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  • 1
    Electronic Resource
    Electronic Resource
    Lipid peroxidation in thioacetamide-induced macronodular rat liver cirrhosis (1991)
    Springer
    Archives of toxicology 65 (1991), S. 199-203 
    Details
    ISSN: 1432-0738
    Keywords: Lipid peroxidation ; Cirrhosis ; Rat liver microsomes ; Hepatocytes ; Cytochrome P-450 ; Fatty acid composition ; Thioacetamide ; Verapamil
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Microsomes and isolated hepatocytes from thioacetamide (TAA)-induced macronodularly cirrhotic rat livers were analysed for their susceptibility to unstimulated and stimulated lipid peroxidation measured as malondialdehyde (MDA) formation. In microsomes from TAA-induced macronodularly cirrhotic livers the MDA production stimulated either by ascorbate-iron or by ADP-iron in a NADPH-regenerating system was decreased. Hepatic microsomes from TAA-treated rats exhibited a reduced cytochrome P450 content and lowered activities of ethylmorphine N-demethylase, ethoxycoumarin O-deethylase and epoxide hydrolase. Besides this, the microsomal fatty acid pattern of phosphatidylcholine and phosphatidylethanolamine was significantly changed after 6 months of TAA administration. The 18∶2/20∶4 ratio of phospholipid fatty acids was markedly increased. In contrast to the microsomes, in isolated hepatocytes from macronodularly cirrhotic livers the iron- and ascorbate-iron-stimulated MDA formation was increased. The hepatocellular GSH content was unaffected by TAA pretreatment, whereas the GSSG content exhibited a significant increase, thus leading to a pronounced reduction of the GSH/GSSG ratio. The calcium channel blocker verapamil (200 μM), known to be able to scavenge OH′ radicals produced by the Fenton reaction, revealed an inhibitory effect on ascorbate-iron- and ADP-iron-stimulated lipid peroxidation in hepatocytes from normal as well as TAA-treated livers which is attributed to its antioxidative properties. In summary, lipid peroxidation is altered in TAA-induced macronodularly cirrhotic rat livers. Furthermore, the data clearly show that isolated microsomes and parenchymal cells prepared from cirrhotic livers react differently to prooxidant stimuli.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02307309
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  • 2
    Electronic Resource
    Electronic Resource
    Hepatic and pancreatic effects of polyenoylphosphatidylcholine in rats with alloxan-induced diabetes (1996)
    New York, NY [u.a.] : Wiley-Blackwell
    Cell Biochemistry and Function 14 (1996), S. 131-137 
    Details
    ISSN: 0263-6484
    Keywords: polyenoylphosphatidylcholine ; liver structure, lipids ; pancreatic structure ; pancreatic islets ; β-cells ; ranules ; alloxan ; experimental diabetes ; liver damage ; glucose content ; Life Sciences ; Molecular Cell Biology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: Polyenoylphosphatidylcholine (PPC: 100 or 300 mg kg-1 b.w., by gastric intubation for 30 days) produced a clearcut protection of the liver of rats treated with alloxan (150 mg kg-1 b.w., i.p.). The liver of rats treated with alloxan was characterized by hydropic dystrophy and lymphocytic infiltrations. Treatment with alloxan increased serum γ-GT and ALAT activities. The liver structure of rats treated with PPC did not differ from the liver of control animals. PPC normalized the biochemical abnormalities caused by the diabetes. The number of pancreatic islets and β/α; cell ratio decreased in the diabetic rats. A number of β-cells in this group did not contain granules. PPC prevented the decrease in the number of islets and the β/α; cell ratio in the pancreas of the diabetic rats. The intensity of staining of β-cell granules in the pancreas of PPC-treated rats had a position intermediate between the control and diabetic groups. Alloxan increased the blood glucose content where treatment with PPC decreased this. The results suggest that PPC acts as a cytoprotector in the liver and pancreas of rats with experimental diabetes induced by alloxan.
    Additional Material: 2 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cbf.657
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    Paper (German National Licenses)
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