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  • 1
    Electronic Resource
    Electronic Resource
    Effect of a cholesterol-rich diet on cholesterol content and phagocytic activity of rat macrophages (1976)
    Springer
    Inflammation research 6 (1976), S. 135-142 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Treatment for 11–13 weeks with a cholesterol-rich diet induced increases in free and esterified serum cholesterol. There was also an increase in free cholesterol of peritoneal macrophages. A 2.2 times rise in the cholesterol to phospholipid ratio of plasma membranes occurred in cholesterol-enriched macrophages. No changes were observed in phagolysosomes. Cholesterol-enriched macrophages showed a 35.8% inhibition of latex particles phagocytosis. When lipid droplets were substituted for latex the inhibition was 81.7%.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01972197
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Time course of protection by N,N'-Diphenyl-p-phenylendiamine (DPPD) against carbon tetrachloride hepatotoxicity (1974)
    Springer
    Inflammation research 4 (1974), S. 383-390 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A preliminary treatment with DPPD (N,N'-diphenyl-p-phenylendiamine) prevents liver fatty infiltration early after carbon tetrachloride poisoning. Double bond shifting in microsomal lipids appears to be depressed 30 minutes after intoxication. A more active protection takes place when low doses of CCl4 are given (25 μl per 100 g body weight) than after a large dose of the poison (250 μl). In later stages of the halogenoalkane challenge, both triglyceride accumulation and lipid peroxidation take place despite of the antioxidant treatment. However, they are less severe and more transient than in unprotected animals. Similarly, liver necrosis, as evidenced by changes in serum activity of alanine aminotransferase appears, to be prevented by DPPD. This compound does not interfere with the hepatic metabolism of carbon tetrachloride, as suggested by the findings of14C binding to liver lipids and exhalation of radioactive CO2 after administration of14CCl4. Moreover, pretreatment with antioxidant partially inhibits the in vitro demethylation of aminopyrine by liver microsomes and significantly potentiates the hypnotic effect of hexobarbital. Further, DPPD, when injected along with phenobarbital, blocks the barbiturate stimulation of microsomal enzymes. A combined dosing with both DPPD and CCl4 causes a more severe inhibition of demethylase activity and hexobarbital metabolism. Our results indicate that DPPD can act as an inhibitor of the enzymes bound to the endoplasmic reticulum, beside its antioxidant properties, during CCl4 intoxication.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01964941
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Behaviour of cyclic nucleotides and Ca2+ levels in liver tissue of rats poisoned by white phosphorus and trichlorobromomethane (1984)
    New York, NY [u.a.] : Wiley-Blackwell
    Cell Biochemistry and Function 2 (1984), S. 111-114 
    Details
    ISSN: 0263-6484
    Keywords: Liver ; hepatotoxins ; trichlorobromomethane ; white phosphorus ; cyclic nucleotides ; Ca2+ ; Chemistry ; Biochemistry and Biotechnology
    Source: Wiley InterScience Backfile Collection 1832-2000
    Topics: Biology , Medicine
    Notes: The content of hepatic cyclic AMP was increased soon after intoxication by white phosphorus. Its level reached a maximum 4 h after poisoning, but in subsequent phases tended to return to normal. In contrast, the cyclic GMP concentration was altered only 24 and 36 h after treatment with the same hepatotoxin. Similar modifications of cAMP and cGMP content were also detected after poisoning by trichlorobromomethane (CBrCl3). As a consequence, an altered cGMP/cAMP ratio was found in both experimental conditions. Further, the modification of cAMP content after white phosphorus was detected prior to liver damage (steatosis and necrosis), while the highest concentration of the cyclic nucleotide in CBrCl3-poisoned rats was found when fatty liver was already evident. In addition, in phosphorus-poisoned rats, the hepatic content of Ca2+ was found to be unmodified during all phases of the intoxication, while after CBrCl3 a phasic increase of the Ca2+ level was observed at 4, 24 and 36 h.
    Additional Material: 6 Ill.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1002/cbf.290020211
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    Paper (German National Licenses)
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