Arachidonic acid metabolism in cultured adult myocardial cells under short-time hypoxic conditions

• Published in: Molecular and cellular biochemistry Vol. 106; no. 1; p. 67
• Main Authors: Härtel, B, Morwinski, R, Heydeck, D, Papies, B
• Format: Journal Article
• Language: English
• Published: Netherlands 24.07.1991
• Subjects: Animals; Arachidonic Acids - blood; Arachidonic Acids - genetics; Arachidonic Acids - metabolism; Cell Survival - drug effects; Cells, Cultured; Creatine Kinase - metabolism; Cyclooxygenase Inhibitors - pharmacology; DNA Probes; Erythrocytes - enzymology; Hypoxia - enzymology; Hypoxia - metabolism; Lipoxygenase Inhibitors - pharmacology; Myocardium - enzymology; Myocardium - metabolism; Nucleic Acid Hybridization; Rats; Rats, Inbred Strains
• ISSN: 0300-8177
• DOI: 10.1007/BF00231190

The present study utilized a cultured adult myocardial cell model to examine the arachidonic acid metabolism under different cell-damaging and normoxic conditions. Cell injury was caused by short-time hypoxia, calcium ionophore A 23187-triggered cell-damage under hypoxia and cell disruption by freezing and thawing. The current study demonstrates that under the cell-damaging conditions cultured adult heart myocytes resemble myocardial cells under normoxic conditions in metabolizing arachidonic acid into triacylglycerols and phospholipids as the major route (a), in formation of ETYA-inhibitable indomethacin-resistant lipid metabolites in minor amounts (b) and in being independent of calcium overload in the metabolic pathways of arachidonic acid metabolism (c). The ETYA-inhibitable components were resolved by HPLC. There was no evidence in formation of lipoxygenase products. The results were supported by negative hybridisation experiments of the total mRNA isolated from adult myocardial cells with a cDNA probe of a red-cell-specific lipoxygenase mRNA. We conclude from these observations that cell injury does not result in expression of lipoxygenase activities in heart myocytes.