In America, more than 80 billion aspirin tablets are consumed each year. Aspirin is the trade name for acetyl salicyclic acid and is effective as an analgesic, antipyretic and anti-inflammatory drug. History Aspirin's predecessors, derivatives of salicylic acids, have been used to treat a variety of conditions for more than 2,500 years. The Greek physician Hippocrates (400 BC) recommended the use of willow bark (a natural source of salicylates) to relieve pain during childbirth. This use of salicylates was also supported by Galen, a 2nd century Roman physician, and mentioned in medical texts of the Middle Ages and Renaissance. In 1757, the Reverend Edward Stone conducted the first scientific study of natural sources of salicylates and wrote about the success of willow bark in curing fevers and aches and pains. Leroux demonstrated in 1829 that salicin is the active agent of willow and was first extracted by Fontana and Brugnatelli. Salicin was synthesized into salicylic acid by the Italian chemist Piria in 1839. It was synthesized by a process discovered by Kolbe and Lautemann in 1860 which led to the introduction of salicylic acid and sodium salicylate (precursors of aspirin) for the treatment of fever and arthritis. However, these compounds were toxic to the stomach and caused diarrhea and vomiting. In 1893 Arthur Eichengrun of Friedrich Bayer & Co commissioned the German chemist Felix Hoffmann to find a less toxic alternative. Hoffmann is back with a related compound. Say no to plagiarism. Get a tailor-made essay on "Why Violent Video Games Shouldn't Be Banned"? Get an original essay By subjecting salicin to a series of chemical reactions, acetylsalicylic acid was created. Acetylsalicylic acid passed chemical tests and was introduced on the market in 1899 under the trade name Aspirin. How does aspirin work? Prostaglandins (PGs) are chemical messengers of the immune system responsible for pain and inflammation. For example, PGE2 acts on nerve endings, causing the sensation of pain. In the 1970s John Vane hypothesized that aspirin might affect the synthesis of prostaglandins (associated with tissue injury). thus reducing pain and inflammation. Knowing that prostaglandins are made up of arachidonic acid (produced from the fatty acids of phospholipids in cell membranes) Vane incubated cell extracts from damaged tissue with arachidonic acid and different concentrations of aspirin. Depending on the dose, Vane found that aspirin inhibited the production of prostaglandins. Further testing established that aspirin inhibits the cyclooxygenase enzyme that converts arachidonic acid to the peroxy radical intermediate and then to compound 6, preventing the production of PGE2. It has been proposed that aspirin ethanolylates the serine residue on the cyclooxygenase enzyme by attacking its hydroxyl group. In the process, an ethanolyl group is transferred from aspirin to serine, and aspirin is converted to salicylic acid. To confirm this theory the serine residue was replaced by alanine (which does not have an OH group). The cyclooxygenase activity of the modified enzyme was not affected by aspirin. When serine was replaced by asparagines, however, the modified enzyme showed no cyclooxygenase activity. This suggests that ethanolylation of the active site of the enzyme prevents the binding of arachidonic acid to its surface so that the enzyme cannot convert arachidonic acid into a prostaglandin. Super aspirins In 1992, chemists discovered that cyclooxygenase (COX) had two forms COX1 and COX2. COX1 converts arachidonic acid into PGl2 which protects the stomach lining while COX2 converts arachidonic acid into.