Eicosanoids
Start with the big picture
Phospholipase A₂ releases arachidonic acid from membrane phospholipids in a rate-limiting step; glucocorticoids inhibit this upstream process. Arachidonic acid is then metabolized through COX, 5-lipoxygenase, and cytochrome P450 epoxygenase pathways. COX products include prostaglandins and thromboxanes, whose effects vary by tissue: prostacyclin supports vasodilation and limits platelet aggregation, while thromboxane promotes vasoconstriction and aggregation. Lipoxygenase products include leukotrienes, which can promote bronchoconstriction, and lipoxins, which support resolution of inflammation. NSAIDs inhibit COX, while leukotriene-pathway drugs target selected asthma-related signals. The full topic also considers omega-3 fatty acids, receptor actions, and rapid inactivation of these short-lived mediators.
What you'll learn
- Describe how arachidonic acid is released from membrane phospholipids.
- Distinguish the main products of the COX, 5-lipoxygenase, and P450 pathways.
- Relate selected prostaglandins, thromboxanes, leukotrienes, and lipoxins to their actions.
- Explain how NSAIDs and leukotriene-pathway drugs modify eicosanoid signaling.
- Summarize how omega-3 fatty acids influence eicosanoid-related mediator production.
Continue your study
Work through the complete notes and reinforce the topic with the study tools available in the full lesson.