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Overheads for Section 3 A brief interlude on digestion Overview of digestion More digestion facts Overview of biochemical pathways Chapter 14  Glycolysis The glycolytic pathway Another view of the glycolytic pathway The test version Details of one individual reaction step Enzyme compexes facilitate channeling The energy landscape of glycolysis The "metabolic" regulation of glycolysis Glycolytic addenda Other carboyhdrates are funneled into the glycolytic path Use of galactose The fates of pyruvate Gluconeogenesis Gluconeogenesis­b Pyr to PEP Two other bypasses Gluconeogenesis and mitochondria The Pentose pathway Alternative views of the Pentose pathway Chapter 15 The role of glycogen phosphorylase The mechanism of GP The breakdown of glycogen Transporting glucose to the blood Activating glucose for synthesis The synthesis of glycogen Regulation of GP  The alloseric regulation of    PFK Coordinate regulation of PFK and FBP The role of F2,6BP Pyruvate Kinase is regulated Coordinate regulation of glycolysis/gluconeogenesis Hormonal influence on glucose metabolism Glycogen synthase is regulated by hormones Synthesis and hydrolysis of F2,6BP More on PFK2 and FBPase2 Summary of hormone regulation in the liver Chapter 16 The TCA cycle in metabolism Some headlines in C-C chemistry C C bond reactions in biochemistry Enolate stabilization in carbon-carbon bonds TPP modifies α-keto acids for decarboxylation TPP and decarboxylation Back to Metabolism The PDC "linking step" PDC is a geometric complex Regulation of PDC Steps of the TCA cycle The test version Mech of citrate synthase, more C-C chem The energy profile of TCA Regulation of the TCA cycle Depletion of TCA intermediates The anaplerotic reactions Chemistry of pryuvate carboxylase The aerobic metabolism of glucose The glyoxylate cycle The glyoxylate shunt Linking TCA and glyoxylate shunt Chapter 17 Lipids from ingestion, storage, or synthesis Fat uptake Lipid mobilization Chylomicrons Lipids released from adipocytes Post lipase chemistry Carnitine mediated transport Beta-oxidation: the big picture Beta-oxidation:detailed chemistry Energy production from ox. of palmitoyl CoA β-ox of oleic acid β-ox of poly unsaturates β-ox of odd numbered fatty acids Peroxisomes in eucaryotes Branched lipids can undergo α Oxidation Synthesis of ketone bodies Use of ketone bodies Ketone bodies in metabolism Chapter 19 The mitochondrion Electron carriers in ETS Overview of ETS ETS complex 1 ETS complex 3 ETS complex 4 The Redox Table Redox example from complex 1 Proton Motive Force The Chemiosmotic theory Some experimental support Motive force of NADH in the ETS The energetics of ATP synthesis The mechanism of ATP synthase ATP synthase in action A movie of the synthase from the side A movie of the synthase from the top A movie of the whole synthesis model Nucleotide translocation The glycerol phosphate shuttle for cytoplasmic NADH The malate-aspartate shuttle Thermogenin and heat Photosynthesis Our Friend, Mr. Sun Photo pigments Harvesting the light spectrum Light harvesting machinery Exciton capture Bacterial photosystems are simple Structure of a bacterial photosystem The "Z" scheme of higher plants Membrane organization of PS Creating a proton gradient The Mn water splitter The energetics of photosynthesis Comparison of mitochondrion and chloroplasts The simplest light pump Photosynthesis - Dark Reacton Headlines Rubisco fixes CO2 The Calvin Cycle Giant Catabolic Roundup catabolic roundup The Cori Cycle Animals can synthesize glucose 6-phosphate via gluconeogenesis just like all other species. However, unlike most species, animals can convert glucose 6-phosphate to glucose, which is secreted into the circulatory system. Mammals, in particular, have a sophisticated cycle of secretion and uptake of glucose. It's called the Cori cycle after the Nobel Laureates: Carl Ferdinand Cori and Gerty Theresa Cori. The glucose 6-phosphate molecules synthesized in the liver can either be converted to glycogen [Glycogen Synthesis] or converted to glucose and secreted into the blood stream. The glucose molecules are taken up by muscle cells where they can be stored as glucogen. During strenuous exercise the glycogen is broken down to glucose 6-phosphate [Glycogen Degradation] and oxdized via the glycolysis pathway. This pathway yields ATP that is used in muscle contraction. If oxygen is limiting, the end product of glucose breakdown isn't CO2 but lactate. Lactate is secreted into the blood stream where it is taken up by the liver and converted to pyruvate by the enzyme lactate dehydrogenase. Pyruvate is the substrate for gluconeogenesis. The synthesis of glucose in the liver requires energy in the form of ATP and this energy is supplied by a variety of sources. The breakdown of fatty acids is the source shown in the figure. The Cori cycle preserves carbon atoms. The six carbon molecule, glucose, is split into two 3-carbon molecules (lactate) that are then converted to another 3-carbon molecule (pyruvate). Two pyruvates are joined to make glucose. Production of biocellulose (bacterial cellulose) 1. Biocellulose Cellulose is the main component of plant cell wall. Some bacteria produce cellulose (celled biocellulose or bacterial cellulose). Plant cellulose and bacterial cellulose have the same chemical structure, but different physical and chemical properties. Figure 1 shows an electron microscopic image of biocellulose and plant cellulose. Bacterial cellulose is produced by an acetic acid-producing bacterium, Acetobacter xylinum. The diameter of biocellulose is about 1/100 of that of plant cellulose and Young's modulus of biocellulose is almost equivalent to that of aluminum. Therefore, biocellulose is expected to be a new biodegradable biopolymer. Fig. 1. Bacterial cellulose and plant cellulose. 2. Production of biocellulose in an airlift reactor In the mass production of biocellulose, conventionally an agitated reactor is used. In our laboratory, we applied an airlift reactor to produce bacterial cellulose because this reactor is simple in structure, its energy requirement is low, its shear stress to cells is small, and the possibility of contamination is low. Figure 2 shows a 50-liter airlift reactor. In the airlift reactor, the productivity of bacterial cellulose was equivalent to that in conventional agitated reactors and its energy requirement was one-tenth of that in agitated reactors. The bacterial cellulose produced in an airlift reactor formed a unique pellet-type cellulose. Fig. 2. 50 liter airlift reactor. 3. Analysis of genes for biocellulose synthesis All genes responsible for biocellulose synthesis have been cloned and their characterization is under way. Figure 3 shows the predicted steps of bacterial cellulose synthesis when glucose is used as the carbon source. The analysis of genes will lead to higher productivity of bacterial cellulose and to new biocellulose with different properties. Fig. 3. The predicted pathway of cellulose synthesis and secretion when glucose is taken into Gluconacetobactor xylinum from the outside of the cell. 4. Future aspects Preservation of forest resources is essential to prevent global warming because the increase in CO 2 concentration can be stopped only by the absorption of CO2 by plants and trees. However, the use of trees for the production of paper and construction materials has continuously depleated forest resources. Bacterial cellulose is the only alternative for plant cellulose because bacteria produce bacterial cellulose in a few days, while trees need more than 30 years to realize full growth. In this respect, bacterial cellulose is the key material for preventing global warming and preservation of the nature. Metabolism of Major Non­Glucose Sugars Fructose Metabolism Diets containing large amounts of sucrose (a disaccharide of glucose and fructose) can utilize  the fructose as a major source of energy. The pathway to utilization of fructose differs in  muscle and liver. Muscle which contains only hexokinase can phosphorylate fructose to F6P which is a direct  glycolytic intermediate. In the liver which contains mostly glucokinase, which is specific for glucose as its substrate,  requires the function of additional enzymes to utilize fructose in glycolysis. Hepatic fructose is  phosphorylated on C­1 by fructokinase yielding fructose­1­phosphate (F1P). In liver the form  of aldolase that predominates (aldolase B) can utilize both F­1,6­BP and F1P as substrates.  Therefore, when presented with F1P the enzyme generates DHAP and glyceraldehyde. The  DHAP is converted, by triose phosphate isomerase, to G3P and enters glycolysis. The  glyceraldehyde can be phosphorylated to G3P by glyceraldehyde kinase or converted to  DHAP through the concerted actions of alcohol dehydrogenase, glycerol kinase and  glycerol phosphate dehydrogenase. Three inherited abnormalities in fructose metabolism have been identified. Essential  fructosuria is a benign metabolic disorder caused by the lack of fructokinase which is  normally present in the liver, pancreatic islets and kidney cortex. The fructosuria of this disease depends on the time and amount of fructose and sucrose intake. Since the disorder is  asymptomatic and harmless it may go undiagnosed. Hereditary fructose intolerance is a potentially lethal disorder resulting from a lack of aldolase  B which is normally present in the liver, small intestine and kidney cortex. The disorder is  characterized by severe hypoglycemia and vomiting following fructose intake. Prolonged intake of fructose by infants with this defect leads to vomiting, poor feeding, jaundice, hepatomegaly,  hemorrhage and eventually hepatic failure and death. The hypoglycemia that result following  fructose uptake is caused by fructose­1­phosphate inhibition of glycogenolysis, by interfering  with the phosphorylase reaction, and inhibition of gluconeogenesis at the deficient aldolase  step. Patients remain symptom free on a diet devoid of fructose and sucrose. Hereditary fructose­1,6­bisphosphatase deficiency results in severely impaired hepatic  gluconeogenesis and leads to episodes of hypoglycemia, apnea, hyperventillation, ketosis and lactic acidosis. These symptoms can take on a lethal course in neonates. Later in life episodes are triggered by fasting and febrile infections. Clinical Significance of Fructose Metabolism   Galactose Metabolism Galactose, which is metabolized from the milk sugar, lactose (a disaccharide of glucose and  galactose), enters glycolysis by its conversion to glucose­1­phosphate (G1P).  This occurs through a series of steps. First the galactose is phosphorylated by galactokinase  to yield galactose­1­phosphate. Epimerization of galactose­1­phosphate to G1P requires the  transfer of UDP from uridine diphosphoglucose (UDP­glucose) catalyzed by galactose­1­ phosphate uridyl transferase (official name: UDP­glucose­­hexose­1­phosphate   uridylyltransferase). This generates UDP­galactose and G1P. The UDP­galactose is  epimerized to UDP­glucose by UDP­galactose­4 epimerase (see reaction mechanism). The  UDP portion is exchanged for phosphate generating glucose­1­phosphate which then is  converted to G6P by phosphoglucose mutase. Galactose on the Web:   Metabolic Pathways of Biochemistry:  Galactose Pathway Clinical Significance of Galactose Metabolism Three inherited disorders of galactose metabolism have been delineated. Classic galactosemia is a major symptom of two enzyme defects.One results from loss of the enzyme galactose­1­ phosphate uridyl transferase.The second form of galactosemia results from a loss of  galactokinase. These two defects are manifest by a failure of neonates to thrive. Vomiting and  diarrhea occur following ingestion of milk, hence individuals are termed lactose intolerant.  Clinical findings of these disorders include impaired liver function (which if left untreated leads  to severe cirrhosis), elevated blood galactose, hypergalactosemia, hyperchloremic metabolic  acidosis, urinary galactitol excretion and hyperaminoaciduria. Unless controlled by exclusion of galactose from the diet, these galactosemias can go on to produce blindness and fatal liver  damage. Even on a galactose­restricted diet, transferase­deficient individuals exhibit urinary  galacitol excretion and persistently elevated erythrocyte galactose­1­phosphate levels.  Blindness is due to the conversion of circulating galactose to the sugar alcohol galacitol, by an  NADPH­dependent galactose reductase that is present in neural tissue and in the lens of the  eye. At normal circulating levels of galactose this enzyme activity causes no pathological  effects. However, a high concentration of galacitol in the lens causes osmotic swelling, with the resultant formation of cataracts and other symptoms. The principal treatment of these  disorders is to eliminate lactose from the diet. The third disorder of galactose metabolism result from a deficiency of UDP­galactose­4­ epimerase. Two different forms of this deficiency have been found. One is benign affecting  only red and white blood cells. The other affects multiple tissues and manifests symptoms  similar to the transferase deficiency. Treatment involves restriction of dietary galactose. Mannose Metabolism The digestion of many polysaccharides and glycoproteins yields mannose which is  phosphorylated by hexokinase to generate mannose­6­phosphate. Mannose­6­phosphate is  converted to fructose­6­phosphate, by the enzyme phosphomannose isomerase,  and then  enters the glycolytic pathway or is converted to glucose­6­phosphate by the gluconeogenic  pathway of hepatocytes. In eukaryotes,mannose  is constituent of N­ and O­linked glycans as well as GPI anchors.  GDP­mannose  is the donor form of mannose. Glycerol Metabolism The predominant source of glycerol is adipose tissue. This molecule is the backbone for the  triacylglycerols. Following release of the fatty acid portions of triacylglycerols the glycerol  backbone is transported to the liver where it it phosphorylated by glycerol kinase yielding  glycerol­3­phosphate. Glycerol­3­phosphate is oxidized to DHAP by glycerol­3­phosphate  dehydrogenase. DHAP then enters the glycolytic if the liver cell needs energy. However, the  more likely fate of glycerol is to enter the gluconeogenesis pathway in order for the liver to  produce glucose for use by the rest of the body. Glucuronate Metabolism Glucuronate is a highly polar molecule which is incorporated into proteoglycans as well as  combining with bilirubin and steroid hormones; it can also be combined with certain drugs to  increase their solubility. Glucuronate is derived from glucose in the uronic acid pathway. The uronic acid pathway is utilized to synthesize UDP­glucuronate, glucuronate and L­ ascorbate. The pathway involves the oxidation of glucosae­6­phosphate to UDP­glucuronate.  The oxidation is uncoupled from energy production. UDP­glucuronate is used in the synthesis  of glycosaminoglycan and proteoglycans as well as forming complexes with bilirubin, steroids  and certain drugs. The glucuronate complexes form to solubilize compounds for excretion. The synthesis of ascorbate (vitamin C) does not occur in primates. The uronic acid pathway is an alternative pathway for the oxidation of glucose that does not  provide a means of producing ATP, but is utilized for the generation of the activated form of  glucuronate, UDP­glucuronate. The uronic acid pathway of glucose conversion to glucuronate  begins by conversion of glucose­6­phosphate is to glucose­1­phosphate by  phosphoglucomutase, and then activated to UDP­glucose by UDP­glucose  pyrophosphorylase. UDP­glucose is oxidized to UDP­glucuronate by the NAD +­requiring  enzyme, UDP­glucose dehydrogenase. UDP­glucuronate then serves as a precursor for the  synthesis of iduronic acid and UDP­xylose and is incorporated into proteoglycans and  glycoproteins or forms conjugates with bilirubin, steroids, xenobiotics, drugs and many  compounds containing hydroxyl (­OH) groups. Clinical Significance of Glucuronate In the adult human, a significant number of erythrocytes die each day. This turnover releases  significant amounts of the iron­free portion of heme, porphyrin, which is subsequently  degraded. The primary sites of porphyrin degradation are found in the reticuloendothelial cells  of the liver, spleen and bone marrow. The breakdown of porphyrin yields bilirubin, a product  that is non­polar and therefore, insoluble. In the liver, to which is transported in the plasma  bound to albumin, bilirubin is solubilized by conjugation to glucuronate. The soluble conjugated bilirubin diglucuronide is then secreted into the bile. An inability to conjugate bilirubin, for  instance in hepatic disease or when the level of bilirubin production exceeds the capacity of  the liver, is a contributory cause of jaundice. The conjugation of glucuronate to certain non­polar drugs is important for their solubilization in  the liver. Glucuronate conjugated drugs are more easily cleared from the blood by the kidneys  for excretion in the urine. The glucuronate­drug conjugation system can, however, lead to drug resistance; chronic exposure to certain drugs, such as barbiturates and AZT, leads to an  increase in the synthesis of the UDP­glucuronyltransferases in the liver that are involved in  glucuronate­drug conjugation. The increased levels of these hepatic enzymes result in a higher rate of drug clearance leading to a reduction in the effective dose of glucuronate cleared drugs. PHOTOSYNTHESIS - - an understandable (not necessarily easy) approach........ Pinus palustris---Pearson Creek Everything should be made as simple as possible, but not simpler. - Albert Einstein (it will take some time to understand this; read deliberately and understand what you have read before going on to the next paragraphs) Photosynthesis is defined as the formation of carbohydrates in living plants from water and carbon dioxide (CO2). It is the most important chemical pathway (series of chemical reactions) on our planet. Almost all of the biomass on Earth was initially created by photosynthesis. Each year 100 quadrillion (or 10 to the 17th) Kilocalories (K.cal.) of useful energy are produced by photosynthesis (about 100 times more energy than is consumed by burning of fossil fuels). At least half of the photosynthesis in the world takes place in oceans, lakes and rivers, brought about by many different microorganisms that constitute the phytoplankton. All organisms on Earth can be classified on the basis of two fundamental physiologic requirements: (A) Energy source: (1) use sunlight for energy: Phototrophs. (2)use chemical compounds for energy : Chemotrophs (B) Carbon source: (1)source is CO2: Autotrophs. (2) source is chemical compounds: Heterotrophs Chemoautotrophs (use chemical compounds for energy and CO2 for carbon)---bacteria (some) Chemoheterotrophs (use chemical compounds for both energy and carbon)----------animals Photoaututrophs (use sunlight for energy and CO2 for carbon)-----plants and photosynthetic bacteria Photoaututrophs utilize sunlight for energy and CO2 for their carbon source by this process of PHOTOSYNTHESIS whereby sunlight is absorbed by a complex compound known as chlorophyll and converted to energy which drives a series of chemical reactions that ultimately removes hydrogen from water or other compounds and then combines the hydrogen with carbon dioxide in a way that produces sugars. Photosynthetic organisms can be divided into two classes: those which produce oxygen and those which do not. Photosynthetic bacteria do not produce oxygen (in fact some of them called anaerobes cannot tolerate oxygen) and this is considered a more primitive type of photosynthesis (in which the hydrogen donor is hydrogen sulfide, lactate or other compounds, but not water). Plants and one type of bacteria (cyanobacteria) do produce oxygen, an evolutionarily more advanced type of photosynthesis (in which the hydrogen donor is water). In a broad chemical sense, the opposite of photosynthesis is respiration. Most of life on this planet (all except in the deep sea vents) depends on the reciprocal photosynthesis-driven production of carbon containing compounds by a series of reducing (adding electrons) chemical reactions carried out by plants and then the opposite process of oxidative (removing electrons) chemical reactions by animals (and plants, which are capable of both photosynthesis and respiration) in which these carbon compounds are broken down to carbon dioxide and water. The oxidative chemical reactions of respiration release energy, some of which is heat and some of it is captured in the form of high energy compunds such as Adenosine triphosphate (ATP) and Nicotinamide adenide dinucleotide phosphate (NADPH). These compounds have a high energy (unstable) terminal phosphate bond and that terminal phosphate is easily detached with the transfer of the energy to drive chemical reactions in the synthesis of other biomolecules. In this case, the ATP loses one phosphate to become the energy-depleted ADP (Adenosine diphosphate) and the NADPH loses one electron to become energy-depleted NADP+. Photosynthesis converts these energy- depleted compounds (ADP and NADP+) back to the high energy forms (ATP and NADPH) and the energy thus produced in this chemical form is utilized to drive the chemical reactions necessary for synthesis of sugars and other carbon containing compounds (e.g., proteins, fats). The production of high energy ATP and NADPH in plants occurs in what is known as Light Phase Reactions (Z Scheme) (requires sunlight). The energy releasing reactions which converts them back to energy-depleted ADP and NADP is known as Dark Phase Reactions (Calvin Cycle) (does not require light) in which the synthesis of glucose and other carbohydrates occurs. So we can summarize by saying that the photosynthetic plants trap solar energy to form ATP and NADPH (Light Phase) and then use these as the energy source to make carbohydrates and other biomolecules from carbon dioxide and water (Dark Phase), simultaneously releasing oxygen in to the atmosphere. The chemoheterotrophic animals reverse this process by using the oxygen to degrade the energy-rich organic products of photosynthesis to CO2 and water in order to generate ATP for their own synthesis of biomolecules. Plant photosynthesis, both the Light Phase and Dark phase reactions, takes place in chloroplasts, which may be regarded as the "power plants" of the green leaf cells. At night, when there is no sunlight energy, ATP continues to be generated for the plant's needs by respiration, i.e., oxidation of (photosynthetically produced) carbohydrate in mitochondria (similar to animals). Chloroplasts have many shapes in different species but are generally fusiform shaped (and much larger than mitochondria) and have many flattened membrane-surrounded vesicles called thylakoids which are arranged in stacks called grana. These thylakoid membranes contain all of the photosynthetic pigments of the chloroplast and all of the enzymes required for Light Phase reactions. The fluid in the stroma surrounding the thylakoid vesicles contains most of the enzymes for Dark phase reactions. There are several light-absorbing pigments in the thylakoid membranes. The most important are the green chlorophylls which are complex protoporphyrin (resembles hemoglobin) molecules which have a magnesiun ion in the center. There are two types of chlorophyll: chlorophyll a, which is always present in all green plants, and a second, chlorophyll b which is also present (about half as much as chlorophyll a) in some plants. The chlorophylls are the major light receptors, absorbing light mostly in the 400 to 500 and 600 to 700 nanometer (nm.)wavelength ranges. The absorption spectra for chlorphylls a and b are shown below. Other pigmented compounds present in the thylakoid membranes include carotenoids (are red, yellow or purple), the most important of which is beta-carotene, the precursor of vitamin A in animals. The carotenoid pigments absorb sunlight at wavelengths other than those absorbed by the chlorophylls and thus are supplementary light receptors. The thylakoid membranes of plant chloroplasts have two different sets of light harvesting chlorophyll and carotenoid molecules combined with a special protein. There are two of these Photochemical Reaction Centers: Photosystem I: has a high ratio of chlorophyll a to chlorophyll b. PhotosystemII: has relatively more chlorophyll b and may also contain a chlorophyll c. The plants and cyanobacteria (which use water as a hydrogen donor and produce oxygen) have Photosystems I and II, whereas the less highly evolved other photosynthetic bacteria(which do not use water as their hydgrogen donor and do not produce oxygen) have only Photosystem I. How does the absorption of light by the chlorophyll pigments in the thylakoid membrane cause the conversion of light energy to chemical (ATP & NADHP) energy? The quick answer is that an electron is stripped from water and transferred to NADP+ to form NADPH which is an endergonic (requires energy imput) reaction.That energy is supplied by the sunlight absorbed in the chloroplasts. And in the process, a phosphorus is added to ADP to produce ATP. When the chlorophyll molecule is excited by light, the energy level of an electron in its structure is "boosted to a higher energy level and this "excited" chlorophyll (now is called an exciton) moves rapidly the the reaction center of the Photosystem I where it transfers its extra energy to an electron which is then expelled from the reaction center and is accepted by the first member of a chain of electron carriers and ultimately reaches NADP+, reducing it to NADPH. The reaction center has lost an electron and this "electron hole" is filled by by stripping electrons from water which leaves hydrogen ion (H+) and molecular oxygen (O2). The pathway of electrons from water to NADP+ has "Z" shape when diagramed and is refered to as the Z Scheme. The Z Scheme diagram shows the pathway of an electron from water (lower right) to NADP+ (upper left). It also shows the energy relationships which are measured as voltage potential shown on the scaleon the right. To raise the energy of the electrons derived from water (+0.82 volts) to the level necessary to reduce NADP+ to NADPH (-0.32 volts), each electron must be boosted twice (vertical red arrows) by light energy absorbed in Photosystems I and II. After each boosting , the energized electrons flow "downhill" (diagonal black lines) and in the process transfer some of their energy to a series of reactions which ultimately adds a phosporus to ADP to produce high energy ATP and reduces NADP+ to NADPH. There is an alternative shunt whereby the electron flow turns back to cytochrome b563 (green line)and this is called cyclic electron flow and it occurs when there is no need for NADPH, so only ATP is produced. How are the electrons lost from Photocenters replaced? The "electron hole" in Photosystem I is filled by the electron which was expelled by sunlight energy from Photosytem II and travels to Photosystem I via the chain of electron carriers (the right red vertical and right black diagonal lines). Then the resulting "electron hole" in Photosystem II is in turn filled by the splitting of water (by an enzyme named water dehydrogenase) into electrons and H+ ions and molecular oxygen. The electrons go to Photosystem II "electron holes" and the H+s go into the fluid medium and the oxygen is released into the air. For each electron flowing from water to NADP+ (a net change in 1.14 volts), two quanta of light are absorbed, one by each Photosystem. Each molecule of oxygen released involves the flow of four electrons from two water molecules to two NADP+s and requires four quanta of sunlight absorbed by each Photosystem to provide the energy to do this. These are the "Light Phase Reactions" of photosynthesis, which produce two high energy chemical products, namely NADPH and ATP. Now what are the "Dark Phase Reactions" (aka Calvin Cycle)? This is the cycle that converts CO2 into glucose. Since it utilizes the chemical energy in the ATP and NADPH, it does not require sunlight (hence the name). It is a complex cycle of mostly phosphorylation (adding or removing phosphate) and oxidative (electron removal) chemical reactions whereby 6 molecules of CO2 are converted into one molecule of glucose. It requires the energy-releasing cleavage of high energy bonds of 18 ATPs and 12 NADPHs . The resulting 18 ADPs and 12 NADP+s are then restored by the Light Phase process to their high energy forms (ATP and NADPH). Therefor these two (Light and Dark) phases are interlinked and complimentary. And in the end, the plants have utilized the energy of sunlight to produce glucose (and ultimately other carbohydrates, proteins and fats) and oxygen from water and carbon dioxide. he Molecule of Life A. Carbohydrates Carbohydrates are a class of organic macromolecules made up of the so called "sugars and starches". There are three classes of carbohydrates, based on the number of sugar units: 1) Monosaccharides 2) Polysaccharides 1) Monosaccharides (simple sugars) These molecules consist of open-chain or ring forms of 3 to 8 carbon atoms. The most common type of monosaccharide is the simple sugar "glucose". Glucose is an important energy source in metabolically active cells. Another important monosaccharides are shown below. Fructose is a common sugar in fruit), and Galactose is the sugar found in milk. Sugars with 6 carbons are called "hexoses". Five carbon sugars are "pentoses". Whereas 7 carbon sugars are called "heptoses". Two very important "pentoses" (5 carbons) are, Ribose found in Ribonucleic Acid, RNA, and Deoxyribose found in Deoxyribonucleic Acid, DNA. Disaccharides When two monosaccharides are joined together they form a "disaccharide". This linking of two sugars involves the removal of a molecule of H 2O (water) and is therefore called a "dehydration linkage". The reaction is called "dehydration synthesis". e.g. Glucose + Glucose = Maltose This forms a bond between the #1 carbon of one glucose and the #4 carbon of the other, therefore it is called an 1-4 linkage, (or Glycosidic Linkage). Other disaccharides are: Glucose + Fructose = Sucrose Glucose + Galactose = Lactose Polysaccharides These are long chains of monosaccharides linked together by dehydration linkages.
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