously selected for resistance to aflatoxin (AR line) and a corresponding control population (NS line) after in vivo pretreatment with saline, sodium phenobarbital (PB), or beta-naphthoflavone (BNF) solutions. PB pretreatment increased survival and BNF pretreatment increased mortality in both the NS and AR lines when a single oral dose of aflatoxin was administered. The rate of in vitro metabolism of AFB1 was greater with microsomes from saline pretreated AR chicks than with microsomes from similarly treated NS chicks. In vivo pretreatment with PB increased AFB1 metabolism by NS and AR microsomes. After BNF pretreatment of vivo, AR microsomes metabolized more AFB1 than NS microsomes, and there was a dramatic decrease in AFB1 metabolism in NS microsomes. AFB1-dihydrodiol was the major metabolite produced by both lines, with aflatoxin M1 and aflatoxin Q1 recovered in small quantities from BNF-pretreated AR microsomal incubations only. These data indicate that increased in vivo resistance of the AR line to acute aflatoxicosis may be related to increased hepatic AFB1 metabolism and that genetic selection has resulted in altered in vitro quantitative and qualitative metabolism of AFB1 in the AR line.

Aflatoxins↗

PubMed1979

Metabolism of aflatoxin B1 and identification of the major aflatoxin B1-DNA adducts formed in cultured human bronchus and colon.

Aflatoxin B1 and benzo(a)pyrene were activated by both cultured human bronchus and human colon as measured by binding to cellular DNA and protein. The binding of aflatoxin B1 to DNA was dose dependent, and the level of binding was higher in cultured human bronchus than it was in the colon. When compared to aflatoxin B1, the binding level of benzo(a)pyrene to both bronchial and colonic DNA was generally higher. The major adducts formed in both tissues by the interaction of aflatoxin B1 and DNA were chromatographically identical to 2,3-dihydro-2-(N7-guanyl)-3-hydroxyaflatoxin B1 (Structure 1) with the guanyl group and hydroxy group in trans-position and an adduct which has been tentatively identified by other investigators as 2,3-dihydro-2-(N5-formyl-2',5',6'-triamino-4'-oxo-N5-pyrimidyl)-3-hydroxyaflatoxin B1 (Structure 11). Seventy % of the radioactivity associated with bronchial DNA was found in these two peaks, and the ratio of radioactivity between the peaks was nearly 1. In colonic DNA, the ratio between Structures 1 and 11 was approximately 2. These observations add aflatoxin B1 to the list of chemical procarcinogens metabolized by cultured human tissues and in which the carcinogen-DNA adducts are similar to the adducts formed in animal tissue susceptible to the carcinogenic action of aflatoxin B1.

Aflatoxins↗

PubMed1990

Risk assessment for aflatoxin: I. Metabolism of aflatoxin B1 by different species.

A comparison of the generation and detoxification of reactive aflatoxin B1 metabolites in different species may elucidate why animal species vary widely in sensitivity to aflatoxin B1 carcinogenicity, in addition to offering some perspective on how sensitive man may be to the carcinogenic effects of this mycotoxin. Scientific literature comparing the ability of cellular fractions from different species to metabolize aflatoxin B1 is reviewed. However, in vitro studies exclude components for multiple metabolic pathways, eliminating the possibility of competition between metabolic activation and detoxification. Quantification of metabolic activation by different species from these studies is therefore limited. The species-specific carcinogenic potency of aflatoxin B1 may be reflected in levels of aflatoxin B1-DNA adducts generated in vivo. The current paucity of quantitative information on human DNA adduct levels does not permit comparisons between different species on this basis.

Aflatoxins↗

PubMed1975

[Spectrophotometric investigations on aflatoxin B1 and aflatoxin G1 (author's transl)].

UV-spectrophotometric and fluorescence-spectrophotometric investigations have been performed on the aflatoxins B1 and G1 with the aim of their unequivocal identification and quantitative estimation in the routine examination. The lower limits of the quantitative and semiquantitative estimations have been found to be 0,4 ng (thin layer chromatography, semiquantitative), Imug/ml (UV-spectroscopy) and 10 ng/ml (fluorescence spectroscopy) for the aflatoxin B1 and 0,3 ng (TLC, semiquantitative), 1 mug/ml (UV-spectroscopy) and 1 ng/ml (fluorescence spectroscopy). Quinine sulfate in 0.1 n sulfuric acid was successfully utilized as a convenient standard substance for quantitative fluorescence spectroscopic estimations of the aflatoxins B1 and G1. In an extensive series of estimations the fluorescence intensity of aflatoxin B1 in chloroform in the range of 0,01-10 mug/ml has been compared with that of equally concentrated solutions of quinine sulfate in sulfuric acid. The ratio of the intensities was 0.5 : 1(0.509 : 1). Similar comparative estimations of aflatoxin G1 in chloroform in the range of 0.001 bis 1 mug/ml and quinine sulfate in sulfuric acid resulted in a ratio of 5 : 1 (4.99 : 1). These ratios have been found using a fluorescence spectrophotometer Beckman SF 1078.

Aflatoxins↗