Prostaglandin synthesis produces lipid compounds that act as chemical messengers in biological processes such as inflammation. Enzymes initiate synthesis, and drugs like aspirin prevent it. Prostaglandins function as cell signaling molecules and are synthesized constantly in the body. COX enzymes mediate synthesis, and COX-2 is released during tissue injury, leading to an inflammatory response. Aspirin inhibits COX enzymes and reduces pain and inflammation. NSAIDs prevent prostaglandin production rather than treating their effects.
Prostaglandin synthesis is the production of lipid compounds within the cells of some animals, including humans. These substances are chemical messengers that mediate biological processes, such as inflammation, and are important in the normal function of many different tissues. Some enzymes initiate prostaglandin synthesis by catalyzing a series of metabolic reactions that convert a fatty acid into the biologically active end product. Drugs such as aspirin prevent the synthesis of prostaglandins and thus reduce pain and inflammation.
In many animal tissues, prostaglandins function as cell signaling molecules that have functions ranging from sending a signal about body temperature to the brain to sensitizing neurons to pain. These lipid compounds come in three main subtypes and together they comprise the eicosanoids, a group of biologically active fatty acids. Prostaglandin synthesis occurs within cells whenever one of the compounds is needed, but they are not stored in specialized compartments as biologically important molecules usually are. With many different effects on neurons, muscles, and epithelium, prostaglandin is synthesized almost constantly within the body.
When enzymes known as cyclooxygenase (COX) are released, prostaglandin synthesis begins through the oxidation of fatty acids, especially arachidonic acid. The fatty acids themselves come from the same sources as the lipids that make up the cell membrane. Oxidation changes their basic structure into whatever type of prostaglandin is needed at the moment. COX 1 is the enzyme responsible for maintaining normal levels of prostaglandins in the body, while COX 2 mediates synthesis when tissues are damaged or infected. Synthesis occurs in almost all cell types, except white blood cells and those without a nucleus.
Whenever tissue injury occurs, various immune cells migrate to the site. This cellular response process triggers the release of COX-2, resulting in the synthesis of prostaglandins in the damaged part of the body. Prostaglandins lead to an inflammatory response, triggering a fever and limiting infection and tissue loss. Another variety regulates some of the blood’s clotting mechanisms, controlling where a clot can and cannot form. The prostaglandin known as PGE-2 effects changes in the uterus, including contractions, and is commonly used medicinally to induce labor or abortion.
Various chemicals can inhibit prostaglandin synthesis: aspirin is a well-known example. Both COX-1 and COX-2 are inhibited by aspirin, which prevents the oxygenation of arachidonic acid required for synthesis. By impeding enzyme activity, aspirin interrupts the inflammatory pathway and reduces fever along with pain sensitivity, as both decrease without the effects of prostaglandin. Along with compounds like ibuprofen, aspirin is one of the nonsteroidal anti-inflammatory drugs (NSAIDs). Unlike steroids such as cortisone, NSAIDs prevent the production of prostaglandins rather than treating their effects.
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