Basic Concept Of Coordination Compounds Biology Essay

introductory Concept Of Coordination Compounds Biology EssayWe live in the world of uncertainty and assumptions, no one and only(a) can predict the next activity, it may be good or crappy notwithstanding thing is how to tackle bad things? chemical science is the most power full tool to understand the world at almost all(prenominal) scale may be huge or femtometer scale. Chemistry is closely associated with humans day to day life , it application in music is major one. Medicine is the life living entity which play vital piece in ones life , but how medicines be made? What are their chemical properties and how they affect our body? Let us study the application of chemistry(co-ordination compounds) in medicines.Basic concept of co-ordination compoundsThe coordination chemistry was notice by Nobel Prize winner Alfred Werner (1866-1919). He received the Nobel Prize in 1913 for his coordination theory of transition metal-amine complexes. In the starting of the twentieth century, inorganic chemistry was not a prominent field until Werner studied the metal-amine complexes such as Co (NH3)6Cl3.He further studied the coordination compound of cobalt and ammonium hydroxide and detect its different properties. He studied different colors and no. of Cl instalments attached to the compounds and on that basis he proposed a table-Solid polishIonized Cl-Complex formulaCoCl36NH3Yellow3Co(NH3)6Cl3CoCl35NH3Purple2Co(NH3)5ClCl2CoCl34NH3Green1trans-Co(NH3)4Cl2ClCoCl34NH3Violet1cis-Co(NH3)4Cl2ClThe structures of the complexes were proposed based on a coordination theatre of 6. The 6 ligands can be amonia corpuscles or chloride ions. both different structures were proposed for the last two compounds, the trans compound has two chloride ions on opposit vertices of an octahedral, whereas the the two chloride ions are adjacent to each(prenominal) other in the cis compound. The cis and trans compounds are known as geometric isomers.Other cobalt complexes studied by Werner are similarly interesting. It has been predicted that the complex Co(NH2CH2CH2NH2)2ClNH32+ should exist in two forms, which are mirror images of each other. Werner isolated solids of the two forms, and structural studies confirmed his interpretations. The ligand NH2CH2CH2NH2 is ethylenediamine (en) often holded by en.Basically coordination compound consists of two moveCentral metal ionLigandsboth metal ion and ligands lie wrong or outside the coordination sphere, coordination sphere is represented by square brackets for example Co(NH3)6Cl3 here Co is the metal ion and NH3,Cl3 are the ligands , one lie inside and the second one is outside.Contain coordinate covalent bonds4) Unusual composition Central metal ion or atom + ligands + counter ion (if needed)5) Called complex ion if chargedFor an instantBasic concept of medicines and how they are discoveredDrug discovery is very time -consuming and expensive process. Estimates of the add up time required to bring a do medicates to a market ranges from 12-15 years at an average cost of $600-800 million. For approximation every 10,000 compounds are evaluated in animal studied , 10 will make it to humans clinical trials in order to get 1 compound on the market for every medicine introduction we need approval for that and once the new drug application (NDA) is submitted to the Food and Drug Administration(FDA) , it can be several months to several years before it is approved for commercial go for. Then study is done and the result are considered and if the results are found are same with the drug that is already in the market then the whole project is rejected so the discovery of new medicine is very costly , that is why medicines costs high when bought.In general medicines are never discovered , what is more apt(predicate) discovered is called lead compound. The lead compound is prototype compound that has a number of personable characteristics , such as the desired biological but may have many a(prenom inal) undesired characteristics for example high toxicity ,other biological activities, absorption worry ,insolubility or metabolism problems , so considering all these things further modified compound is formed which is called clinical drug ,which is ready for many clinical researches. The drug discovered without lead are called penicillins How does a medicine make believes on human body?The quest for knowledge to established how the drug act in a living system has been a thought provoking topic to scientist be capaciousing to various disciplines such as medicinal chemistry, biochemistry and pharmacology.Factors affecting the drugs to reach the active sitesAbsorption-biological tissue layer play a vital role towards the absorption of a drug molecule. Soon after drug is taken orally ,it makes the way through the GI tract, cross the various membranes and finally reaches the active site. It has been observed that drug moves from a region of high drug concentration to low drug conce ntration. However the set up of diffusion solely depends upon the magnitude of the concentration gradient (C). across the biological membrane.Rate = -kC(abs) C(bl), c(bl) is concentration present in blood and C(abs) is the concentration of drug at active site.Distribution As soon as drug finds its way into the blood stream, it tries to approach the site of biological perform. Hence , the distribution of a drug is markedly influenced by such vital factor as tissue distribution and membrane penetration ,which largely depends on the physio-chemical characteristics of the drug.Metabolism (biotransformation)-when a drug molecule gets converted into the body to an altogether different form, the phenomenon is called biotransformation. Mostly the metabolism occurs in the liver. The metabolism products are more polar than the parent drug.Inside liver ,in metabolism two important reactions takeChange in the functional groupeg. The side chain or ring hydroxylation reduction of nitrogroup.C onjugationthe drug substance undergoes sum whereby the metabolized product combines with various solubilizing groups.Excretion this is also very important process and may be done with the help of a number of process ,namely renal excretion, biliary excretion , excretion through lungs and above all by drug metabolism(biotransformation).COMMON TYPES OF MEDICINES USED IN DAILY LIFESome of the medicines which we use in daily life areCISPLATIN discretionment of cancerParacetamol - surmounts body temp.Aspirin reduces painLocal anesthetic1 )Cisplatin -Cisplatin is a chemotherapy drug which is utilize to treat cancers including sarcoma, small cell lung cancer, germ cell tumors, lymphoma, and ovarian cancer. While it is often considered an alkylating agent, it contains no alkyls groups and does not instigate alkylating reactions, so it is properly designated as an alkylating-like drug. Cisplatin is platinum-based and was the first medicine developed in that drug class. Other drugs in this class include carboplatin, a drug with fewer and less severe side effects introduced in the 1980s, and oxaliplatin, a drug which is part of the FOLFOX treatment for colorectal cancer. The other names for cisplatin are DDP, cisplatinum, and cis-diamminedichloridoplatinum(II) (CDDP).Cisplatin was actually first created in the mid 19th Century and is also known as Peyrones chloride. (The disoverer was Michel Peyrone.) It wasnt until the 1960s that scientists started getting interested in its biological effects, and cisplatin went ito clinical trials for cancer therapy in 1971. By the late 1970s it was already widely used and is still used today despite the many newer chemotherapy drugs developed over the past decades. construction of cisplatin-Structure of cisplatin is tetrahydral (sp3) in shape. Here one atom of platinum is bound to 2 chlorine atoms and 2 ammonia atoms.Working mechanism of cisplatin-The way that cisplatin operates is by forming a platinum complex inside of a cell whi ch binds to DNA and cross-links DNA. When DNA is cross-linked in this manner, it sticks the cells to undergo apoptosis, or systematic cell death. One of the methods it uses causes apoptosis through cross-linking is by damaging the DNA so that the repair mechanisms for DNA are activated, and once the repair mechanisms are activated and the cells are found to not be salvageable, the death of those cells is triggered instead.Cisplatin undergoes aquation to form Pt(NH3)2Cl(OH2)+ and Pt(NH3)2(OH2)22+ once inside the cell. The platinum atom of cisplatin binds covalently to the N7 position of purines to form 1,2- or 1,3-intrastrand crosslinks, and interstrand crosslinks. Cisplatin-DNA adducts cause various cellular responses, such as replication arrest, transcription inhibition, cell-cycle arrest, DNA repair and apoptosis.2 ParacetamolParacetamol is vernacularly used for relief in headache , and other minor pain and aches. It also serve as major ingredient in tatty and flu remedies in c ollaboration with opioid analgesics, it can also be used in management of several major disease such as cancer.Structure of paracetamolIn some publications, it is described as 4-hydroxyacetanilide or N-acetyl-p-aminophenol and in the US Pharmacopoeia it is known as acetaminophen.Paracetamol is a white, odourless crystalline powder with a venomous taste, soluble in 70 move of water (1 in 20 boiling water), 7 parts of alcohol (95%), 13 parts of acetone, 40 parts of glycerol, 9 parts of propylene glycol, 50 parts of chloroform, or 10 parts of methyl alcohol. It is also soluble in solutions of alkali hydroxides. It is insoluble in benzene and ether. A saturated aqueous solution has a pH of about 6 and is stable (half-life over 20 years) but stability decreases in acid or alkaline conditions, the paracetamol being slowly broken down into acetic acid and p-aminophenol.Mixtures of paracetamol and aspirin are stable in dry conditions, but tablets containing these two ingredients, particul arly in the presence of moisture, magnesium stearate, or codeine, produce some diacetyl-p- aminophenol when stored at room temperature, and this latter compound is hydrolyzed in the presence of moisture to paracetamol and p-aminophenol.Mechanism of workingOver 100 years after it was first discovered, we are now learning what the mechanism of action is that makes paracetamol such an effective and profitable medicine. It now appears paracetamol has a highly targeted action in the disposition, block an enzyme involved in the transmission of pain.As with many medicines, the effectiveness of paracetamol was discovered without knowing how it works. Its trend of action was known to be different to other pain relievers, but although it produces pain relief throughout the body the exact mechanism was not clear.The intersection of prostaglandins is part of the bodys inflammatory response to injury, and inhibition of prostaglandin production around the body by blocking the cyclooxygenase enzymes known as cox-1 and COX-2 has long been known to be the mechanism of action of aspirin and other non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen. However, their action in blocking COX-1 is known to be responsible for also causing the unwanted gastrointestinal side effects associated with these drugs.Paracetamol has no significant action on COX-1 and COX-2, which left its mode of action a mystery but did explain its lack of anti-inflammatory action and also, more importantly, its freedom from gastrointestinal side effects typical of NSAIDs.Early work (1) had suggested that the fever reducing action of paracetamol was due to activity in the mastermind while its lack of any clinically useful anti-inflammatory action was concordant with a lack of prostaglandin inhibition peripherally in the body.Now, recent research (2) has shown the presence of a new, previously unknown cyclooxygenase enzyme COX-3, found in the brain and spinal cord, which is selectively inh ibited by paracetamol, and is distinct from the two already known cyclooxygenase enzymes COX-1 and COX-2. It is now believed that this selective inhibition of the enzyme COX-3 in the brain and spinal cord explains the effectiveness of paracetamol in relieving pain and reducing fever without having unwanted gastrointestinal side effects.3 AspirinIn 1897 Flex Hoffman a German chemist employed by bayer and company was researching on the arthritic pain of his father ,then he began his study on the acetalsalicyclic acid and discovered a stable compound which was further refined to Aspirin Acetylsalicylic acid, marketed everywhere as Aspirin (USAN), is a salicylate drug mostly used as an febrifuge to reduce fever, as an anti-inflammatory medication to reduce swelling, and as an analgesic to alleviate minor pains and aches. To wit, aspirin is often used to relieve whacky to moderate pain and to reduce fever from typical maladies such as headaches, toothaches, muscle aches, and the common cold.This medication may also be used to reduce arthritic swelling and pain as well. This salicytate drug is classified as a nonsteroidal anti-inflammatory drug or NSAID, and it works by blocking a certain natural substance in your body to reduce inflammation and throbbing aches.Structure of AspirinAspirin, also known as acetylsalicylic acid, has a chemical formula of C9H8O4.Working mechanism of aspirin-Many kinds of prostaglandin exist in the body to serve a plethora of physiological functions, some of which are irritable, others beneficial. Prostaglandins are among the chemicals secreted by the bodysimmune system when it fights off bacteria and other invaders in injuries. Located around wounds , these chemicals cause pain and inflammation. Following bacterial infection, prostaglandins are also produced the hypothalamus, the brains center for controlling body temperature, resulting in a rise in temperature. In their capacities to cause pain, inflammation, and fever, prostaglandins are nuisances. Inhibiting their production, consequently reducing pain, inflammation, and fever, is the main healthful value of aspirin.On the other hand, prostaglandins secreted by the stand out regulate acid production and maintain the mucous secretion lining that protects the stomach from digesting itself. Prostaglandins in the bloods platelets cause the platelets to beat out together to initiate blood clotting in wounds. In these capacities, prostaglandins are crucial to a healthy body. Inhibiting their production leads to aspirins undesirable side effects, including upset stomach and excessive bleeding.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.Enzymes are protein catalysts that speed up chemical reactions without being themselves used up in the reactions. An enzym e 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 tamper 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.Vanes success attracted many researchers to the area. Their investigations spread from aspirin to similar drugs that suppress pain and inflammation. By 1974, it was fairly well established that all NSAIDs act with similar mechanisms. They are all COX inhibitors.Aspirin, ibuprofen, naproxen, and many other non-steroidal anti-inflammatory drugs (NSAIDs) work as COX inh ibitors. They suppress the catalytic functions of the enzymes COX1 and COX2. COX2, which appears up injuries and other inflammatory stimuli, is deemed bad. It catalyzes the synthesis of prostaglandins that, located near sites of injuries, cause pain and inflammation. Inhibition of COX2 is responsible for the therapeutic effects of reducing pain, inflammation, and fever. COX1, which is present in many parts of the body, is deemed good. It catalyzes the synthesis of prostaglandins that perform many physiological functions, e.g., maintaining the mucus lining of the stomach or causing platelets in the blood to stick and form clots over wounds. Inhibition of COX1 is responsible for the drugs side effect of stomach irritation. In reducing the risk of blood clots, it is also responsible for aspirins efficacy in heart attack prevention. A new class of NSAID, COX2 inhibitor, is designed to target bad COX2 selectively and leave good COX1 alone, thus reducing pain and inflammation without upse tting the stomach.4-local anestheticCocaine is a naturally occurring compound indigenous to the AndesMountains, western hemisphere Indies, and Java. It was the first anesthetic to be discovered and is the only naturally occurring local anesthetic all others are synthetically derived. Cocainewas introduced into Europe in the 1800s pursuance its isolation from coca beans. Sigmund Freud, the noted Austrian psychoanalyst, used cocaine on his patients and became addicted through self-experimentation.In the latter half of the 1800s, interest in the drug became widespread, and many of cocaines pharmacologic actions and adverse effects were elucidated during this time. In the 1880s, Koller introduced cocaine to the field of ophthalmology, and Hall introduced it to dentistry. Halsted was the first to report the use of cocaine for facial expression blocks in the unify States in 1885 and also became addicted to the drug through self-experimentation.Procaine, the first synthetic derivative o f cocaine, was developed in 1904. Lofgren later developed lidocaine, the most widely used cocaine derivative, during World War II in 1943.Chemical structureAll local anesthetics have an intermediate chain linking an amine on one end to an aromatic ring on the other. The amine end is hydrophilic, and the aromatic end is lipophilic. Variation of the amine or aromatic ends changes the chemical activity of the drug.Two basic classes of local anesthetics exist, the amino amides and the amino esters. Amino amides have an amide link between the intermediate chain and the aromatic end, whereas amino esters have an ester link between the intermediate chain and the aromatic end.Amino esters and amino amides differ in several respects. Amino esters are metabolized in the plasma via pseudocholinesterases, whereas amino amides are metabolized in the liver. Amino esters are unstable in solution, but amino amides are very stable in solution. Amino esters are much more likely than amino amides to c auseallergic hypersensitivity reactions.Commonly used amino amides include lidocaine, mepivacaine, prilocaine, bupivacaine, etidocaine, and ropivacaine and levobupivacaine. Commonly used amino esters include cocaine, procaine, tetracaine,chloroprocaine,and benzocaine. An easy way to remember which drug belongs in which category is that all of the amino amides contain the letter i twice, as does the term amino amides.The newest additions to clinically available local anesthetics, namely ropivacaine and levobupivacaine, represent exploitation of the S enantiomer of these chemicals to create anesthetics which are less toxic, more potent, and longer acting.WORKINGLocal anesthetics produce anesthesia by inhibiting excitation of nerve endings or by blocking conduction in peripheral nerves. This is achieved by anesthetics reversibly binding to and inactivating sodium occupations. Sodium influx through these channels is necessity for the depolarization of nerve cell membranes and subseque nt propagation of impulses along the course of the nerve. When a nerve loses depolarization and capacity to propagate an impulse, the individual loses sensation in the area supplied by the nerve.The order of affinity of local anesthetics for different sodium channel states is open is better than inactivated, which is better than resting.Thus, theopen state of the sodium channel is the primary target of local anesthetic molecules.The blocking of propagated action potentials is therefore a function of the frequency of depolarization. The mechanism for differential block, the block of pain experience without motor block, isstill unclear.*