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  • hepatocyte cultures  (2)
  • lipopolysaccharide  (2)
  • 1
    Electronic Resource
    Electronic Resource
    Involvement of cytochrome b5 in the cytotoxic response to Escherichia coli Lipopolysaccharide (1989)
    Springer
    Molecular and cellular biochemistry 87 (1989), S. 79-84 
    Details
    ISSN: 1573-4919
    Keywords: endotoxins ; cytochrome b5 ; cytochrome P450 ; hepatocyte cultures ; detoxification
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Cytotoxic lesions, induced by Gram-negative lipopolysaccharides (LPS), occur mainly in liver where the microsomal compartment of hepatocytes is involved in the detoxification mechanisms as well as in the biosynthesis of different active metabolites. The alterations induced by LPS from E. coli 0111: 134 on cytochrome b5 and its correlation with cytochrome P450, have been studied using an in vivo reversible endotoxic shock model and 24 h non-replicative hepatocyte monolayers. Results show that cytochrome b5 is directly affected by LPS that induces also a membrane damage with an active release of lactate dehydrogenase (LDH). The increase of cytochrome b5 levels may enhance the efficiency of the electron transport, thus facilitating the cytochrome P450-associate oxidations and reactions involved in the repair mechanisms of membranes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00421085
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  • 2
    Electronic Resource
    Electronic Resource
    Effect of Escherichia coli lipopolysaccharide on phosphatidylcholine biosynthesis by rat lung and alveolar type II cells (1990)
    Springer
    Molecular and cellular biochemistry 93 (1990), S. 167-172 
    Details
    ISSN: 1573-4919
    Keywords: endotoxic shock ; lipopolysaccharide ; type II cells ; phosphatidylcholine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Summary Alterations in pulmonary surfactant are partly responsible for the respiratory insufficiency seen under septic shock process. We have used an experimental model of LPS-induced shock in rats to examine the cells responsible for the pulmonary surfactant synthesis and its relationship to lung injury. (14C)Choline incorporation into phosphatidylcholine was significantly reduced in lung homogenates or type II cells obtained from LPS-treated animals. Addition of LPS in vitro fails to increase (14C)choline incorporation in type II cells obtained from LPS-treated animals. We suggest that this depression of pulmonary phosphatidylcholine synthesis may partly explain the occurrence of respiratory failure with septic shock.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00226188
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  • 3
    Electronic Resource
    Electronic Resource
    Influence of E. coli lipopolysaccharide binding to rat alveolar type II cells on their functional properties (1985)
    Springer
    Molecular and cellular biochemistry 68 (1985), S. 59-66 
    Details
    ISSN: 1573-4919
    Keywords: endotoxic shock ; lipopolysaccharide ; pneumocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Summary The interaction between lipopolysaccharide from E. coli0111:B4 and rat alveolar type II pneumocytes and its influence on the functional properties of the cells and their membranes were studied. Type II cells were isolated by a novel procedure involving digestion of the lung connective tissue with elastase and Percoll-gradient centrifugation. Binding of (14C)lipopolysaccharide to type II cells resulted in a partially reversible, non-specific, high affinity process. (l4C)Choline incorporation into phosphatidylcholine by type II cells was stimulated by lipopolysaccharide, the maximum effect being observed at 10–20 μg/ml. 45Ca2+ uptake by type II cells was also increased by lipopolysaccharide. Using plasma membranes from lung homogenates an increase of membrane microviscosity versus the amount of lipopolysaccharide was shown. These results indicate that E. coli lipopolysaccharide interacts with alveolar type 11 cells by binding reversibly to particular ingredients of the membrane bilayer and induces a modification of ion permeability and fluidity of the membrane.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00219389
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  • 4
    Electronic Resource
    Electronic Resource
    Effect of Escherichia coli lipopolysaccharide on the microviscosity of liver plasma membranes and hepatocyte suspensions and monolayers (1987)
    New York, NY [u.a.] : Wiley-Blackwell
    Cell Biochemistry and Function 5 (1987), S. 55-61 
    Details
    ISSN: 0263-6484
    Keywords: Endotoxins ; membranes ; hepatocytes ; hepatocyte cultures ; microviscosity ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The fluorescence probe 1,6-diphenylhexa-1,3,5-triene (DPH) was used for monitoring structural perturbations induced by lipopolysaccharide (LPS) of Escherichia coli (0111 : B4) in plasma membranes of rat liver. Changes in microviscosity were observed in plasma membrane preparations from control rats after treatment with LPS and in plasma membrane preparations from liver perfused with LPS. In both systems fluorescence polarization was measured from which microviscosity was calculated. This parameter increases with LPS treatment. From temperature dependence studies was inferred that LPS interaction with plasma membrane preparations induces an increase of both the polarization term (r0/r-1)-1 and flow activation energy (ΔE). Addition of LPS to hepatocyte suspensions also induces an increase on microviscosity and a delay in the fall of microviscosity induced by a temperature rise in hepatocyte monolayers grown on microcover slides.These data suggest that LPS interaction can be attributed to its binding to membrane hydrophobic regions in a non-specific manner.
    Additional Material: 4 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cbf.290050107
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