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Tuesday, September 6

  1. page home edited ... FUCKING GAYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY…

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    FUCKING GAYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY #betterthanAnzBank#PoddleCorp #Givebackher
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Monday, September 5

  1. page home edited ... FUCKING GAYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY…

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    FUCKING GAYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY #betterthanlockie#betterthanAnzBank
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Sunday, September 4

  1. page ibuprofen edited David Sungwoo Son HEY GUYS ITS YA BOY TMARTN HERE SUB TO MY CHANNEL PLEASE https://www.youtube.…

    David Sungwoo Son HEY GUYS ITS YA BOY TMARTN HERE SUB TO MY CHANNEL PLEASE
    https://www.youtube.com/user/Matroix THANKS <3
    hi im rick harrision and this is my pawn shop
    Ibuprofen is well known drug that possesses pain-relieving and fever-reducing properties. Ibuprofen is Non-steroidalanti-inflammatory drug (NSAID). It relieves aches and pains due to headache, toothache, backache, menstrualcramps, cold, muscular aches, and minor pain of arthritis from most of peoplein the earth today. It is enough to saythat the Ibuprofen is the most famous drug in the world now. Its IUPAC name is (R&S)-2-2(4-(2-methylpropyl)phenyl)propanoicacid). Chemical formula is C_13 H_18 O_2. Molar mass is 206.29g/mol. And its melting point is 76 °C. Here is the synthesis structure of the Ibuprofen (1).
    {ibuprofensynthesis.gif}
    Ibuprofen was discovered by Dr. Stewart Adamsand Boots Group in the United Kingdom in 1950s, parented in 1961. It becameavailable in the United States in 1974 (2). The founder Stewart Adams won the OBE, andthe Boots Group won the Queen’s Award
    ill suck your penis for Technical Achievement due to their development of the Ibuprofen. The Bootsgroup licensed Ibuprofen to two large drug companies; Whitehall Laboratoriesfor ‘Advil’ and Upjohn who used Bristol-Meyers to market their product ‘Nuprin’ (3). After all, the Ibuprofen has been existed somany different names and different places. This is the timeline of Ibuprofen's history.
    1955 The discovery is madethat anti-inflammatory drugs reduce inflammation of the skin caused byultra-violet light. This gives a simple screening test for new chemical compounds(called new chemical entities or NCEs in the jargon) that the research chemists produced.
    1961 A patent (see Figure 7)is filed for the compound 2-(4-isobutylphenyl) propanoic acid - later calledibuprofen.
    1964 Ibuprofen is selectedfor further development.
    1966 Clinical trials ofibuprofen take place at the Northern General Hospital in Edinburgh and show itsanti-inflammatory effect in patients.
    1969 Ibuprofen is launchedin the UK on prescription only.
    1974 it became available in United States.
    1983 Because of its safetyrecord, ibuprofen is made available without prescription.
    Ibuprofen relieves human’s pain asworking to inhibit human’s enzyme for mediator of pain. The clinical effects of Ibuprofen (NSAID) arebased on the inhibition of the enzyme cyclooxygenase (COX), which catalyses therate limiting step in the formation of prostanoids, prostaglandins (PGs) andthromboxane A2 (TxA2). The production ofPGs is induced at sites of inflammations where they are involved in propagationof inflammation, pain and fever. Inhibition of PGs production alleviates most of the pathologic effects associated with inflammation (4). Prostaglandinshave both positive and negative effects in the body. Prostaglandins are, forexample, protective against the development of stomach ulcers, but they canalso mediate inflammation (as well as the pain response). There are more than one kind of enzymes inhuman body. This is important tounderstand of the therapeutic effects of ibuprofen. COX-1 is present at near constant levels inthe body under all conditions (that is, it is a constitutive enzyme), whereasthe levels of COX-2 could increase in response to inflammatory conditions(i.e., it is an inducible enzyme). Thisled to the idea that the side effects of ibuprofen and aspirin (includingstomach ulcers) probably arose from inhibition of the constitutive COX-1enzyme, whereas the therapeutic benefits arose from inhibition of the inducibleCOX-2 enzyme.
    Ibuprofeninhibits COX-1 and COX-2. Ibuprofen binds non-covalently to a COX enzyme andthus competes with the enzyme's natural substrate. (This is referred to asreversible inhibition). However,Acetaminophen AKA the Advil’s biggest rival ‘Tylenol’ does not interact witheither COX-1 or COX-2, but it is now understood that it may interact with anewly identified cyclooxygenase, COX-3 (5).
    Ibuprofen contains a chiral centerand is employed therapeutically as a racemic mixture. However, without few exceptions, theS-enantiomer is better for human body’s metabolism since it’s primarilyresponsible for the inhibition of cyclooxygenase activity (COX) (6).
    Ibuprofen overdose is associatedwith either asymptomatic or mildly symptomatic presentation to the emergencydepartment. Mild gastrointestinal upsetor mild central nervous system depression may occur (7). However, serious complications can develop tothe patient ingests a large amount of the drug. This patient took 90 800-mg ibuprofen in order to commit suicide. He had 38 hours of blood vomiting, feeling ‘veryill’ and severe skin dryness. This case demonstrates that serious toxicity can occur by ibuprofen overdose (8). It also demonstrates why you should consider a safer alternative with no side effects, for example serrapeptase is a natural enzyme which helps remove inflammation.
    References
    1) http://www.advil.com/OurProducts/Advil.aspx
    2) International Ibuprofen Foundation. "The History ofIbuprofen." Available from http://www.ibuprofen-foundation.com/history.htm.
    3) http://ibuprofendrug.com/ibuprofen-history
    4) Synthesis of ibuprofen heterocyclic amides and investigation oftheir analgesic and toxicological properties, European Journal of Medicinal Chemistry, Volume 38, Issue 5, May2003, Pages 513-518 Maria Teresa Cocco, Cenzo Congiu, ValentinaOnnis, Micaela Morelli, Omar Cauli
    5) Flower, Rod J. (2003). "The Development of Cox 2Inhibitors." Nature Reviews Drug Discovery 2(3):179–191.
    6) Regioselective and stereoselective metabolism of ibuprofen by humancytochrome, Biochemical Pharmacology,Volume 54, Issue 1, 1 July 1997, Pages 33-41Mitchell A. Hamman, Gary A. Thompson, Stephen D. Hall
    7) Ibuprofen overdose presenting with severe agitation and hypothermia, The American Journal of Emergency Medicine, Volume 16, Issue 5, September1998, Pages 549-550, Albert Ritter, Barnet Eskin
    8) Ibuprofen overdose, The American Journal of Emergency Medicine, Volume13, Issue 3, May 1995, Page 375, Timothy R. Wolfe
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  2. page ibuprofen edited ... David Sungwoo Son HEY GUYS ITS YA BOY TMARTN HERE SUB TO MY CHANNEL PLEASE https://www.youtub…
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    David Sungwoo Son HEY GUYS ITS YA BOY TMARTN HERE SUB TO MY CHANNEL PLEASE
    https://www.youtube.com/user/Matroix THANKS <3
    hi im rick harrision and this is my pawn shop
    Ibuprofen is well known drug that possesses pain-relieving and fever-reducing properties. Ibuprofen is Non-steroidalanti-inflammatory drug (NSAID). It relieves aches and pains due to headache, toothache, backache, menstrualcramps, cold, muscular aches, and minor pain of arthritis from most of peoplein the earth today. It is enough to saythat the Ibuprofen is the most famous drug in the world now. Its IUPAC name is (R&S)-2-2(4-(2-methylpropyl)phenyl)propanoicacid). Chemical formula is C_13 H_18 O_2. Molar mass is 206.29g/mol. And its melting point is 76 °C. Here is the synthesis structure of the Ibuprofen (1).
    {ibuprofensynthesis.gif}
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  3. page ibuprofen edited David David Sungwoo Son HEY GUYS ITS YA BOY TMARTN HERE SUB TO MY CHANNEL PLEASE https://www…
    David
    David
    Sungwoo Son HEY GUYS ITS YA BOY TMARTN HERE SUB TO MY CHANNEL PLEASE
    https://www.youtube.com/user/Matroix THANKS <3

    Ibuprofen is well known drug that possesses pain-relieving and fever-reducing properties. Ibuprofen is Non-steroidalanti-inflammatory drug (NSAID). It relieves aches and pains due to headache, toothache, backache, menstrualcramps, cold, muscular aches, and minor pain of arthritis from most of peoplein the earth today. It is enough to saythat the Ibuprofen is the most famous drug in the world now. Its IUPAC name is (R&S)-2-2(4-(2-methylpropyl)phenyl)propanoicacid). Chemical formula is C_13 H_18 O_2. Molar mass is 206.29g/mol. And its melting point is 76 °C. Here is the synthesis structure of the Ibuprofen (1).
    {ibuprofensynthesis.gif}
    (view changes)
  4. page _intro edited This project was created by a Chem 263 organic chemistry III class at Bellevue College in Spring 2…
    This project was created by a Chem 263 organic chemistry III class at Bellevue College in Spring 2011.
    I would like to thank the students for their contributions! Some of the themes observed:
    1) Serendipity in science - a little luck goes a long way! (Nylon, penicillin)
    2) Molecular structure influences its physical and chemical properties, especially in the human body. Thus, structure is closely linked to function. Molecules similar in structure can mimic each other and function in the same way. Altering molecular structure leads to different functions. (Genistein, prednisone, allopurinol)
    3) Though our understanding of chemistry is extensive, it is still a very complex science and there is plenty of room for more study and more discoveries!
    Do you have any insights to add? Please do so here:
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  5. page serotonin edited Serotonin Nikki Johal | Chemistry 263 | Spring 2011| Bellevue College Serotonin (Figure 1), 5-h…
    Serotonin
    Nikki Johal | Chemistry 263 | Spring 2011| Bellevue College
    Serotonin (Figure 1), 5-hydroxytryptamine (5-HT), is a molecule used by certain neurons as a neurotransmitter, classified in general as a monoamine, which have a chemical template comprised of a basic amino group separated from an aromatic nucleus by a two carbon aliphatic chain (1).
    {serotonin.png}
    Figure 1. Structure of Serotonin.
    Mechanism and Biosynthesis
    Serotonin is biosynthetically derived by two steps, the first being the ring hydroxylation of the essential amino acid tryptophan by tryptophan hydroxylase, which is also the rate limiting step and second step is the side chain decarboxylation by aromatic amino acid decarboxylase (Figure 2).
    {serotonin2.png}
    Figure 2. Mechanism for derivation of serotonin from tryptophan.
    Serotonin, is found in many places in the mammalian body including the heart, brain, and throughout the cardiovascular system. However, it is primarily found in the gastrointestinal tract, where it controls digestion and intestinal functions. However, serotonin derives most of its attention in the human body from its functionality as a neurotransmitter in the brain (4). This is particularly because of its involvement in major mood and psychiatric disorders such as depression, obsessive compulsive disorder, and panic and anxiety disorders. Serotonin deficiency is one of the leading causes of psychiatric disorders to date such as, anxiety, depression, panic attacks, obesity, insomnia, eating disorders, chronic pain, migraines, alcohol abuse, and fibromyalgia. The World Health Organization, claims that as many as 121 million people are facing depression at the hands of serotonin deficiency. This is due to serotonin’s effect as a neurotransmitter that regulates emotional functions of the brain (6). This is evidenced by the attribution of negative thoughts, low self-esteem, obsessive thoughts and behaviors, and premenstrual syndrome as symptoms of low serotonin levels in the brain. Serotonin deficiency is usually caused by low brain cell production of serotonin; an overworked, stressed, or impaired immune system; brain damage; or a combination of the above factors. Pharmaceuticals have taken advantage of serotonin’s increased application in psychology, and have opened up a new area of drug research and production involving Selective Serotonin Reuptake Inhibitors (SSRIs) (5). These drugs work selectively on serotonin, but do not interfere with the functionality of other neurotransmitters or chemical processes within the brain. This is because SSRIs do not actually increase the production of serotonin in the brain. Rather, SSRI molecules insert themselves in serotonin receptors between neuron synapses, blocking the rather quick reabsorption of serotonin molecles by neurons (3). This keeps serotonin levels in the brain higher. However, these drugs have also borne new health conditions, the most well-known to be Serotonin Syndrome, or hyperserotonemia. This condition is a potentially life-threatening drug reaction to too much serotonin in the body, and usually occurs when two drugs that affect serotonin levels in the body such as SSRIs are taken together at the same time (7).
    References
    Hernandez-Rodriguez, J., & Chagoya G. 1985. Brain Serotonin Synthesis and Na+, K+-ATPase Activity are Increased Postnatally after Prenatal Administration of L-Tryptophan. Developmental Brain Research. 25, 221-226.
    Schaechter, J.D., & Wurtman R.J. 1990. Serotonin release varies with brain tryptophan levels. Brain Research. 532, 203-210.
    Kalat, James W. Biological Psychology. Belmont, CA: Wadsworth, Cengage Learning, 2009. Print.
    Voet, D, G., J, & W., C. (2007). Principles of biochemistry. Egully.com.
    Baumel, S. (1999). Serotonin. Keats Pub
    Vanhoutte, Paul M. Serotonin: from Cell Biology to Pharmacology and Therapeutics. Dordrecht: Kluwer Academic, 1993. Print
    C., J, & Monte, T. (1998). Natural prozac: learning to release your body's own anti-depressants. HarperOne.
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  6. page epinephrine edited |===[Epinephrine]==------- By Joseph S. Medina | Bellevue College | Chemistry 263 | Jennie Mayer …
    |===[Epinephrine]==-------
    By Joseph S. Medina | Bellevue College | Chemistry 263 | Jennie Mayer | Spring 2011
    EPI- WHAT?
    Sometimes I'd like to think myself as an "adrenaline junkie". My adrenaline addiction was derived from an experience at only the ripe age of seven years-old. A tranquil day for an elementary student bicycle-riding through the skirts of the enchanting neighborhood back roads. Serene was the first thought until my eyes met with an angry feral doberman pinscher. Instantaneously, like a slap to my fragile, little heart, I realized this wild beast wanted me for lunch. The sight of his salivating chewers and evil beady eyes made me bike faster than I had ever biked before. Fortunately for adrenaline like a kick in the rear end, I avoided becoming rare meat at the doghouse. Epinephrine is a hormone/neurotransmitter belonging to a group of biogenic amines called catecholamines. It is the key to the short-term reaction, the “fight-or-flight response”, that occurs in conjunction with the activation of the sympathetic nervous system.1 In short, the "fight-or-flight response" is a biological innate system that allows us to respond quickly and effectively to stressful or threatening situations so that we may adapt to survive. Epinephrine, commonly known as adrenaline, facilitates the massive increase of glucose into the bloodstream from liver and muscle tissue. Glucose is the staple energy fuel for our bodies, hence the term “adrenaline rush”, which is essentially a rush of energy. Massive amounts of glucose were released into my pedaling leg muscles quickly turning them into something like pinwheels caught in a 100 MPH twister. Epinephrine is only produced in the adrenal glands of the kidney. The energy rush you feel can be contributed to an increase in rate and force of contraction at the heart, arterial blood pressure, pulse rate, and oxygen consumption (metabolic functions).2 Epinephrine also relaxes smooth muscle, which opens blood vessels- thus increasing blood delivery to targeted tissues (a vasodilator). 1 The release of epinephrine into the bloodstream becomes an efficient powerhouse that only gets faster, strong, and better. One research group conducted an experiment to determine how the body responds to epinephrine. Subjects received injections of saline solution or epinephrine. The data results (Figure 1) showed that subjects had a substantial increase in free fatty-acid and glucose concentration in blood as opposed to the control group that received only saline solution. The data confirmed the increases in pulse rate, blood pressure, and oxygen consumption by the brain. 3
    {photo.JPG}
    Figure 1. What Effect Does Epinephrine Have on the Body? Each data point on the graphs represents a human volunteer. The data in the table are average values from seven volunteers.
    BIO-SYNTHESIZE THIS!
    Epinephrine is bio-synthesized from the amino acid, tyrosine. The hydroxylation of tyrosine forms an intermediate called, L-DOPA., which has two adjacent OH groups on the aromatic ring. By decarboxylation this of this intermediate, dopamine, is formed. Oxidation of dopamine gives way to norepinephrine and then alkylation, specifically, methylation finally gives our favorite product, epinephrine. The molecules, norepinephrine, epinephrine, and dopamine make up the family catecholamines (amines from the adrenal glands). Biosynthesis map below:
    {400px-Catecholamines_biosynthesis.svg.png}
    @ THE HOT ZONE: SITE OF BIOLOGICAL ACTION
    To understand what happens at the cellular level when the body is under stress, we must follow the molecule to the epinephrine receptors known as beta-adrenergic receptors (Figure 2). When epinephrine reaches these receptors at muscle and liver tissue, the ligand binding causes a conformation change in the receptor to allow interaction with a triomeric Gs protein (consisting of subunit proteins alpha, beta, and gamma). This receptor-protein interaction allows GDP to be traded for GTP to allow the alpha subunit of the Gs protein to bind to a near-by adenylate cyclase. Here, the binded alpha subunit activates the enzyme to facilitate the conversion of ATP to cyclic adenosine monophosphate, cAMP. This important molecule, is a second-messenger that increases in concentration to activate a signal transduction cascade of complex enzymatic reactions that amplifies the effect of the hormone. The key to the cascade of these enzymatic reactions is phosphorylation. These enzymes, known as kinases, place a phosphate group at specific sites of proteins or enzymes. The end results of these reactions is an enzyme that breaks down glycogen that is stored in liver and muscle tissue and converts it to a mass production of glucose. 1, 4
    {1424.jpg} Figure 2.
    (Left) An image showing basic molecular action when epinephrine reaches its target receptor, beta-adrenergic receptor.
    VIDEO
    An animation (with sound) of the biological action behind epinephrine to beta receptors.
    Epinephrine also plays an important secondary role. The hormone through its interaction with second messenger cAMP, prevents dephosphorylating of an enzyme that the first enzyme in fatty acid synthesis, acetyl-coenzyme A. By preventing the desphorylated enzyme, it is inactive and synthesis of fatty acids is stopped. This is significant since when under stress, the body can concentrate its mass production of glucose for energy rather than the competition of storing the energy as glycogen or fat. 1
    A QUICK SIDE-NOTE
    Ligand binding of epinephrine is non-selective, meaning that when epinephrine reaches its receptors it does not choose who it may bind with: it binds to both alpha-adrenergic receptors and beta-adrenergic receptors. However, epinephrine primarily binds to beta-adrenergic receptors and norepinephrine primarily binds to alpha-adrenergic receptors (Figure 2). Both work in conjunction to implement both vasodilation and vasoconstriction on specific body organs and tissue. The predominant effect of epinephrine is the binding on beta receptors to increase heart rate and force of contraction at the heart. Some of the effects of epinephrine is vasoconstriction on blood vessels in the bronchials via alpha-adrenergic receptors and relaxation of smooth muscles of the GI tract. Essentially the idea is that epinephrine has a variety of effects on each bodily organ and contraction and dilation of certain tissues is important to provide the most efficient use of energy during times of stress. 6
    A LIFE SAVER ON DECK- CLINICAL USAGE
    Clinically, epinephrine has been the big hitter in emergency and life-threatening situations for some time. When a patient’s heart has reached a dead-stop such as in the case of cardiac arrest, its immediate and substantial effects of increasing heart rate and force of contraction proves to save many lives everyday. Epinephrine binding to beta receptors allows an increase in cardiac output. During anaphylactic shock, which can happen especially during ingestion of allergens causes a tightening of bronchial tissue leaving the patient difficulty or the complete inability to breathe. Epinephrine's vasodilation effects can relax smooth muscle and open the airway allowing the patient to breathe normally again. 4 Many studies have also confirmed that epinephrine is effective for treating children with croup, a severe cough that can lead to major swelling inside the throat. Treatment with epinephrine is only used severe cases and rarely administered. The racemate epinephrine was found effective in treating croup, but a research group found that its active form, L-epinephrine was significantly more effective in treating croup than its racemic version.5 Epinephrine is also used effectively with local anesthesia by restricting blood vessels; Locally by restricting the blood vessels at the target site, epinephrine can retard the absorption of the anesthetic and prolong its effects. 5
    CONCLUSION
    Without a doubt, epinephrine is one of the most essential molecules in our bodies. Simply put, it has and continues to help us survive evolutionarily whether it meant running away from a sabretooth tiger in the Eocene Epoch or winning your 100-meter dash to the finish line today. It induces a multitude of physiological effects that are advantageous to any stressful situation by preparing the body in a perfect harmony of energetic processes. Since its laboratory synthesis, epinephrine has dramatically changed the medical field due to its vasoconstrictive effects to treat an array of conditions usually involving a debilitating inflammatory effect of functional tissue. Although other chemicals have been synthesized that prove to have much longer effects for treating medical conditions, we cannot discredit its prototypical and natural ability to save us just when we need it to. There is an appreciated value of the synthesized molecule by those patients in the emergency room who accidentally ate that tantalizing cookie with hidden nuts or even an appreciated value of the naturally produced epinephrine by a seven year-old boy who just needed enough time to outrun that little nasty doberman demon to live at least one more elementary day.
    REFERENCES
    1. Bering Larry C. 2011. Epinephrine. [online]. Available from: http://www.chemistryexplained.com/Di-Fa/Epinephrine.html
    2. Bowen, A. 1998 Adrenal Medullary Hormone. [online]. Available from : http://www.vivo.colostate.edu/hbooks/pathphys/endocrine/adrenal/medhormones.html
    3. Freeman, S. Biological Science. 8th Edition. Prentice Hall; 2008.
    4. Ophardt, C. 2003. Adrenergic Drugs I. [online]. Available from: http://www.elmhurst.edu/~chm/vchembook/663adrenergic.html
    5. Bjornson, C., Rusell, KF.. Nebulized epinephrine for Croup in Children. COCHRANE DATABASE OF SYSTEMATIC REVIEWS. 2011. VOLUME 2 ARTICLE
    CD006619. Available from ISI Web of Knowledge.
    6. Klabunde, R. 2008. CV Physiology: Circulating Catecholamines. [online]. Available from: http://www.cvphysiology.com/Blood%20Pressure/BP018.htm
    7. DeBehke D. MD. Use of Cardiopulmonary Bypass, High-Dose Epinephrine, and Standard-Dose Epinephrine in Resuscitation From Post-Countershock Electromechanical Dissociation. Annals of Emergency Medicine. 1992. VOLUME 21 ISSUE 9: 1051-1057. Available from: Science Direct
    8. Harrison K. 2007. Norepinephrine. [online]. Available from: http://www.3dchem.com/molecules.asp?ID=288
    9. Southwick S. Role of Norepinephrine in the Pathophysiology and Treatment of Posttraumatic Stress Disorder. BIOL PSYCHIATRY. 1999. VOL 46: 1192-1204. Available from: ScienceDirect
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  7. page dextromethorphan edited ... No. Thanks for reading! fuck off now
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    Thanks for reading!
    fuck off now
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  8. page vitamin_c edited Vitamin C Between the 1500’s and 1700’s many people, especially sailors and explorers, were dying…
    Vitamin C
    Between the 1500’s and 1700’s many people, especially sailors and explorers, were dying of a disease called scurvy. Scurvy causes spots on the skin, spongy gums and bleeding of mucous membranes. It wasn’t until 1742 that James Lind, a British doctor, noticed a correlation between diet and scurvy. He noticed that people who had diets rich in fruits and vegetables did not get scurvy and so he gave lemon juice to those who were diagnosed with scurvy and sure enough they were cured; he was the first to notice that there was something in the citrus fruit that cured scurvy. It wasn’t until later that scientists found that the cause of scurvy was a deficiency in Vitamin C1. Two British chemists Sir Walter Norman Haworth and Sir Edmund Hirst were the first scientists to synthesize Vitamin C in 1934. It has a chemical formula of C6H8O6 and a molecular mass of 176.14g/mol. Vitamin C is only the L-enantiomer of ascorbate, the D-enantiomer has no effect in our bodies2.
    Vitamin C, also known as ascorbic acid, has many vital roles in the human body. It assists in the synthesis of norepinephrine, a neurotransmitter, as well as in the synthesis of carnitine, a molecule that is needed to transport fat to the mitochondria that is then converted to energy1. Vitamin C plays a major role in collagen synthesis. Collagen is the main component in connective tissue that makes up tendons, ligaments, skin, cartilage and much more. Vitamin C is a reducing agent and is able to maintain ferrous iron in the reduced form. The reduced ferrous iron is necessary for collagen biosynthesis. In the immune system, vitamin C influences the function and production of leukocytes, more specifically, neutrophils, lymphocytes and phagocytes which all play an important role in defending the body from infectious disease and foreign materials. Vitamin C also speeds up T-cell production in response to infection as well as blocking the pathway that leads to apoptosis of T-cells. In short, vitamin C enhances the immune response1,2.
    Vitamin C is probably most known for its antioxidant properties. Vitamin C is a water-soluble antioxidant. Free radicals are molecules that are highly reactive because they contain an unpaired electron that will react with anything to get its pair back. There are three steps; the initiation step is where the free radical is formed. The problem with free radicals is that when the free radical reacts with another molecule, that molecule will turn into a free radical itself causing a chain reaction, which makes up the second step that is called propagation. The third step, termination, is when two free radicals react with each other. When free radicals react with living cells, it can cause damage or death of the cell. Vitamin C comes into play because it can stop the free radical chain reaction. Because of this trait, vitamin C is thought to have anti-aging and anti-cancer effects. It also helps prevent against atherosclerosis. This is a condition where the build of cholesterol and plaque causes the artery wall to thicken which can lead to heart attack, stroke and cardiovascular disease3.
    The biosynthetic pathway is as follows, D-glucuronate (formed from glucose) is converted to L-gluconate and then to L-gulono-gamma-lactone, which in turn is further reduced (via L-xylo-hexulonolactone) to L-ascorbic acid (2-oxo-L-gulono-gamm-lactone). The final enzymatic step is catalyzed by L-gulonolactone oxidase. However, humans as well as some other primates, some bats, birds, insects, fish and guinea pigs do not have the enzyme, L-gulonolactone oxidase, which means our bodies cannot synthesize vitamin c, we must ingest it1.
    Vitamin C is found in red berries, kiwi, red and green bell peppers, tomatoes, broccoli, spinach, guava, papaya, orange, strawberries and citrus fruits5.
    Luckily, overdose of vitamin c is rare because any excess is usually expelled through the urine. However, some common side effects are diarrhea, nausea, abdominal cramps and other gastrointestinal disturbances.
    1. Hughes, R. . (n.d.). Iv .a.3. - vitamin c. Retrieved from http://www.cambridge.org/us/books/kiple/vitaminc.htm [[#_ftn1|[1]]]
    2. Vitamin c. (n.d.). Retrieved from http://www.worldofmolecules.com/antioxidants/vitaminc.htm
    3. Vitamin c. Unpublished manuscript, Linus Pauling Institute, Oregon State University, Corvallis, Oregon. Retrieved from http://lpi.oregonstate.edu/infocenter/vitamins/vitaminC/
    4. Evans, W. (2000). Vitamin e, vitamin c, and exercise. The American Journal of Clinical Nutrition, 71. Retrieved from http://www.ajcn.org/content/72/2/647S.full
    5. Levine, M. (2006). Intravenously administered vitamin c as cancer therapy: three cases. CMAJ, Retrieved from http://www.cmaj.ca/cgi/content/full/174/7/937
    6. Naidu, A. (2003). Vitamin c in human health and disease is still a mystery?. Nutritional Journal , 2(7), Retrieved from http://www.nutritionj.com/content/2/1/7
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