In America, more than 80 billion aspirin tablets are consumed each year. Aspirin is a trade name for acetylsalicyclic acid and is effective as an analgesic, antipyretic and anti-inflammatory. Aspirin's predecessors, derived from salicylic acid, have been used to treat a variety of conditions for over 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 advocated by Galen, a second-century Roman physician, and mentioned in medical texts from the Middle Ages and the Renaissance. In 1757, the Rev. Edward Stone conducted the first scientific study of natural sources of salicylates and wrote about the success of willow bark in treating fevers and body aches. Leroux showed in 1829 that salicin is the active agent in willow and was first extracted by Fontana and Brugnatelli. Salicin was transformed 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. German chemist Felix Hoffmann was commissioned by Arthur Eichengrun of Friedrich Bayer & Co in 1893 to find a less toxic alternative. Hoffmann came back with a related compound. Say no to plagiarism. Get a tailor-made essay on “Why Violent Video Games Should Not Be Banned”? Get the original essay By subjecting salicin to a series of chemical reactions, acetylsalicylic acid was created. Acetylsalicylic acid successfully passed chemical tests and was introduced to 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 a sensation of pain. In the 1970s, John Vane hypothesized that aspirin might affect prostaglandin synthesis (associated with tissue damage). thereby reducing pain and inflammation. Knowing that prostaglandins are made from arachidonic acid (produced by fatty acids in cell membrane phospholipids), Vane incubated cell extracts from damaged tissues with arachidonic acid and different concentrations of aspirin. Depending on the dose, Vane found that aspirin inhibited prostaglandin production. Additional experiments established that aspirin inhibits the cyclooxygenase enzyme that converts arachidonic acid to the intermediate peroxy radical and then to compound 6, thereby preventing the production of PGE2. It has been proposed that aspirin ethanolylates serine. residue on the cyclooxygenase enzyme by attacking its hydroxl group. During the process, an ethanol 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. However, when serine was replaced with asparagines, the modified enzyme did not show cyclooxygenase activity. This suggests that ethanolylation of the enzyme's active site prevents arachidonic acid from binding to its surface, so the enzyme cannot convert arachidonic acid to prostaglandin. Super Aspirins In 1992,.