Correction of mesiolinguoversion of the upper lateral incisors with lingual appliances

The genotoxic potentials of boric acid in Escherichia coli PQ37 was assessed along in the presence of aflatoxin B1 using SOS chromotest. Boric acid induced beta-galactosidase synthesis on the tester bacteria both on the presence and absence of S9 activation mixture. Therefore, the inorganic acid may not require metabolic activation to be genotoxic for this bacteria. When present together with aflatoxin B1 in the assay medium, boric acid increased the degree of beta-galactosidase synthesis induced by the maximal inducing concentration of aflatoxin B1 before the toxin's activation. However, the degree of enzyme synthesis induced was significantly decreased when boric acid was present after aflatoxin activation. This suggests that boric acid may not interfere with nor block the expoxidation of aflatoxin B1. It may however interact with the expoxide thereby inhibiting its activity. Boric acid may be a genotoxin and could possibly act as a syngenotoxic and/or a cogenotoxic agent.     

Quantitation of aflatoxin B1-N7-guanine adduct in urine by enzyme-linked immunosorbent assay coupled with immunoaffinity chromatography

A specific and sensitive method to quantitate aflatoxin B1-N7-guanine adduct in urine samples by immunoaffinity chromatography coupled with indirect competitive enzyme-linked immunosorbent assay (ELISA) is reported. A novel in vitro method to synthesize an antigen (bovine serum albumin-guanine-aflatoxin B1) and its use to produce polyclonal antibodies specific to the hapten aflatoxin B1-N7-guanine are discussed. An indirect competitive ELISA developed to quantitate aflatoxin adduct showed a 50% inhibition at 15.6 pmol aflatoxin B1-N7-guanine (y = 66.73 + (-19.8)chi; r = -0.997). Interference by aflatoxin B1 was less than 5%, and no interference by guanine, aflatoxin G1 and aflatoxin M1 was observed. An immunoaffinity column was also developed, by using these polyclonal antibodies, for single-step purification of aflatoxin B1-N7-guanine. The immunoaffinity column and the indirect competitive ELISA were evaluated and validated by quantitation of aflatoxin B1-N7-guanine in urine from rats dosed with aflatoxin B1 (1 mg/kg body weight). Spiking studies with standard aflatoxin B1-N7-guanine adduct at 2 and 4 micrograms/mL phosphate-buffered saline gave 96 and 100% recoveries, respectively, for immunoaffinity cleanup column. The method also was tested successfully for quantitating aflatoxin B1-N7-guanine adduct in spiked human urine. Recoveries of the adduct were 79-90%.     

The anticarcinogen 3,3'-diindolylmethane is an inhibitor of cytochrome P-450

Dietary indole-3-carbinol inhibits carcinogenesis in rodents and trout. Several mechanisms of inhibition may exist. We reported previously that 3,3'-diindolylmethane, an in vivo derivative of indole-3-carbinol, is a potent noncompetitive inhibitor of trout cytochrome P450 (CYP) 1A-dependent ethoxyresorufin O-deethylase with Ki values in the low micromolar range. We now report a similar potent inhibition by 3,3'-diindolylmethane of rat and human CYP1A1, human CYP1A2, and rat CYP2B1 using various CYP-specific or preferential activity assays. 3,3'-Diindolylmethane also inhibited in vitro CYP-mediated metabolism of the ubiquitous food contaminant and potent hepatocarcinogen, aflatoxin B1. There was no inhibition of cytochrome c reductase. In addition, we found 3,3'-diindolylmethane to be a substrate for rat hepatic microsomal monooxygenase(s) and tentatively identified a monohydroxylated metabolite. These observations indicate that 3,3'-diindolylmethane can inhibit the catalytic activities of a range of CYP isoforms from lower and higher vertebrates in vitro. This broadly based inhibition of CYP-mediated activation of procarcinogens may be an indole-3-carbinol anticarcinogenic mechanism applicable to all species, including humans.     

The effect of 9-beta-D-arabinofuranosyl-2-fluoroadenine and 1-beta-D-arabinofuranosylcytosine on the cell cycle phase distribution, topoisomerase II level, mitoxantrone cytotoxicity, and DNA strand break production in K562 human leukemia cells

The UvrA and UvrB proteins form part of the UvrABc endonuclease, which is responsible for nucleotide excision repair in Escherichia coli. Using a mobility shift gel assay we have studied the binding of UvrA dimer, UvrB monomer and UvA(2)B trimer complexes with 40, 50 and 136 bp (32)P-end-labelled DNA fragments adducted with aflatoxin B(1). UvrA was shown to re-associate with adduct specific UvrB: DNA complexes, a phenomenon which could be reversed by the addition of 500 mM potassium chloride or anti-UvrA anti-sera. Re-association was shown to be UvrA concentration dependent. Re-association of UvrA(2)B to the UvrB:DNA complex was not seen. We have also shown that the UvrB:DNA complex, in the case of aflatoxin B(1), is extremely stable with a half-life excess of 400 min and that fragment termini are not a specific substrate for UvrA binding.     

Transvaginal ultrasonography of female urethral carcinoma treated with radiation therapy: report of two cases

Rats were given aflatoxin B1 (7.5 microg/200 g b.w.) and alpha-tocopherol (0.9 mg/200 g b.w.) for 14 days oral intubation to investigate the effect of alpha-tocopherol on the toxicity of aflatoxin B1 on rat's testes. There were significant alterations in testicular sorbitol dehydrogenase, lactic dehydrogenase, glucose-6-phosphate dehydrogenase, gamma glutamyl transpeptidase; reduced quality of sperm and marked pathological changes in the testis of rats given aflatoxin B1 alone. Alpha-tocopherol supplementation increased the aflatoxin blood level. A reduction in the toxicity of free radicals by alpha-tocopherol in association with a reduction in aflatoxin metabolism seem to be responsible for the protective influence observed.     

Comparison of three methods for determining aflatoxins in melon seeds

The suitability of 3 methods for determining aflatoxins in melon seeds was examined. The first 2 are the Contaminants Branch (CB) method and the Best Foods (BF) method, both official methods for determining aflatoxins in peanuts and peanut products. The third method, the modified CB method-Rapid Modification of the Cottonseed (CB-RCS-Mod) method, devised in this work, was derived by combining steps from the CB method and the Rapid Modification of the Cottonseed method. The CB method was superior to the other 2 methods for quantitation of aflatoxins. It gave better recoveries and cleaner extracts that exhibit less fluorescent interference for thin-layer chromatography (TLC) than the BF method. Also, its solvent efficiency was better than that of the CB-RCS-Mod method. With the CB method, recoveries from spiked samples were 85.0% for aflatoxin B1 and 90.0% for aflatoxin B2. Recoveries of G aflatoxins were more variable, averaging 90.0% for aflatoxin G1 and 72.5% for aflatoxin G2. Total aflatoxin recovery was 86.5% for the CB method. At a low aflatoxin contamination level (8 micrograms B1/kg sample), aflatoxin B1 was detectable by the CB method but not by the BF method. Detection of aflatoxins in BF method sample extracts by TLC was not improved by the use of chloroform-acetone-water (88 + 12 + 1), benzene-ethanol-water, or ether-methanol-water (96 + 3 + 1) in place of the standard chloroform-acetone (88 + 12) developer. Use of ether-methanol-water (96 + 3 + 1) for detecting aflatoxins by TLC in the CB method extracts increased interference compared with the standard chloroform-acetone (88 + 12) developer.     

Down-regulation of human FEN-1 gene expression during differentiation of promyelocytic leukemia cells

The presence of aflatoxin in corn and corn dust during relatively normal years and the increased risk of Aspergillus flavus infestation during drought conditions suggest that airborne agricultural exposures should be of considerable concern. Liquid extraction, thin layer chromatography, and high pressure liquid chromatography were used for the analysis of aflatoxin B1 in grain dust and bulk corn samples. A total of 24 samples of airborne dust were collected from 8 farms during harvest, 22 samples from 9 farms during animal feeding, and 14 sets of Andersen samples from 11 farms during bin cleaning. A total of 14 samples of settled dust and 18 samples of bulk corn were also collected and analyzed. The airborne concentration of aflatoxin B1 found in dust collected during harvest and grain unloading ranged from 0.04 to 92 ng/m3. Higher levels of aflatoxin B1 were found in the airborne dust samples collected from enclosed animal feeding buildings (5-421 ng/m3) and during bin cleaning (124-4849 ng/m3). Aflatoxin B1 up to 5100 ng/g were detected in settled dust collected from an enclosed animal feeding building; however, no apparent correlation was found between the airborne concentration of aflatoxin B1 and its concentration in settled dust or bulk corn. The data demonstrate that farmers and farm workers may be exposed to potentially hazardous concentrations of aflatoxin B1, particularly during bin cleaning and animal feeding in enclosed buildings.     

Measurement of intrahepatic shunted blood flow by ethanol-1-14C method as compared with D-galactose-1-14C method

The interaction of aflatoxin B1 with a number of biologically important substances has been investigated by spectrophotometric and fluorimetric techniques. The ultra-violet absorption of tryptophan, adenosine, RNA and DNA were altered by the addition of aflatoxin B1. Some amino-acids, purine and pyrimidine derivatives, bovine-serum albumin and DNA quenched the fluorescence of aflatoxin B1. Fluorescence polarization data suggested that the interaction of aflatoxin B1 with bovine-serum albumin was stronger than that with DNA.     

Aflatoxin and p53 abnormality in duck hepatocellular carcinoma

Recent studies have revealed that a point mutation at codon 249 in the p53 gene predominates in hepatocellular carcinoma (HCC) cases from Southern Africa and China, where infection with hepatitis B virus (HBV) and contamination of aflatoxin B1 in food are risk factors for HCC. This unique mutation from G to T at the third base in codon 249 observed in human HCC cases is suggested to be linked to aflatoxin exposure. Six ducks with HCC, five of which were fed a diet containing aflatoxin B1 for 1-2 years, were analysed for the presence of point mutations at this codon of the p53 gene by polymerase chain reaction and direct nucleotide sequencing. None of the six ducks with HCC showed the change at this codon regardless of duck hepatitis B virus infection. This suggests that aflatoxin B1 itself might not be involved in the unique mutation at codon 249 in hepatocarcinogenesis, or that other factors coincident with aflatoxin may be responsible for this unique mutation.     

Synthesis and characterization of aflatoxin B1 mercapturic acids and their identification in rat urine

Biologic effects of the hepatocarcinogenic mycotoxin aflatoxin B1 are principally induced by one of its metabolites, the exo-aflatoxin B1 epoxide which produces both DNA and protein adducts in vivo. Detoxication of the exo-aflatoxin B1 epoxide can be mediated in part by glutathione S-transferases whose induction could be important in chemoprotection interventions. Thus, biomarkers of the enzymatic conjugation of exo-aflatoxin B1 epoxide with glutathione may be important indices of protection against the toxic effects of this agent. Since glutathione conjugates undergo further metabolic processing in vivo to yield mercapturic acids, increased urinary excretion of exo-aflatoxin B1 mercapturate could be expected during chemoprotection intervention. To determine if this mercapturic acid could be used as a biomarker, techniques for its specific measurement were developed using monoclonal antibody immunoaffinity chromatography and reverse phase high-performance liquid chromatography with ultraviolet absorbance and mass spectral detection. First, a synthetic exo-aflatoxin B1 mercapturate was characterized using mass spectrometry, ultraviolet absorbance, circular dichroism spectrometry, and chemical derivatization. In vivo metabolite characterization was then facilitated by comparison with the synthetically prepared exo-aflatoxin B1 mercapturate and both aflatoxin B1-glutathione conjugate diastereoisomers. In rats, 1% of the aflatoxin dose was excreted as exo-aflatoxin B1 mercapturate within 24 h. The finding that exo-aflatoxin B1 mercapturate was excreted in urine in a dose-dependent manner provides the basis for investigating its applicability as a biomarker of glutathione S-transferase status in aflatoxin chemoprotection studies.     

Immunochemical approaches to AGE-structures: characterization of anti-AGE antibodies

An extractionless method for determining aflatoxin M1 (AFM1), a major metabolite of aflatoxin B1 (AFB1), in human urine was developed. The biological fluid is injected directly into the chromatographic system after simple dilution and centrifugation. A pre-column, packed with a cation-exchange phase and coupled on-line to a column-switching liquid chromatography (LC) system, is used for sample pre-treatment and concentration. The analytes are non-selectively desorbed with the LC eluent and cleaned by means of a column-switching procedure. Pre-treatment and analysis were performed within 40 min. Average AFMI recovery reached 97% in the 10-100 ng/l range of urine. The detection limit of AFM1 in urine and milk was 2.5 ng/l for 1 ml of injected sample. A comparison with an immunoaffinity column clean-up and LC method was performed. The method was applied to determine AFM1 in the urine of AFB1 gavaged rats, and in the urine of both potentially exposed and supposedly unexposed workers. The method was also extended to milk.     

Evaluation of maxillofacial vascular abnormalities with Tc-99m RBC

Cassava bread was prepared by pre-gelling, battering and baking cassava flour to which were added, in moderate amounts, sugar, yeast solution and edible oil. Baking was at 215 degrees C for 40 min. No mould was isolated from the cassava bread and the mean value of aflatoxin B1 (AFB1) for the three subsamples of cassava bread was 0.03 microgram/kg. The cassava tuber (Manihot esculenta Crantz), which was used for the production of cassava bread had an initial AFB1 level of 1.91 micrograms/kg and the dominant mycoflora were Penicillium oxalicum, Aspergillus flavus, Fusarium spp and some unidentified fungi.     

Iodine-123 labelled nor-beta-CIT binds to the serotonin transporter in vivo as assessed by biodistribution studies in rats

Flavobacterium aurantiacum NRRL B-184 possesses the ability to degrade aflatoxin B1 in solution and in several food items. Aflatoxin B1 is a potent carcinogen that causes significant economic losses to the agricultural and food industry. The role of trace metal ions (Cu2+, Mn2+, Zn2+, and Co2+) were studied in an effort to understand the enzymatic system involved in aflatoxin B1 degradation by F aurantiacum. The effect of divalent chelators (EDTA and 1,10-phenanthroline [OPT]) in the presence of the trace metal ions was studied as well. Aflatoxin B1 (10 microg/ml) was added to 72-h cultures of F aurantiacum that had been washed and resuspended in phosphate buffer (pH 7.0). HPLC was used to determine aflatoxin B1 concentration in these cultures. Incubating cells at 30 degrees C with 1 and 10 mM Cu2+, Mn2+, and Zn2+ significantly decreased aflatoxin B degradation after 4 and 24 h (P < 0.05). Decreased degradation was also observed with 1 and 10 mM Cu2+ and Zn2+ after 48 h and with 0.1 mM Cu2+ after 24 and 48 h. Co2+ did not have a significant effect on aflatoxin B1 degradation. EDTA and OPT did not counter the inhibition in the presence of Cu2+. The addition of 1 mM EDTA countered the inhibition by 1 mM Mn2+ after 4 and 24 h, but 1 mM OPT did not counter the inhibition by 10 mM Mn2+ after 4 and 24 h. OPT countered the inhibition by 1 mM Zn2+ after 4 and 48 h. These trace elements inhibit aflatoxin B1 degradation by F aurantiacum. In addition, their presence necessitates higher concentrations (>1 mM) of EDTA and OPT for the removal of their inhibitory effect.     

Stimulation of beta-adrenoceptors inhibits endotoxin-induced IL-12 production in normal and IL-10 deficient mice

The influence of water activity (a(w)) on the kinetics of aflatoxin and zearalenone production in amaranth grains at 25 degrees C was studied. Minimum a(w) for aflatoxin production in this substrate was 0.825. Accumulation of the four aflatoxins (B1, B2, G1 and G2) was similar at a(w) 0.825 (maximum 81.2 microg/kg after 42 days) and 0.868 (maximum 109.6 microg/kg after 49 days). Maximum accumulation of total aflatoxins at a(w) 0.902 (260.4 microg/kg) was detected after 21 days, with an appreciable increment in the concentration of aflatoxins B1 and G1. These quantities were lower than those reported for aflatoxin production on other cereals and legumes, indicating that amaranth is not a good substrate for aflatoxin production. Zearalenone was not detected at a(w) 0.902. Maximum accumulation of zearalenone was 1.5 microg/g after 35 days at a(w) 0.925 and 11.1 microg/g after 49 days at a(w) 0.950.     

A two-year prospective study of the effect of ursodeoxycholic acid on urinary bile acid excretion and liver morphology in cystic fibrosis-associated liver disease

Mice constitutively express glutathione S-transferase mGSTA3-3 in liver. This isoform possesses uniquely high conjugating activity toward aflatoxin B1-8,9-epoxide (AFBO), thereby protecting mice from aflatoxin B1-induced hepatocarcinogenicity. In contrast, rats constitutively express a closely related GST isoenzyme, rGSTA3-3, with low AFBO activity and, therefore, are sensitive to aflatoxin B1 exposure. Although the two GSTs share 86% sequence identity and have similar catalytic activities toward 1-chloro-2,4-dinitrobenzene (CDNB), they have an approximately 1000-fold difference in catalytic activity toward AFBO. To identify amino acids that confer high activity toward AFBO, non-conserved rGSTA3-3 residues were replaced with mGSTA3-3 residues in two regions believed to form the substrate binding site. Twenty-one mutant rGSTA3-3 enzymes were generated by site-directed mutagenesis using combinations of nine different residues. Except for the E208D mutant, single mutations of rGSTA3-3 produced enzymes with no detectable AFBO activity. Generally, AFBO conjugation activity increased in additive fashion as mGSTA3-3 residues were introduced into the rGSTA3-3 enzyme with the six site mutant E104I/H108Y/Y111H/L207F/E208D/V217K displaying the highest AFBO activity (40 nmol/mg/min) of all the mutant enzymes. When this mutant enzyme was further modified by three additional substitutions (D103E/I105M/V106I) AFBO conjugation activity decreased 14-fold to 2. 8 nmol/mg/min. Although wild-type mGSTA3-3 AFBO conjugation activity (265 nmol/mg/min) could not be obtained by our rGSTA3-3 mutants, we were able to identify six mGSTA3-3 residues; Ile104, Tyr108, His111, Phe207, Asp208, and Lys217 that, when collectively substituted into rGSTA3-3, substantially increased (>200-fold) glutathione conjugation activity toward AFBO.     

Pleiotropic and differential phenotypic expression of two sn (snowflake) mutant alleles of Neurospora crassa: analysis in homokaryotic and heterokaryotic cells

The effects of N-benzylimidazole (BI) on mutagenic activation of six groups of carcinogens were studied with the Ames liquid incubation assay. Intragastric (i.g.) treatment of male Wistar rats for 3 days with BI produced an over 3-fold induction of hepatic microsomal cytochrome P-450 (CYP). The mutagenic activities of five N-nitrosamines on S. typhimurium TA100 and two arylamines on TA98 were induced up to 5 times above controls and much higher inductions on strain TA98 were observed with aflatoxin B1, two polycyclic hydrocarbons, two aminoazo compounds and six amino acid pyrolysates, which are all known to be metabolically activated by CYP I and/or II species. Compared with the reported results for rats treated with polychlorobiphenyls (PCB), the numbers of revertant colonies were the same or higher (0.7-1.8-fold), indicating that BI and PCB show a similar pattern of induction of CYP-dependent properties. However, intraperitoneally treated liver S9 was inferior to the i.g. treated S9 for all the mutagenic activations of 18 carcinogens. In conclusion, these results demonstrate the use of BI for metabolic induction to be an effective alternative for induction with either PCB or a combination of phenobarbital and beta-naphthoflavone.     

Transient intervention with oltipraz protects against aflatoxin-induced hepatic tumorigenesis

Oltipraz [5-(2-pyrazinyl)-4-methyl-1,2-dithiole-3-thione] protects against aflatoxin B1-induced hepatocarcinogenesis in rats when fed before and during carcinogen exposure; however, such an exposure-chemoprotection intervention paradigm is not directly relevant to most human populations. To model and assess the possible efficacy of short term interventions targeted at individuals at risk for sustained exposure to aflatoxins, 175-g male F344 rats were treated daily with 25 micrograms of aflatoxin B1, p.o., for 28 days. One week after the start of aflatoxin B1 exposure, half of the animals were fed a diet supplemented with 0.075% oltipraz for 10 days; these rats were then restored to the unsupplemented AIN-76A diet for the remainder of the experimental period. Livers were analyzed 2 or 3 months after the last aflatoxin B1 dose for burden of glutathione S-transferase P (GST-P)-positive foci, as an index of presumptive preneoplastic tumors. The transient intervention with oltipraz reduced the volume percent of hepatic GST-P-positive foci by 54% (P = 0.047) and 72% (P = 0.004) at 2 and 3 months, respectively. A strong positive correlation was also observed between the extent of fibrosis in the livers of these animals and the hepatic burden of GST-P-positive foci, implying that cytotoxicity is associated with the tumorigenic process. This protection may reflect alterations in the metabolism and disposition of aflatoxin B1 induced by oltipraz. Glutathione S-transferase catalyze the detoxication of aflatoxin-8,9-oxide and were found to be rapidly induced in the livers of animals after the beginning of the oltipraz intervention. Glutathione S-transferase activity remained significantly (P < 0.05) higher until 9 days after the end of the oltipraz intervention. In contrast, levels of hepatic aflatoxin-DNA adducts were not significantly reduced until 4 days after the beginning of the intervention but remained significantly (P < 0.05) lower up to 11 days after the end of the intervention. The cumulative reduction in levels of hepatic aflatoxin-DNA adducts (approximately 25%) by the oltipraz intervention underestimated the reduction in the hepatic burden of GST-P-positive foci. The significant protection against presumptive preneoplastic tumors, despite the delay of intervention, suggests that oltipraz may exert substantial activity against the cytotoxic and autopromoting action of repeated exposures to aflatoxin B1 and supports the utility of intervention trials with oltipraz in individuals chronically consuming aflatoxin B1-contaminated foods, particularly in regions with high incidences of liver cancer.     

Enzymatic deconjugation of erythrocyte polyglutamyl folates during preparation for folate assay: investigation with reversed-phase liquid chromatography

Erythrocyte (RBC) folates occur mainly as 5-methyltetrahydrofolate polyglutamates. Determination of RBC folate concentration requires an initial deconjugation of these polyglutamates. In this study, existing HPLC methods were adapted to investigate the rate and extent of this deconjugation process. The action of endogenous plasma pteroyl-polyglutamate hydrolase activity was strongly affected by the conditions of sample preparation, with pH of the incubation mixture more critical to effective deconjugation than incubation time. Dilution of whole blood with 10 g/L ascorbic acid yielded fast hydrolysis of long-chain polyglutamates, and total conversion to 5-methyltetrahydrofolate monoglutamate occurred after 90 min of incubation at 37 degrees C. In contrast, dilution of whole blood with 10 g/L sodium ascorbate, with up to 90 min of incubation at 37 degrees C, yielded a mixture of polyglutamates of 5-methyltetrahydrofolate (glun = 1-8). As documented by direct HPLC analysis and in concurrent assays with Lactobacillus casei, acidification provided by ascorbic acid can have dramatic effects on the measurement of RBC folates.     

Direct synthesis of aflatoxin B1-N7 guanine adduct: a reference standard for biological monitoring of dietary aflatoxin exposure in molecular epidemiological studies

Aflatoxin B1-N7-guanine and aflatoxin B1-human serum albumin adducts have been established as biomarkers of dietary aflatoxin exposure in epidemiological studies. Earlier chemical oxidants were used to synthesize aflatoxin B1-8,9-epoxide in vitro and its subsequent interaction with DNA or synthetic oligodeoxynucleotide was used as a source of authentic aflatoxin B1-N7-guanine adduct. In the present communication we report a simple single step procedure for the synthesis of aflatoxin B1-N7-guanine adduct using free guanine and m-chloroperbenzoic acid as the chemical oxidant for the production of AFB1-8,9-epoxide. At a molar ratio of 1:1 of AFB1-8,9-epoxide and guanine the recovery of the AFB1-N7-guanine adduct was found to be 60% while at higher molar ratios (1:2 and 1:4) of guanine the recovery of the AFB1-N7-guanine adduct was found to be low (30-40%). HPLC analysis of the AFB1-N7 guanine adduct showed a retention time identical with the retention time of the AFB1-N7-guanine adduct synthesized using calf thymus DNA. TLC-fluorodensitometric analysis indicated that the Rf of the AFB1-N7-guanine adduct was zero. Spectral analysis of the adduct synthesized showed an excitation wavelength of 360 nm and emission wavelength at 440 nm in phosphate buffer (100 mM, pH 7.4). Further, the formation of the AFB1-N7-guanine adduct was confirmed by perchloric acid treatment resulting in the destruction of the adduct. The AFB1-N7-guanine adduct thus synthesized was stable in both acidic as well as lyophilized conditions over a period of 2 weeks. The antibody capture assay showed that the antibodies produced against the antigen BSA-guanine-N7-AFB1 also cross-reacted with calf thymus DNA-AFB1 adduct, indicating specificity to the guanine-N7-AFB1 moiety. The method developed may find immediate application as a source of authentic reference standard in molecular epidemiological studies.     

Buttockectomy as a limbsaving procedure for locally advanced soft tissue sarcoma of the buttock region

Cord blood was obtained from 164 neonates at birth and investigated for the presence of aflatoxins. 14 of the samples were neonates without jaundice and 150 from neonates with jaundice. There was significant reduction (P > 0.05) in birth weight of jaundiced neonates with aflatoxin. Neonates with jaundice have high mean concentration of aflatoxin B1 (32.3 ng/ml and 35.6 ng/ml). Aflatoxin G1 was not detected in any of the groups. The rate of detection was higher in wet (81.8%) than dry season (50.0%). These findings show that neonates are exposed to aflatoxin prenatally and that high incidence of jaundice occurred in the wet warm months.