Excretion of Fumonisin B1, Hydrolyzed Fumonisin B1, and the Fumonisin B1−Fructose Adduct in Rats

The excretion of fumonisin B1 (FB1), hydrolyzed FB1 (HFB1), and FB1−fructose addition products (FB1−fructose) was determined in male Fisher 344/NHsd rats. Rats were dosed by gavage with 0.69, 6.93, or 69.3 μmol/kg of body weight FB1, HFB1, or FB1−fructose. Excretion of unchanged FB1, HFB1, and HFB1 after hydrolysis was determined in urine and feces by analytical reverse phase HPLC and fluorometric detection of the o-phthaldialdehyde derivatives. Average total FB1 backbone excretion in feces was 101, 76, and 50% of the dose for FB1, HFB1, and FB1−fructose, respectively. No effect of dose level was found on the percentage of the dose excreted as total FB1 after hydrolysis. FB1−fructose appears to be absorbed to the highest extent, followed by HFB1. FB1 appears to be excreted nearly completely in the feces. The greater absorption of HFB1 may explain the greater toxicity of HFB1 compared to FB1 on a molar basis. However, the detoxification of FB1 by formation of the fructose adduct cannot be explained by reduced absorption. Average total FB1 backbone excretion in urine was 2.7, 5.0, and 5.3% of the dose for FB1, HFB1, or FB1−fructose, respectively

L’imprimé et l’artiste : édition, ex-libris, affiches et revues au temps de l’Art nouveau à Strasbourg

Il faut attendre les années 1890 pour que le paysage artistique alsacien, meurtri par le conflit de 1870, amorce son renouvellement générationnel et s’engage dans les courants modernistes de la fin du siècle qui animent les capitales européennes. Cette génération s’épanouit dans un contexte favorable à plusieurs titres. D’une part les autorités allemandes, désireuses de développer les arts décoratifs mais aussi, à travers ceux-ci, d’en diffuser un modèle germanique, créent la « Kunstgewerbesc..

Characterization of Fumonisin B1-GlucoseReaction Kinetics and Products

The reaction of fumonisin B1 with the reducing sugar D-glucose can block the primary amine group of fumonisin B1 and may detoxify this mycotoxin. A method to separate hundred milligram quantities of fumonisin B1-glucose reaction products from the excess D-glucose with a reversed-phase C18 cartridge was developed. Mass spectrometry revealed that there were four primary products in this chain reaction when fumonisin B1 was heated with D-glucose at 65 C for 48 h: N-methyl-fumonisin B1, N-carboxymethyl-fumonisin B1, N-(3-hydroxyacetonyl)-fumonisin B1, and N-(2-hydroxy, 2-car- boxyethyl)-fumonisin B1. The N-(1-deoxy-D-fructos-1-yl) fumonisin B1 (fumonisin B1-glucose Schiff’s base) was detected by mass spectrometry when fumonisin B1 was heated with D-glucose at 60 C. The nonenzymatic browning reaction of fumonisin B1 with excess D-glucose followed apparent first- order kinetics. The activation energy, Ea, was 105.7 kJ/mol. Fumonisin B1 in contaminated corn could precipitate the nonenzymatic browning reaction with 0.1 M D-glucose at 60 and 8

Glucose Reaction with Fumonisin B1 Partially Reduces Its Toxicity in Swine

Acute and subacute intraperitoneal doses of fumonisin B1 (FB1) were administered to test the efficacy of the FB1-glucose reaction products in detoxifying FB1 in swine. In the acute study at 11 µmol of FB1/kg of body weight, five of six pigs administered FB1 and four of six pigs administered FB1- glucose died from acute pulmonary edema. Analysis of weight gain, serum aspartate aminotransferase and γ-glutamyltransferase, total cholesterol, and pathological evaluation did not provide evidence of protection against FB1 toxicity by the FB1-glucose reaction products. In the subacute study at 5.5 µmol of FB1/kg of body weight, one pig administered FB1 died from liver damage. Analysis of serum aspartate aminotransferase, γ-glutamyltransferase, and total bilirubin showed protection against FB1 toxicity by the FB1-glucose reaction products. The levels of sphinganine and sphinganine/sphingosine ratios in serum and liver as well as pathologic findings provided definitive evidence of protection against the FB1 toxic effects by this detoxification procedure (p \u3c 0.05)

Inhibition of lentivirus replication by aqueous extracts of Prunella vulgaris

<p>Abstract</p> <p>Background</p> <p>Various members of the mint family have been used historically in Chinese and Native American medicine. Many of these same family members, including <it>Prunella vulgaris</it>, have been reported to have anti-viral activities. To further characterize the anti-lentiviral activities of <it>P. vulgaris</it>, water and ethanol extractions were tested for their ability to inhibit equine infectious anemia virus (EIAV) replication.</p> <p>Results</p> <p>Aqueous extracts contained more anti-viral activity than did ethanol extracts, displaying potent anti-lentiviral activity against virus in cell lines as well as in primary cell cultures with little to no cellular cytotoxicity. Time-of-addition studies demonstrated that the extracts were effective when added during the first four h of the viral life cycle, suggesting that the botanical constituents were targeting the virion itself or early entry events. Further analysis revealed that the extracts did not destroy EIAV virion integrity, but prevented viral particles from binding to the surface of permissive cells. Modest levels of anti-EIAV activity were also detected when the cells were treated with the extracts prior to infection, indicating that anti-EIAV botanical constituents could interact with both viral particles and permissive cells to interfere with infectivity. Size fractionation of the extract demonstrated that eight of the nine fractions generated from aqueous extracts displayed anti-viral activity. Separation of ethanol soluble and insoluble compounds in the eight active fractions revealed that ethanol-soluble constituents were responsible for the anti-viral activity in one fraction whereas ethanol-insoluble constituents were important for the anti-viral activity in two of the other fractions. In three of the five fractions that lost activity upon sub-fractionation, anti-viral activity was restored upon reconstitution of the fractions, indicating that synergistic anti-viral activity is present in several of the fractions.</p> <p>Conclusion</p> <p>Our findings indicate that multiple <it>Prunella </it>constituents have profound anti-viral activity against EIAV, providing additional evidence of the broad anti-viral abilities of these extracts. The ability of the aqueous extracts to prevent entry of viral particles into permissive cells suggests that these extracts may function as promising microbicides against lentiviruses.</p

Inhibition of HIV-1 infection by aqueous extracts of Prunella vulgaris L.

<p>Abstract</p> <p>Background</p> <p>The mint family (Lamiaceae) produces a wide variety of constituents with medicinal properties. Several family members have been reported to have antiviral activity, including lemon balm (<it>Melissa officinalis </it>L.), sage (<it>Salvia </it>spp.), peppermint (<it>Mentha </it>× <it>piperita </it>L.), hyssop (<it>Hyssopus officinalis </it>L.), basil (<it>Ocimum </it>spp.) and self-heal (<it>Prunell</it>a <it>vulgaris </it>L.). To further characterize the anti-lentiviral activities of <it>Prunella vulgaris</it>, water and ethanol extracts were tested for their ability to inhibit HIV-1 infection.</p> <p>Results</p> <p>Aqueous extracts contained more anti-viral activity than did ethanol extracts, displaying potent antiviral activity against HIV-1 at sub μg/mL concentrations with little to no cellular cytotoxicity at concentrations more than 100-fold higher. Time-of-addition studies demonstrated that aqueous extracts were effective when added during the first five hours following initiation of infection, suggesting that the botanical constituents were targeting entry events. Further analysis revealed that extracts inhibited both virus/cell interactions and post-binding events. While only 40% inhibition was maximally achieved in our virus/cell interaction studies, extract effectively blocked post-binding events at concentrations similar to those that blocked infection, suggesting that it was targeting of these latter steps that was most important for mediating inhibition of virus infectivity.</p> <p>Conclusions</p> <p>We demonstrate that aqueous <it>P. vulgaris </it>extracts inhibited HIV-1 infectivity. Our studies suggest that inhibition occurs primarily by interference of early, post-virion binding events. The ability of aqueous extracts to inhibit early events within the HIV life cycle suggests that these extracts, or purified constituents responsible for the antiviral activity, are promising microbicides and/or antivirals against HIV-1.</p