What is the difference between a reversible enzyme inhibitor and an irreversible enzyme inhibitor Reversible are not permanent while irreversible are permanent This means that a reversible inhibitor simply sits in the active site while the irreversible inhibitor covalently binds to the enzyme What is the difference between a receptor agonist and antagonist An agonist binds to the receptor just like the natural NT forcing it to change shape and sends the signal to the interior of the cell An antagonist binds to the receptor but does not force the receptor to change its shape thus no activity occurs inside the cell Which type of inhibitor is aspirin Which enzyme does aspirin inhibit Aspirin inhibits the cyclooxygenase COX enzymes by covalently reacting with a serine OH in the active site More specifically the ester group of aspirin gets attacked by the OH Thus aspirin is an irreversible inhibitor Recently it has been discovered that there are 3 COX enzymes and it is COX 2 that is mostly responsible for the production of prostaglandins The over production of prostaglandins is one cause of inflammation and ultimately pain Aspirin is not specific for COX 2 and thus some people have adverse reactions to aspirin Some newer drugs inhibit COX 2 and thus are not as likely to produce side effects How does the binding of a NT to its receptor protein transmits a signal to the inside of a cell When a NT binds to a receptor protein outside the cell the protein is forced to change its shape This shape change causes the molecules inside the cell to do get into gear and do something How do sulfanilimides and penicillin attack bacteria i e in what ways are bacterial cells different from human cells Sulfanilimides inhibit an enzyme dihydropteroate synthetase that bacterial cells have but human cells do not Bacteria need folic acid to survive and sulfanilimides inhibit the enzyme that is responsible for the synthesis of folic acid One of the substrates for the enzyme is gamma amino butyric acid GABA and the sulfanilamide resembles the GABA Sulfanilimide occupies that same place as GABA in the active site and thus it is a reversible inhibitor Bacteria cells have cell walls while human cells have cell membranes Cell walls are stronger because the sugar chains are covalently connected cross linked via short peptides Membranes are composed of phospholipid tails that are not covalently linked Penicillin inhibits the enzyme transpeptidase that connects the peptides between the sugar chains And if the bacterial cell wall is not cross linked the cell will not survive Structure Activity Relationship The relationship between the chemical or 3D structure of a molecule and its biological activity Penicillin is one of the first drugs to be studied This is because synthetic organic chemistry had evolved to the stage where we could synthesize variations of the natural product Thus chemists synthesized versions of penicillins where all of the functional groups were altered from the natural version How have bacteria been able to resist our anti bacterial drugs such as penicillin And how has the medical community responded to these drug resistant bacteria The bacteria have created enzymes B lactamases that cleave the 4 membered ring amide bond of the penicillin so that the drug is no longer active The medical community has fought back by adding B lactamase inhibitors to the penicillin common version is Augmentin so that the B lactamase enzyme is inhibited and the drug is remains active Illustrate the life cycle of the NT acetylcholine 1 synthesis of acetylcholine 2 acetylcholine goes to vesicle and is shot towards the receptor 3 acetylcholine binds to its receptor signal is sent to the inside of cell 4 acetylcholine wanders over to the acetylcholineesterase ACE to be chopped 5 the choline goes back to nerve cell and binds to receptor protein How do we know there are at least two types of receptors for acetylcholine In the nervous system acetylcholine is found to bind all over the body and elicits different response In general the two types are classified as muscarinic and nicotinic How do the organophosphorous ACE inhibitors work The organophosphorous ACE inhibitors example mustard gases covalently bind to the Ser OH in the active site of the enzyme The fact that these agents are so deadly to humans illustrates the importance of acetylcholine and the acetylcholine cycle to our survival Why are the insecticides malathion and parathion active in plants but not humans These insecticides have P S instead of P O However insects have an enzyme that can convert P S to P O and thus it can inhibit ACE in vivo Humans do not the enzyme and thus our ACE is not inhibited How do the structures of morphine codeine and heroin differ And how do these differences alter the biological activity of these drugs Codeine is not active in vitro in a test tube which means the benzene OH of morphine is crucial for biological activity The fact that codeine is 20 as active as morphine in vivo in living bodies tells us that our bodies are able to convert some codeine into morphine The fact that 6 acetylmorphine is much more active than morphine in vivo means it crosses the blood brain barrier more easily than morphine Also it means that the other OH is not required for biological activity The fact that heroin is more active in vivo than morphine tells us that the benzene ester can be converted into OH very easily unlike codeine and it crosses the blood brain barrier easier than morphine