PMID: 2117403Aug 1, 1990Paper

Reduced arachidonate metabolism in ATP-depleted myocardial cells occurs early in cell injury

The American Journal of Physiology
G E RevtyakW B Campbell

Abstract

Exposure of cultured neonatal rat myocardial cells to metabolic inhibitors results in cellular ATP depletion. If prolonged, arachidonic acid is released from membrane phospholipid and irreversible cell injury may ensue. The present study was undertaken to identify the major products of arachidonic acid formed when myocardial cells are depleted of ATP by the metabolic inhibitors 2-deoxy-D-glucose (2-DG) and oligomycin (OG). Under basal conditions, myocardial cells metabolize [3H]arachidonic acid to 6-keto-[3H]prostaglandin (PG)F1 alpha, [3H]PGE2, [3H]PGF2 alpha, 12-[3H]hydroxy-6,8,11,14-eicosatetraenoic acid (12-[3H]HETE) and 11-[3H]HETE, indicating that these cells contain both cyclooxygenase and lipoxygenase pathways. After exposure of myocardial cells to 10 mM 2-DG and 0.1 micrograms/ml OG for 4 h, the basal release of 6-keto-PGF1 alpha and PGE2 is reduced by 3.4-fold and 2-fold, respectively. Supernatants obtained from cells prelabeled with [3H]arachidonic acid and treated with 2-DG and OG for 4 or 12 h did not contain detectable [3H]prostaglandins or [3H]HETEs, but only [3H]arachidonic acid when compared with untreated cells. After 4 and 12 h of treatment with 2-DG and OG, there was a 3.4- and 4.4-fold net release of endoge...Continue Reading

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