Effects of nordihydroguaiaretic acid and indomethacin on the viability and functional activities of normal and carbon tetrachioride-injured rat hepatocytes cultured alone and with Kupffer cells

In order to study the contribution of eicosanoids to the regulation of the functions of normal and carbon tetrachloride (CCl4)-injured liver cells, primary cultures of hepatocytes (HC) either alone or in coculture with Kupffer cells (KC) were exposed for 4 and 24 h to lipoxygenase inhibitor (nordihy...

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Published inActa physiologica et pharmacologica Bulgarica Vol. 23; no. 2; p. 33
Main Authors Makogon, N V, Lushnikova, I V, Korneitchuk, A N, Alexeyeva, I N
Format Journal Article
LanguageEnglish
Published Bulgaria 1998
Subjects
Alanine Transaminase - metabolism
Animals
Carbon Tetrachloride - toxicity
Cell Respiration - drug effects
Cell Survival - drug effects
Cells, Cultured
Cyclooxygenase Inhibitors - pharmacology
Drug Interactions
Indomethacin - pharmacology
Kupffer Cells - drug effects
Lipoxygenase Inhibitors - pharmacology
Liver - cytology
Liver - drug effects
Liver - metabolism
Male
Masoprocol - pharmacology
Mitochondria, Liver - drug effects
Mitochondria, Liver - enzymology
Mitochondria, Liver - metabolism
Rats
Rats, Wistar
Urea - metabolism
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Summary:In order to study the contribution of eicosanoids to the regulation of the functions of normal and carbon tetrachloride (CCl4)-injured liver cells, primary cultures of hepatocytes (HC) either alone or in coculture with Kupffer cells (KC) were exposed for 4 and 24 h to lipoxygenase inhibitor (nordihydroguaiaretic acid-NDGA) or cyclooxygenase inhibitor (indomethacin-IND) in the presence and in the absence of CCl4. Treatment with CCl4 resulted in increased ALT release and a decreased mitochondrial respiration (MR) in HC and their cocultures with KC. The addition of NDGA decreased ALT levels and increased MR in control and CCL4-injured cells. Urea production (UP) was not significantly affected by NDGA. In contrast, addition of IND) decreased UP by HC (4 h), and did not alter ALT release and MR in control and CCl4-treated cells. These results indicate that arachidonic acid metabolites are involved in the regulation of HC flinctions. There is also evidence that a protective action of lipoxygenase inhibitors on CCl4-injured liver is mediated, at least partly, by their direct effects on HC and KC, in particular by increasing the mitochondrial respiration.
ISSN:0323-9950