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Eicosanoid biosynthesis enzymes are a heterogeneous group of enzymes comprising cyclooxygenases (COX-1, COX-2: prostaglandin-endoperoxide synthases), lipoxygenases (5-LOX, 12-LOX, 15-LOX), cytochrome P450 monooxygenases, and phospholipase A2 (PLA2)[1][3][5][7][9]. These enzymes mediate the conversion of polyunsaturated fatty acids into eicosanoids—prostaglandins, thromboxanes, leukotrienes, lipoxins, and specialized pro-resolving lipid mediators—which play central roles in both normal physiology (homeostasis, vascular tone, platelet function) and pathology (pain, fever, inflammation, cancer, cardiovascular disease, asthma, allergy, and infection)[4][5][7][9]. Many widely used anti-inflammatory and analgesic drugs, especially NSAIDs and COX-2 selective inhibitors, exert their therapeutic effects by inhibiting these enzymes, but safety concerns around gastrointestinal and cardiovascular side effects persist. The enzymes within this group represent proven and important therapeutic targets, although the designation "Eicosanoid biosynthesis enzymes" requires further specification to indicate exactly which enzyme is involved in any given context.
Enzyme inhibition (blocking COX, LOX, or CYP enzymes reduces specific eicosanoid production) Acetylation (aspirin acetylates COX-1, inhibiting thromboxane A2 synthesis) Selective isoform inhibition (COX-2 inhibitors target inflammation while sparing homeostatic functions)[2][4][8][10]
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