Exacerbation or facilitation of allergic reactions to unrelated allergens has also been reported: starting an immunostimulating treatment has been associated with exacerbation of underlying eczema, asthma, or rhinitis.
Among Eichengrün’s first ideas was to find a derivative of salicylic acid that would be as therapeutically effective but with less undesirable side effects. He hired a young chemist Felix Hoffmann who, because of his arthritic father, had a personal passion in the project. Hoffmann came up with acetylsalicylic acid.
Synthesis of Aspirin | Sharmaine Bungabong - …
First generation COX2 inhibitors, Celebrex and Vioxx, reached consumers in 1999. Nicknamed “super aspirins,” they are comparable to aspirin in reducing pain and inflammation. Large scale clinical trials also found that they cause significantly less gastrointestinal irritation than the old COX inhibitors. Gastrointestinal side effects of COX inhibitors were blamed for roughly 100,000 hospitalizations and 15,000 deaths each year in the United States alone. Rheumatoid arthritic patients who had to take high dosages for long periods suffered most. To them COX2 inhibitors that promise to lessen the toll were godsend.
the balanced chemical reaction for the synthesis of aspirin
Enzymes are protein catalysts that speed up chemical reactions without being themselves used up in the reactions. An enzyme is a huge molecule with an active area that works somehow like a mold that accepts certain raw pieces and casts them into a final form. Imagine a mold that stamps a rod and a bowl into a spoon. Spoon production would be disrupted if someone throws a monkey range into the mold. Such a monkey range – an enzyme inhibitor – would make a desirable drug if it stops an enzyme from producing disease-inducing chemicals. Aspirin is an enzyme inhibitor. It suppresses the action of the enzyme COX, stops the production of prostaglandin, thus disrupting the pathways to pain, inflammation, elevated temperature, and stomach protection.
Full Report: Synthesis of Aspirin ..
Blood clotting is a complex process. The blood contains, besides red and white blood cells, partial cells called platelets. The disc-like platelets are produced in the bone marrow and cannot reproduce themselves because they contain no nucleus. They usually lie dormant in the blood, awakened only by chemicals released by injured tissues or a tear in the artery’s plaque. These stimulants activate the COX1 enzyme in the platelets to produce a prostaglandin, which causes the platelets to stick together, triggering the cascade of reactions that result in clotting of blood. By inhibiting COX1 from synthesizing the prostaglandin, aspirin reduces the stickiness of platelets, hence the chance of forming blood clots. For this antiplatelet purpose aspirin is uniquely effective. All other aspirin-like drugs inhibit COX temporarily, aspirin alone inhibits it permanently. One dose of aspirin has antiplatelet effects that last through the platelet’s lifetime, about ten days.
Synthesis of Aspirin..equation? | Yahoo Answers
How does aspirin curb prostaglandin production? The many kinds of prostaglandin are synthesized by a host of complicated biochemical pathways. However, all pathways share a common stage facilitated by an enzyme called COX, whose action aspirin suppresses.
synthesis of aspirin - Course Hero
Basic science and knowledge about underlying mechanisms strengthen the case for “an aspirin a day keeps heart attacks away.” However, they are not sufficient to prove it. We saw earlier that tissue bioassay is better than whole animal experiments in isolating a process and uncovering its underlying mechanism, which is buried under myriad processes going on in a life animal. The advantage in discovery can become a disadvantage in applying its results. In isolating a process we ignore its interaction with other processes in the context of application. These interactions can generate side effects or even derail the process itself. In the test tube, aspirin inhibits COX1 in platelets and hence the formation of a prostaglandin that promotes blood clots; fine. In the body, the situation is far more complex. For instance, aspirin also inhibits COX2 in blood vessels and hence the formation of another prostaglandin that prevents blood clots. How would the two processes of opposing effects balance out? Another question, would taking aspirin years on end, even at low dosages, increase the risk of bleeding in the brain? These and many other questions involving the functioning of the body as a whole cannot be answered by test-tube experiments on individual processes. That is why governments require drugs to pass clinical trials in human subjects to prove their effectiveness and safety.