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  • 1
    Electronic Resource
    Electronic Resource
    Die gewebsverteilung von 1,2-14c-vinylchlorid bei der ratte (1977)
    Springer
    International archives of occupational and environmental health 39 (1977), S. 27-32 
    Details
    ISSN: 1432-1246
    Keywords: Vinyl chloride ; Distribution in organs ; Inhibiton of vinyl chloride metabolism ; Vinylchlorid ; Gewebsverteilung ; Inhibition des Vinylchlorid-Stoffwechsels
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Wird Vinylchlorid aus der Atmosphere eingeatmet, so stellt sich ein Gleichgewicht zwischen dem Vinylchlorid in der Luft und dem Organismus ein. In erster Linie reichert sich nicht metabolisiertes Vinylchlorid im Fettgewebe an. Für dieses Verteilungsverhalten dürfte die Lipophilie des Vinylchlorid Ausschlag gebend sein. Das Konzentrationsverhältnis von Vinylchlorid in einzelnen Organen bleibt über den gesamten untersuchten Konzentrationsbereich von 25 his 10.000 ppm Vinylchlorid in der Expositionsatmosphäre konstant. Aus dem Gleichgewicht wird Vinylchlorid dem Metabolismus zugeführt. Metabolite reichern sich, im Gegensatz zum unveränderten Vinylchlorid, vor allem in Leber und Niere an.
    Notes: Summary Rats have been pretieatet with 6-nitro-1.2.3-benzothiadiazole which completely blocks metabolism of vinyl chloride. If the animals are exposed to atmospheric vinyl chloride, formation of an equilibrium between the compound in the gas phase and in the animal's orgnism is observed. Unmetabolized vinyl chloride is concentrated in adipose tissue. The distribution pattern of vinyl chloride in different organs of the rat is constant over the concentration range of 25–10,000 ppm of vinyl chloride in the exposure atmosphere. Distribution of metabolites of vinyl chloride contrasts to that of the original compound; metabolites primarily are concentrated in liver and in kidneys.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00381548
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  • 2
    Electronic Resource
    Electronic Resource
    The significance of covalent binding of catechols to proteins in vivo (1977)
    Springer
    Archives of toxicology 39 (1977), S. 31-39 
    Details
    ISSN: 1432-0738
    Keywords: Catechols ; Isoproterenol ; Ethinyloestradiol ; Covalent protein binding ; Reactive metabolites ; Rat liver microsomes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Wenn Ratten mit 14 μg/kg 3H-Isoproterenol behandelt wurden, konnte bis 48 h danach in der Leber 3H-Radioaktivität gemessen werden. Diese Menge war nicht unterschiedlich in Lebern von Tieren, welche mit Diäthylmaleat vorbehandelt waren. Nach erschöpfender Extraktion konnte eine beträchtliche Menge an 3H-Radioaktivität aus Isoproterenol in den Proteinen von Gesamtleber (Homogenat), Cytosol und von Mikrosomen gefunden werden. In der Cytosolfraktion von Diäthylmaleat vorbehandelten Tieren wurde die zweifache Menge von Isoproterenol-Radioaktivität in den extrahierten Proteinen gefunden, im Vergleich zu Kontrollen. In der mikrosomalen Fraktion gab es keinen Unterschied bei der Radioaktivitätsmenge, die in Proteine eingebaut war. In allen Fraktionen nahm die Radioaktivität, die in den extrahierten Proteinen meßbar war, mit einer Halbwertszeit von etwa 24 h ab. Die in vivo-Ergebnisse über kovalente Proteinbindung von Isoproterenol werden verglichen mit der irreversiblen Proteinbindung von Äthinylöstradiol in vivo. Quantitativ werden diese in vivo-Befunde mit den Resultaten zur irreversiblen Proteinbindung verglichen, die während Inkubationen von Isoproterenol oder Äthinylöstradiol mit Rattenlebermikrosomen erhalten wurden.
    Notes: Abstract When rats were dosed with 14 μg/kg 3H-isoproterenol, 3H-radioactivity was measurable in the liver until 48 h. This amount was not different in livers of animals which have been pretreated with diethyl maleate. After exhaustive extraction, a significant amount of 3H-radioactivity from isoproterenol could be detected in the proteins of total liver (homogenate), of cytosol and of microsomes. In the cytosol fraction of diethyl maleate pretreated animals twice the amount of isoproterenol-radioactivity was found in the extracted proteins compared to controls. In the microsomal fraction there was no difference between diethyl maleate pretreated and control animals in the amount of radioactivity incorporated into proteins. In all fractions the radioactivity measurable in the extracted proteins declined with a half life time of about 24 h. The in vivo results on covalent binding of isoproterenol are compared to the irreversible protein binding of ethinyloestradiol in vivo. Quantitatively, these in vivo data are compared to the results on irreversible protein binding obtained during incubations of isoproterenol or ethinyloestradiol with rat liver microsomes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00343273
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  • 3
    Electronic Resource
    Electronic Resource
    Disposition of [1,2-14C] vinyl chloride in the rat (1976)
    Springer
    Archives of toxicology 35 (1976), S. 153-162 
    Details
    ISSN: 1432-0738
    Keywords: Vinylchloride ; 3-Bromophenyl-4(5)-imidazole ; 6-Nitro-1,2,3-benzothiadiazole ; Inhibition of vinyl chloride metabolism ; Induction of vinyl chloride metabolism ; Vinylchlorid ; 3-Bromphenyl-4(5)-imidazol ; 6-Nitro-1,2,3-benzothiadiazol ; Induktion des Vinylchlorid-Stoffwechsels ; Hemmung des Vinylchlorid-Stoffwechsels
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung In einem geschlossenen System wurden Ratten initialen Konzentrationen an [1,2-14C] Vinylchlorid von unter 100 ppm ausgesetzt. Bei einer Besetzung des Systems durch 3 Ratten wurde in der Atmosphäre eine Halbwertszeit des gasförmigen Vinylchlorid von 1,13 ± 0,12 Std gemessen. Bei einem Volumen des Systems von 10,3 l ergab die Berechnung der Vinylchlorid Clearance, daß nur ca. 40% des von den Ratten eingeatmeten Vinylchlorid resorbiert wurde. Aus diesem Grunde führten Änderungen der Atemtätigkeit nicht zu Änderungen der Aufnahmegeschwindigkeit von Vinylchlorid. Durch sehr wirksame Inhibitoren von Cytochrom-P-450-abhängigen mikrosomalen Oxidationen (3-Bromphenyl-4(5)-imidazol und 6-Nitro-1,2,3-benzothiadiazol) konnte die Aufnahme von Vinylchlorid vollständig verhindert werden. SKF 525 A und 5,6-Dimethyl-1,2,3-benzothiadiazol waren in dieser Hinsicht weit weniger wirksam. Durch Vorbehandlung der Ratten mit DDT und, zum geringeren Maße, mit Clotrimazol wurde die Aufnahme von Vinylchlorid gesteigert. Keine signifikante Steigerung trat auf nach Vorbehandlung mit Phenobarbital, 3-Methylcholanthren, Rifampicin und nach chronischer Alkoholgabe. Unmittelbar nach Beendigung der Exposition wurden die höchsten Radioaktivitätswerte in Leber und Niere festgestellt. Die Metabolite von 14C-Vinylchlorid wurden sehr schnell ausgeschieden. Bereits nach 24 Std wurden im Urin 69,4±2,6% der inkorporierten Radioaktivität gemessen.
    Notes: Abstract Rats were exposed to [1,2-14C] vinyl chloride in a closed system at initial concentrations below 100 ppm. When the system was occupied by 3 rats, a half-life of vinyl chloride in the system's atmosphere of 1.13 ± 0.12 h was observed. The volume of the system was 10.3 l. Calculation of the clearance of vinyl chloride from the system revealed that about 40% of inspired vinyl chloride is absorbed by lung. Therefore, changes in respiration did not influence uptake of vinyl chloride. Uptake of vinyl chloride by the rats was completely blocked by acute pretreatment with potent inhibitors of cytochrome-P-450-dependent microsomal drug metabolism (i.e., by 35 mg/kg 3-bromophenyl-4(5)-imidazole or 50 mg/kg 6-nitro-1,2,3-benzothiadiazole in 0.6 ml/kg DMSO). A weaker inhibition was observed after dosing SKF 525 A or 5,6-dimethyl-1,2,3-benzothiadiazole (50 mg/kg in 0.6 ml/kg DMSO). Metyrapone did not cause inhibition. Uptake of vinyl chloride was increased by pretreatment with DDT and, to a lesser extent, with clotrimazol. No significant stimulation of uptake was observed after pretreatment with phenobarbital, 3-methylcholanthrene, rifampicin, or chronic ethanol treatment. Immediately after exposure, highest radioactivity levels were observed in liver and kidney. The radioactive metabolites of 14C-vinyl chloride were rapidly excreted, largely by the kidneys. Excretion of radioactivity in the urine was 69.4 ± 2.6% within 24 h.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00293562
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  • 4
    Electronic Resource
    Electronic Resource
    Molecular aspects of catechol and pyrogallol inhibition of liver microsomal lipid peroxidation stimulated by ferrous ion-ADP-complexes or by carbon tetrachloride (1977)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 300 (1977), S. 179-187 
    Details
    ISSN: 1432-1912
    Keywords: Catechols ; Pyrogallols ; Lipid peroxidation ; Liver microsomes ; Carbon tetrachloride
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Lipid peroxidation was induced in rat liver microsomes either by iron-ADP-complexes or by carbon tetrachloride in the presence of NADPH. Different compounds containing catechol or pyrogallol structures were examined for their activities to inhibit lipid peroxidation in both systems. In general, all compounds tested showed similar inhibitory activities on lipid peroxidation, if induced by ferrous ion-ADP-complexes or by carbon tetrachloride. This inhibition is explained by the suggestion that catechols and pyrogallos inhibit at the lipid site of the membrane, rather than at the enzymic site. Compounds not containing catechol or pyrogallol groups inhibited lipid peroxidation only weakly. O-Methylation resulted in a decrease of the inhibitory effect. Catecholor pyrogallol-derivatives which contained polar functional side chains, like carboxyl- or amino groups showed minor inhibitory effects compared to the esterified or N-alkylated compounds. Dihydroxychlorpromazine, 2-hydroxy-estradiol and 2-hydroxyethinylestradiol were the most effective inhbitors of microsomal lipid peroxidation (I50-values of 1×10−6 to 2×10−7 M). The inhibitory activity of α-tocopherol, glutathione and ascorbic acid, naturally occurring antioxidants, was about three orders of magnitude lower. Inhibition of lipid peroxidation induced by NADPH-cytochrome c reductase and iron-ADP-complexes in the presence of NADPH and liposomes was also observed with catechols. From our results we assume that the molecular structure of a catechol or pyrogallol functional group is a prequisite for an effective inhibition of lipid peroxidation by these chemicals. Furthermore, the results are discussed in relation to the requisite membrane affinity of catechols, pyrogallols and other antioxidants which might be used for inhibition studies on lipid peroxidation in vivo.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00505049
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