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Leukotrienes as mediators in frog virus 3‐induced hepatitis in rats
Author(s) -
Hagmann Wolfgang,
Steffan AnneMarie,
Kirn André,
Keppler Dietrich
Publication year - 1987
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840070419
Subject(s) - leukotriene , in vivo , virus , leukotriene c4 , leukotriene e4 , leukotriene d4 , biology , metabolite , medicine , in vitro , cyclooxygenase , endocrinology , lipoxygenase , arachidonate 5 lipoxygenase , enzyme , immunology , biochemistry , arachidonic acid , microbiology and biotechnology , asthma
The role of leukotrienes was investigated in frog virus 3‐induced hepatitis in rats. Frog virus 3 elicited an enhanced generation of cysteinyl leukotrienes in vivo as monitored by measurement of N ‐acetyl‐leukotriene E 4 as the major endogenous metabolite of cysteinyl leukotrienes secreted into rat bile. N ‐Acetyl‐leukotriene E 4 concentrations were elevated for more than 4 hr after frog virus 3 injection. In vitro experiments using cultured rat liver Kupffer cells of high purity indicated that these cells can produce and metabolize leukotrienes and are thus a possible source of leukotrienes elicited in vivo by frog virus 3. The selective 5‐lipoxygenase inhibitor AA 861 and the dual inhibitor of arachidonate lipoxygenase and cyclooxygenase, BW 755C, reduced the hepatocellular injury after a high dose of frog virus 3 by about 50 and 80%, respectively, as judged from plasma activities of ALT and sorbitol dehydrogenase at 24 hr after frog virus 3 administration. Our in vivo and in vitro studies argue in favor of an important role of leukotrienes as mediators in frog virus 3 hepatitis in rats.