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COX-2 inhibitors and metabolism of essential fatty acids.
Med Sci Monit. 2005 Jul; 11(7):RA233-7.MS

Abstract

Selective COX-2 inhibitors increase the risk of myocardial infarction and stroke that is attributed to their ability to inhibit prostacyclin (PGI2), lipoxins, resolvins, and endothelial nitric oxide (eNO) but not platelet COX-1 derived thromboxane A2 (TXA2). In contrast, aspirin blocks both COX-1 and COX-2 enzymes that, in turn, increases intracellular concentrations of dihomo-gamma-linolenic acid (DGLA), arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and reduced formation of eicosanoids. On the other hand, such an increase is much less with specific COX-2 inhibitors since they do not block the formation of eicosanoids through COX-1 pathway. DGLA, AA and EPA form precursors to PGE1, PGI2, and PGI3 respectively, which are potent vasodilators and platelet anti-aggregators, and thus aid in the prevention of thrombus formation. EPA has anti-arrhythmic action, and EPA, DHA (docosahexaenoic acid), DGLA, and PGE1 have anti-inflammatory actions as well. EPA, DHA, and AA augment eNO formation that has anti-atherosclerotic action. Hence, combining EFAs with COX-2 inhibitors will prevent thrombotic cardiovascular events.

Authors+Show Affiliations

UND Life Sciences, Cleveland Heights, OH 44106, USA. undurti@hotmail.com

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

15990700

Citation

Das, Undurti N.. "COX-2 Inhibitors and Metabolism of Essential Fatty Acids." Medical Science Monitor : International Medical Journal of Experimental and Clinical Research, vol. 11, no. 7, 2005, pp. RA233-7.
Das UN. COX-2 inhibitors and metabolism of essential fatty acids. Med Sci Monit. 2005;11(7):RA233-7.
Das, U. N. (2005). COX-2 inhibitors and metabolism of essential fatty acids. Medical Science Monitor : International Medical Journal of Experimental and Clinical Research, 11(7), RA233-7.
Das UN. COX-2 Inhibitors and Metabolism of Essential Fatty Acids. Med Sci Monit. 2005;11(7):RA233-7. PubMed PMID: 15990700.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - COX-2 inhibitors and metabolism of essential fatty acids. A1 - Das,Undurti N, Y1 - 2005/06/29/ PY - 2005/03/21/received PY - 2005/04/13/accepted PY - 2005/7/2/pubmed PY - 2005/8/27/medline PY - 2005/7/2/entrez SP - RA233 EP - 7 JF - Medical science monitor : international medical journal of experimental and clinical research JO - Med Sci Monit VL - 11 IS - 7 N2 - Selective COX-2 inhibitors increase the risk of myocardial infarction and stroke that is attributed to their ability to inhibit prostacyclin (PGI2), lipoxins, resolvins, and endothelial nitric oxide (eNO) but not platelet COX-1 derived thromboxane A2 (TXA2). In contrast, aspirin blocks both COX-1 and COX-2 enzymes that, in turn, increases intracellular concentrations of dihomo-gamma-linolenic acid (DGLA), arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and reduced formation of eicosanoids. On the other hand, such an increase is much less with specific COX-2 inhibitors since they do not block the formation of eicosanoids through COX-1 pathway. DGLA, AA and EPA form precursors to PGE1, PGI2, and PGI3 respectively, which are potent vasodilators and platelet anti-aggregators, and thus aid in the prevention of thrombus formation. EPA has anti-arrhythmic action, and EPA, DHA (docosahexaenoic acid), DGLA, and PGE1 have anti-inflammatory actions as well. EPA, DHA, and AA augment eNO formation that has anti-atherosclerotic action. Hence, combining EFAs with COX-2 inhibitors will prevent thrombotic cardiovascular events. SN - 1234-1010 UR - https://www.unboundmedicine.com/medline/citation/15990700/COX_2_inhibitors_and_metabolism_of_essential_fatty_acids_ L2 - https://www.medscimonit.com/download/index/idArt/16986 DB - PRIME DP - Unbound Medicine ER -