
doi: 10.1007/bf02737594
pmid: 10436856
The metabolism of AA reflects a carefully balanced series of biochemical pathways. The level of free arachidonate in a cells is controlled by de novo synthesis, dietary uptake, and transcellular metabolism. Lysophospholipids are key controlling substrates for a variety of acyl transferase and transacylase reactions, whose combined effect is to remodel cellular membranes placing AA in up to 20 different molecular species of phospholipids. PLA2 enzymes, both cytosolic and secretory, can release AA for subsequent metabolism via lipoxygenase, COX, and cytochrome P450 enzymes into a variety of eicosanoid products. Reactions are often tissue- and cell-specific, and provide a spectrum of inflammatory mediator release in which many of the molecular details remain to be elucidated.
Arachidonic Acid, Models, Immunological, Animals, Humans, Lung Injury, Inflammation Mediators, Lung
Arachidonic Acid, Models, Immunological, Animals, Humans, Lung Injury, Inflammation Mediators, Lung
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