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Possible involvement of eicosanoids in the zymosan and arachidonic‐acid‐induced oxygen uptake, glycogenolysis and Ca 2+ mobilization in the perfused rat liver
Author(s) -
DIETER Peter,
ALTIN Joseph G.,
DECKER Karl,
BYGRAVE Fyfe L.
Publication year - 1987
Publication title -
european journal of biochemistry
Language(s) - English
Resource type - Journals
eISSN - 1432-1033
pISSN - 0014-2956
DOI - 10.1111/j.1432-1033.1987.tb11460.x
Subject(s) - zymosan , arachidonic acid , glycogenolysis , nordihydroguaiaretic acid , chemistry , endocrinology , phenylephrine , medicine , cyclooxygenase , biochemistry , pharmacology , metabolism , biology , enzyme , in vitro , blood pressure
Exposure of perfused rat livers to zymosan, arachidonic acid and phenylephrine, but not to latex particles, induces pronounced oxygen uptake, glycogenolysis and Ca 2+ mobilization. The oxygen uptake induced by arachidonic acid and by zymosan remains elevated even after the agents have been removed. NaN 3 was found to be much more effective in inhibiting the oxygen uptake induced by phenylephrine than that induced by zymosan or arachidonic acid. Glucose release induced by zymosan and by arachidonic acid reaches a maximum after about 2 min and then declines very rapidly even while the agents are still being infused. In contrast, glucose release induced by phenylephrine remains elevated for the duration of the infusion. Ca 2+ fluxes induced by arachidonic acid are similar to those induced by phenylephrine in that efflux occurs when the agent is administered and influx occurs only when the agent is removed. This contrasts to the Ca 2+ flux changes induced by zymosan where both Ca 2+ efflux and Ca 2+ influx occur even while zymosan is still being infused. Glucose release induced by zymosan is inhibited by bromophenacylbromide and nordihydroguaiaretic acid, but not by indomethacin. Indomethacin, however inhibits the arachidonic‐acid‐induced glucose release which is also inhibited by nordihydroguaiaretic acid but not by bromophenacylbromide. Indomethacin inhibits also the arachidonic‐acid‐induced Ca 2+ flux changes whereas the zymosan‐ and the phenylephrine‐induced Ca 2+ flux changes are not inhibited by the cyclooxygenase inhibitor. The data presented in this paper suggest that in the perfused rat liver the zymosan‐induced glycogenolysis, as well as the Ca 2+ flux changes and glycogenolysis induced by arachidonic acid, are mediated by eicosanoids.

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