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  • 1985-1989  (2)
  • 1965-1969
  • Effects on hepatic mitochondrial function  (1)
  • Time-dependent suppression  (1)
Material
Years
  • 1985-1989  (2)
  • 1965-1969
Year
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    International journal of legal medicine 96 (1986), S. 1-10 
    ISSN: 1437-1596
    Keywords: Carbon monoxide ; Effects on hepatic mitochondrial function ; Cyanide effects on hepatic mitochondrial function ; Kohlenmonoxid, Funktionsstörung der Mitochondrien ; Zyanid, Funktionsstörungen der Mitochondrien
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine , Law
    Description / Table of Contents: Zusammenfassung Der Einfluß von Kohlenmonoxid und Blausäure auf die Funktion der Lebermitochondrien wurde untersucht. Alle Versuche wurden an Ratten in Pentobarbitalnarkose durchgeführt. Unmittelbar nachdem die Bauchhöhle der Ratten geöffnet wurde, wurden einzelne Tiere in einer Versuchskammer aus transparentem Kunststoff für 3min einem Prüfungsgas ausgesetzt. Jedes Prüfungsgas wurde in einer durch ein Plastikrohr mit der Versuchskammer verbundenen Gaskammer hergestellt. HCN wurde aus NaCN und H2SO4 hergestellt. Bei CO-Versuchen wurden verschiedene Mengen von CO in die Kammer eingeführt. Unmittelbar nach den Versuchen wurden etwa 2g Leber in situ mit einer abgekühlten Klemme gefroren. Eine Blutprobe wurde von der Wunde entnommen. Die Konzentrationen des Azetoazetats, β-Hydroxybutyrats, Adenosintriphosphats, Adenosindiphosphats und Adenosinmonophosphats der Leber wurden bestimmt, und anhand von ihren Werten wurden “redox state” (ein Verhältnis von Azetoazetats zu β-Hydroxybutyrats) und “energy charge” (ein Verhältnis von Summa von ATP und 0.5 ADP zu Summa von ATP, ADP und AMP) berechnet. In vergifteten Ratten verminderten sich “redox state” mit der zunehmenden Konzentration der Toxika im Blut. Als die HbCO-Konzentration 40% überstieg, trat eine Art Wende, bei der die Geschwindigkeit der Verminderung sich reduziert, ein. Für Zyanid war diese Wende 2.0μg/ml. Im Vergleich zu “redox state” verminderte sich “energy charge” langsamer. Aber die Geschwindigkeit der Verminderung beschleunigte sich, wenn die Blutkonzentration der Toxika eine Grenze überschritt. Die o.g. Wenden waren 40% für HbCO und 2.0μg/ml für Zyanid. In kombinierten Versuchen wurden Tiere einem Gasgemisch (CO und niederer Konzentration von HCN) ausgesetzt. Es wurde angenommen, daß es keine Wechselwirkung zwischen CO und HCN gibt.
    Notes: Summary The effects of carbon monoxide and cyanide on the hepatic redox state and energy charge were investigated. Rats were used for the experiment under pentobarbital anesthesia. Immediately after laparotomy, a rat was placed in an animal chamber made of a transparent plastic box and exposed to a test gas for 3 min. Every test gas was produced in a gas chamber connected to the animal chamber with a flexible tube. HCN was produced from NaCN and H2SO4. In the CO inhalation experiment, various amounts of CO were introduced into the gas chamber. Immediately after an exposure, about 2g liver was frozen in situ with a precooled clamp. Oozed blood from the wound surface was sampled. Concentrations of ATP, ADP, AMP, acetoacetate, and β-hydroxybutyrate in hepatic mitochondria were determined, and the redox state and the energy charge were calculated. For cyanide as well as CO, significant negative correlations were found between the concentration in the blood and the redox state. The same held true for the energy charge. The redox state showed a slight increase at low concentrations of both gases; however, thereafter it began to decrease sharply with increases in concentrations. When concentrations of the toxicant in the blood reached certain levels, a kind of turning point, beyond which the redox state does not decrease any more, was observed. It was about 40% for HbCO and about 2.0μg/ml for cyanide, and the points seemed to be related to the concentrations, beyond which cells are irreversibly damaged. On the other hand, the energy charge did not change at low concentrations. With an increase in toxicant concentrations, the energy charge decreased drastically. The rate of decrease in the energy charge became higher when blood concentrations exceeded certain levels. It was about 40% for HbCO and 2.0μg/ml for cyanide. The presence of low levels of blood cyanide did not affect the relationship between the energy charge and the HbCO concentration.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Archives of dermatological research 278 (1986), S. 329-334 
    ISSN: 1432-069X
    Keywords: Melanoma metastasis ; Interferon ; Time-dependent suppression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of murine α/β interferon (IFN) on experimental metastasis was investigated using B16-F10 melanoma cells. Since the outcome of metastasis of blood-borne tumor cells is mainly determined within the first 24 h after i.v. inoculation of tumor cells, i.p. injection of IFN was focused on this critical early phase. The inhibition of pulmonary metastases by IFN was found to be maximal when given 3 h prior to tumor cell inoculation, while mice with 24-h and 12-h pretreatment and simultaneous IFN treatment also showed a reduction in metastases, but to a lesser extent. However, mice receiving IFN 2 h after tumor cell inoculation did not show any reduction. Tumor cells cultured for 24 h in IFN-containing medium showed no reduction in metastases. Administration of anti-asialo GMl prior to IFN treatment was found to eliminate the inhibitory effect of IFN 3 h pretreatment. However, natural killer (NK) cell activity in vitro measured at 3 h, 13 h and 24 h after IFN administration was enhanced to the same extent, not paralleling the inhibitory effect on pulmonary metastases. These data indicate that prepared host status against blood-borne tumor cells is established by IFN pretreatment, being maximal when injected several hours prior to tumor cell inoculation, and that this effect is substantially dependent on NK cell activity, though the implication of other factors is not excluded.
    Type of Medium: Electronic Resource
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