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PubMed1982

Development of Aspergillus parasiticus and formation of aflatoxin B1 under the influence of conidiogenesis affecting compounds.

The influence of various inhibitors of hyphal growth, sporulation and biosynthesis of aflatoxin B1 in Aspergillus parasiticus NRRL2999 was studied. 6-Thioguanine, DL-ethionine, fluoroacetic acid and phenylboric acid, inhibitors of maturation of fungal conidiophores and of conidiogenesis, were added at various concentrations to malt extract agar. Lower concentrations of 6-thioguanine and DL-ethionine did not inhibit the growth of hyphae and the sporulation. Phenylboric acid reduced conidiogenesis more than hyphal growth. The yields of aflatoxin B1 were significantly reduced. Additions of fluoroacetic acid did not greatly affect the growth of hyphae but totally inhibited the production of conidia and concurrently significantly reduced the formation of aflatoxin B1. An interrelation between conidiogenesis and onset of secondary metabolism in A. parasiticus is evident.

Aflatoxin B1↗
PubMed1999

Alterations of phosphatidylinositol signal transduction pathway in hepatic mitochondria following aflatoxin B1 administration.

A single dose of aflatoxin B1 (7 mg/kg body wt) to male rats significantly stimulated the turnover of mitochondrial phosphoinositides 1-7 hr following its administration. The elevation of phosphatidylinositol 3,4,5-trisphosphate was most pronounced whose level continued to be moderately high even at 17 hr period. The level of diacylglycerol showed a marked increase from 4 hr till 7 hr after carcinogen treatment, whereas that of inositol 1,4,5-trisphosphate recorded an increase with a maximum at 7 hr followed by a gradual decrease to near normal level at 24 hr period. The activation of phosphatidylinositol cycle together with an activation of PI 3-kinase, whose product PIP3 is known to be involved in apoptosis might contribute to the early step in the manifestation of toxicity and/or carcinogenicity.

Aflatoxin B1↗
PubMedDate not supplied

Interaction of aflatoxin B1 with bacterial DNA: possible relationship to bacteriophage induction in lysogenic Bacillus megaterium.

Studies were conducted to determine possible interactions between aflatoxin B1 and deoxyribonucleic acid (DNA) and induction of bacteriophage formation in lysogenic Bacillus megaterium NRRL-B-3695. At pH 7.4, the spectrophotometric characteristics of B1 with various concentrations of calf thymus DNA were altered with both a hypochromic shift and a shift of the wavelength for maximum absorbance of the toxin. Aflatoxin B1 apparently interacted with DNA as indicated by spectrophotometric analysis and ultrafiltration studies. Under alkaline conditions (pH 10.0), spectrophotometric characteristics of this interaction were altered from those observed at pH 7.4. Toxin incubated at pH 7.4 could induce bacteriophage formation but failed to do so at pH 10. Preincubation of toxin with calf thymus DNA did not block subsequent induction. It is proposed that a bacterial DNA-toxin interaction, involving an alkaline-labile bond of aflatoxin B1, is necessary to cause induction of bacteriophage formation in lysogenic B. megaterium.

Aflatoxin B1↗
PubMed1978

This layer chromatographic determination of aflatoxin B1 in corn silage.

A procedure is described for the purification and quantitation of aflatoxin B1 in corn silage. The toxin is extracted and partially purified using parts of the AOAC minicolumn detection method. The extract is further cleaned up on a 2-step minicolumn and is then analyzed by using thin layer chromatography. Essentially all interferences are removed when the procedure is applied to moldy and non-moldy corn silage. The estimated limit of detection is 5 microgram aflatoxin B1/kg corn silage, and 73 +/- 8% of the added aflatoxin B1 (20 and 85 microgram/kg) was recovered. No aflatoxin B1 was detected in 270 samples collected from 19 silage piles in late fall 1976 and early spring 1977. This procedure also removes interferences associated with moldy corn and mixed feeds.

Aflatoxins↗
PubMedDate not supplied

Resistance of C57Bl/6 mice to immunosuppressive effects of aflatoxin B1 and relationship with neuroendocrine mechanisms.

Aflatoxin B1 (AFB1) a secondary metabolite of Aspergillus flavus and A. parasiticus, is known for its carcinogenicity and immunosuppressive effects. We previously reported on the immunosuppressive effects of AFB1 in Swiss and CD-1 mice. This study concerned the involvement of the hypothalamus-pituitary-adrenal gland axis in the immunosuppressive effects of AFB1 in C57Bl/6 mice. Animals were treated orally with 30, 150 or 750 micrograms/kg AFB1 daily for four weeks. Splenic lymphocytes were assayed to investigate their phenotyping using flow cytometry, proliferative response against mitogens and allogeneic lymphocytes, cytolytic cell activity, and IL-2 production. Antibody-mediated immunocompetence was checked using sheep red blood cell (SRBC)-challenged animals by plaque-forming cell assay and enzyme-linked immunosorbent assay. The dose of AFB1 for the immunosuppressive effects on blastogenic response, IL-2 production, and primary antibody production of splenic cells was much higher than previous studies involving other mice strains. AFB1 decreased the amount of circulating anti-SRBC antibody, and the helper-T cell and B cell populations in phenotyping splenic lymphocytes. There were no significant changes in natural killer cell activity, mixed lymphocyte response, hypothalamic biogenic amine concentrations, and corticotropin releasing factor, and of adrenocorticotropic hormone and corticosterone in plasma. Results were confirmed using adrenalectomized mice. The hypothalamic-pituitary-adrenal axis does not appear to have a major role in AFB1-induced immunotoxicity.

Aflatoxin B1↗
PubMed1996

Glutathione S-transferase-catalyzed conjugation of bioactivated aflatoxin B1 in rabbit lung and liver.

Aflatoxin B1 (AFB1) requires bioactivation to AFB1-8,9-epoxide for carcinogenicity, and glutathione S-transferase (GST)-catalyzed conjugation of activated AFB1 with glutathione (GSH) is a critical determinant of susceptibility to the mycotoxin. Incubations containing [3H]AFB1, rabbit liver microsomes, an NADPH-generating system, 1 mM GSH, and GST-containing lung or liver cytosol were performed to assess the abilities of lung and liver GSTs to conjugate AFB1-8,9-epoxide. [3H]AFB1-GSH was isolated by isocratic reverse-phase high-performance liquid chromatography (HPLC) and quantitated by liquid scintillation spectroscopy. Maximal [3H]AFB1-GSH formation rates were significantly lower for lung than for liver (0.3 +/- 0.1 and 1.7 +/- 0.4 nmol/mg/hr, respectively). Immunoprecipitation of rabbit pulmonary cytosolic GSTs with anti-alpha or anti-mu GST antisera decreased [3H]AFB1-GSH production by approximately 45 and 51%, respectively, indicating that alpha-class and mu-class GSTs are of similar importance in catalyzing this reaction in the lung. Because mu-class GSTs comprise only a small proportion of total lung GST content, these enzymes have high specific activity toward AFB1-8,9-epoxide. In contrast, the pi-class GST appeared to play a negligible role. Using a rat liver microsomal system to generate both AFB1 exo- and endoepoxide isomers, and analysis based on chiral HPLC, we found that rabbit liver cytosolic GSTs catalyzed formation of both AFB1 exo- and endo-epoxide-GSH conjugates, whereas pulmonary cytosolic GSTs catalyzed formation of only the exo stereoisomer at detectable levels. Despite a preference for conjugating the more mutagenic AFB1 exo-epoxide isomer, the relatively low capacity for GST-catalyzed detoxification of bioactivated AFB1 in lung may be an important factor in the susceptibility of the lung to AFB1 toxicity.

Aflatoxin B1↗
PubMed1992

Ultrastructural studies on interaction of infectious bursal disease virus (IBDV) and aflatoxin B1 on chick embryo fibroblast cell culture.

Light and electron microscopic evaluation of chick embryo fibroblast (CEF) cell culture inoculated with graded doses (0.25, 2.5 and 25 micrograms/ml medium) of aflatoxin B1 with and without infectious bursal disease virus (IBDV) was undertaken. The light microscopy revealed degeneration, detachment and necrosis of fibroblasts and multiple plaques formation in IBDV infected group without and with (0.25, 2.5 micrograms) aflatoxin B1. The cultures infected with virus, with or without 25 micrograms aflatoxin B1 showed complete detachment from glass surface. Electron microscopy of these cultures showed marked pyknotic or bizarre shaped nuclei, pronounced degenerative changes in the rough endoplasmic reticulum (RER), mitochondria and the presence of multiple vacuoles in the cytoplasm. The viruses were spherical, arrayed, complete, generally closer to nuclei and RER and indistinctly membrane bound. The viruses were either localised or scattered in the cytoplasm. Cultures containing 25 micrograms aflatoxin B1 without or infected with virus showed marked necrosis of cells. In latter group only a few viruses were seen either in infected cells or free in culture. Control cultures failed to show cytopathic changes as observed in the other three groups.

Aflatoxin B1↗
PubMedDate not supplied

Determination of aflatoxin B1 in baby food (infant formula) by immunoaffinity column cleanup liquid chromatography with postcolumn bromination: collaborative study.

A collaborative study was conducted to evaluate the effectiveness of an immunoaffinity column cleanup liquid chromatography (LC) method for determination of aflatoxin B, in a milk powder based infant formula at a possible future European regulatory limit (0.1 ng/g). The test portion was extracted with methanol-water (8 + 2 [v + v]), filtered, diluted with water, and applied to an immunoaffinity column. The column was washed with water to remove interfering compounds, and the purified aflatoxin B1 was eluted with methanol. The separation and determination of the aflatoxin B1 was performed by reversed-phase LC and detected by fluorescence after postcolumn derivatization (PCD) involving bromination. PCD was achieved with either pyridinum hydrobromide perbromide (PBPB) or an electrochemical (Kobra) cell by addition of bromide to the mobile phase. The baby food (infant formula) test samples, both spiked and naturally contaminated with aflatoxin B1, were sent to 14 laboratories in 13 different European countries. Test portions were spiked at levels of 0.1 and 0.2 ng/g for aflatoxin B1. Recoveries ranged from 101 to 92%. Based on results for spiked test samples (blind pairs at 2 levels) and naturally contaminated test samples (blind pairs at 3 levels), the relative standard deviation for repeatability (RSDr) ranged from 3.5 to 14%. The relative standard deviation for reproducibility (RSDR) ranged from 9 to 23%. Nine participants used PBPB derivatization, and

Aflatoxin B1↗
PubMed1979

The reduced mutagenicity of aflatoxin B1 due to hydroxylation: observations on five Salmonella typhimurium tester strains.

The mutagenicity of aflatoxin M1 relative to that of aflatoxin B1, the parent compound, was studied in 5 Ames' tester strains of Salmonella typhimurium (TA 98, TA 100, TA 1535, TA 1537, TA 1538). Aflatoxins B1 and M1 are both highly mutagenic in microsome-mediated system in TA 100. The prediction of the relative carcinogenicity of aflatoxin M1 to aflatoxin B1 posed by the mutation of TA 100 is probably more authentic than by TA 98.

Aflatoxins↗
PubMed1983

Modification of the effects of aflatoxin B1 and warfarin in young pigs given selenium.

Selenium may be related to the hepatic metabolism of the coumarin compounds aflatoxin B1 and warfarin. Selenium evidently increased the pharmacologic activity of warfarin, probably due to a displacement of warfarin from albumin by selenium, the close relationship among selenium, vitamin E, and sulphur-containing groups (eg, glutathione), or the antioxidant effect of selenium. A diet containing selenium in a concentration of 2.5 mg/kg of feed was protective against the toxic effects of both coumarins in pigs given 4 daily oral doses of 0.2 mg/kg of body weight. Selenium, as glutathione peroxidase, at least in part, protects the hepatic cells against the toxic effects of aflatoxin B1 and warfarin. The protection was demonstrated by alteration of clinical responses and hematologic (prothrombin times), electrophoretic, and clinical chemistry values. It also was demonstrated that selenium at 2.5 mg/kg of feed does not produce toxic effects; however, dietary selenium at a concentration of 5 mg/kg (and in the presence of both toxic agents) was toxic for young pigs within the 3-week experimental period. Warfarin was more active as an anticoagulant than aflatoxin B1.

Aflatoxin B1↗
PubMed1987

Appearance of enzyme activities catalyzing conversion of sterigmatocystin to aflatoxin B1 in late-growth-phase Aspergillus parasiticus cultures.

Two activities involved in terminal pathway conversion of sterigmatocystin to aflatoxin B1 were isolated from an aflatoxin-nonproducing mutant of Aspergillus parasiticus (avn-1), and the time course of appearance of the activities in culture was determined. Subcellular fractionation of fungal mycelia resolved the two activities into a postmicrosomal activity which catalyzed conversion of sterigmatocystin to O-methylsterigmatocystin and a microsomal activity which converted O-methylsterigmatocystin to aflatoxin B1. The two activities were absent in 24-h-old cells, increased to optimum levels during the stationary phase, and then declined.

Aflatoxin B1↗
PubMed1976

Formation of a derivative of aflatoxin B1 on a sephadex column with a 1% aqueous solution of methanol.

A PARTIAL SEPARATION OF AFLATOXINS B1 and B2 on a Sephadex column with a 1% aqueous solution of methanol as mobile phase was achieved. The chromatographic system is, however, not neutral for aflatoxin B1. During elution a derivative--probably aflatoxin B1 hemiacetal-is produced. The derivative forms blue fluorescent spots on Adsorbosil-1 plates with Rf 0.15 when developed in chloroform/acetone (90 + 10).

Aflatoxins↗
PubMed1990

Glucose alters rat liver S9-mediated mutagenesis, metabolism and DNA-binding of aflatoxin B1.

The administration of 30% glucose in drinking water to rats for 48 h caused a significant increase in the hepatic S9-mediated mutagenicity of aflatoxin B1, in Salmonella typhimurium TA100 and in the binding of alfatoxin B1, to calf thymus DNA in vitro. These effects correlated with a reduction in the metabolism and detoxification of aflatoxin B1, by S9 from glucose-treated rats and suggest that the oral intake of sugar may affect the hepatocarcinogenicity of aflatoxin B1.

Administration, Oral↗
PubMed2005

A cross sectional study of hepatitis B, C, some trace elements, heavy metals, aflatoxin B1 and schistosomiasis in a rural population, Egypt.

Chronic liver diseases are disastrous to health. Many factors are associated with their prevalence, hence endemicity. These are mainly infectious, parasitic and toxic. A survey was conducted in a village south to Cairo. Large industries concerned with iron and steel industry, metals smelting, cement manufacturing and electric station were located north to the village. A systematic random sample of houses was selected. All individuals inside the houses were invited to share in the study. Sample size was 84 individuals. Hepatitis markers were done (HBsAg and anti-HCV antibodies). The levels of some heavy metals were assessed; which were lead, mercury, arsenic, aluminum, manganese, nickel, chromium and cadmium. Levels of some trace elements were assessed. These were copper, iron, selenium and zinc. Aflatoxin B1 was assessed in serum. Assessment of schistosomal circulating antigen and antibodies was carried out. Abdominal ultrasonograghy was done to assess liver condition. Univariate logistic regression analysis was done to assess the association between studied variables and HBsAg or anti-HCV sero-positive subjects. The association between studied variables and bilharzial or fatty liver, diagnosed by ultrasonography, were also assessed. The univariate logistic regression analysis revealed odds ratios at the following results. For HBsAg seropositive subjects, aflatoxin B1, lead, chromium and schistosomal antigen and antibodies were higher than negative ones where odds ratios were; 6.2, 1.6, 1.6, 1.6 and 1.7, respectively. None of the variables showed statistically significant difference. For anti-HCV antibodies sero-positive subjects, aflatoxin B1 and chromium had the highest odds ratios among the studied variables, (odds ratios were 2.5 and 2.4, respectively). Bilharzial liver showed higher significant positivity of anti-HCV antibodies and insignificant decreased level of zinc than negative ones (odds ratios were 7.2 and 4.5, respectively). Fatty liver cases showed higher statistically significant positivity of anti-HCV antibodies and chromium than negative ones. Odds ratios were 8.0 and 7.1, respectively. Statistically significant lower level of aflatoxin B1 was shown in fatty liver than normal liver subjects. Multivariate logistic regression analysis for fatty liver showed that only anti-HCV antibodies sero-positivity had statistically significant odds ratio in comparison to chromium level and aflatoxin B1. It is concluded that some heavy metals, and Aflatoxin B1 had a definite association with liver diseases in the area under study. Having anti-HCV antibodies had a relation with fatty liver and with bilharzial liver more than having HBsAg. It is recommended that environmental management to factories nearby the village is urgently needed to decrease exposure to heavy metals. Prevention of hepatitis infection and aflatoxin exposure through different means is also recommended, other wise health care authorities would be confronted with unusual cases of HCC in the nearby future.

Adolescent↗
PubMed1985

[Microsomal and photochemical oxidation of aflatoxin B1].

The UV irradiation (lambda = 362 nm) of aflatoxin B1 (AfB1) dissolved in water resulted in the formation of an oxidized product. The process was not inhibited by ionol, a routine inhibitor of the radical processes. The oxidized product was not found in the system where AfB1 was metabolized by the 3-methylcholanthrene-activated rat liver microsomes. It is suggested that the product is identical with 2,3-dihydrodiol of AfB1.

Aflatoxin B1↗
PubMed1982

Toxicity of aflatoxin B1 to penaeid shrimp.

Single intramuscular injections of aflatoxin B1 into the tail muscle of Penaeus stylirostris produced 24- and 96-h median lethal doses of 100.5 (78.3 to 129.0) and 49.5 (29.8 to 82.3) mg/kg, respectively. A toxicity curve showed no threshold at the levels tested. The mortality response in a feeding study with P. vannamei was not dose dependent, but tissue and organ damage were similar to that seen in injected animals.

Administration, Oral↗
PubMedDate not supplied

Sperm production rates, sperm physiology and fertility in rats chronically treated with sublethal doses of aflatoxin B1.

Rats chronically treated with sublethal doses of aflatoxin B1 suffered severe testicular degeneration and impaired spermatocytogenesis with a concomitant drop in the rate and efficiency of spermatozoal production. Although the major part of sperm maturation was disturbed, there was no noticeable reduction in the viability of spermatozoa in storage, hence a fairly high degree of fertilisation occurred. That the treatment made the uterine environment less compatible with normal foetal development was demonstrated by the smaller litter size and higher embryo mortality.

Aflatoxin B1↗
PubMed1984

Zinc, copper, manganese and iron in rat organs after the administration and withdrawal of aflatoxin B1.

The in vivo levels of zinc, copper, manganese and iron were determined in the testis, kidney and three brain regions (cerebellum, cerebrum and medulla oblongata) from rats intraperitoneally injected with 20 micrograms per kg body weight of aflatoxin B1 for 6 weeks. Similar investigations were made after a recovery period of 6 weeks. The results obtained were compared with those of pair-fed control rats. The aflatoxin B1-induced decrease in testicular zinc was not reversed after the recovery of the rats. On the contrary, the significantly increased zinc concentration in the other organs following aflatoxin B1 exposure, reverted to the control level, as judged by significant levels. Only in the kidney was there accumulation of copper, even after the cessation of aflatoxin B1 administration. The marked increase in the manganese concentration of all the organs following repeated toxin administration, persisted only in the brain regions after the recovery. Aflatoxin B1 treatment significantly decreased the iron concentration in the testis, kidney, cerebellum and cerebrum. Recovery did not alter this trend. Iron concentration in the medulla oblongata was, however, not significantly changed in the presence of aflatoxin B1. The present data suggest that the repeated administration of aflatoxin B1 to rats could result in either a permanent or temporary re-distribution of these elements in the organs examined.

Aflatoxin B1↗