See also Evolution of Metabolism within Metabolism

See also Bacterial Metabolism

Introduction:

The metabolic processes and reactions that occur in our cells are the essence of life. They are also very intricate and detailed. The following is meant to be only an overview of some of the important reactions. Living matter obtain their energy by means of either respiration or fermentation. Both catabolic systems convert the chemical energy of organic molecules to high energy bonds in adenosin triphosphate (ATP). Energy production in respiration is accomplished by means of three well understood pathways, glycolysis, the tricarboxylic acid cycle (Krebs cycle), and oxidative phosphorylation (sometimes cells the electron transport chain, or ETC). Energy production in fermentation is accomplished by a variety of pathways, all referred to as substrate level phosphorylation.

Cellular respiration is the omplete oxidaiton of glucose. Aerobic respriation uses oxygen as the ifnal electron acceptor for redox reactions. Anadrobic respiration uitlizes inorganic molecuels as acceptors.

Glycolysis is the splitting of the six-carbon glucose molecule into two three carbon pyrivate molecules while reducing coenzymes and producing ATP. All of the major respiratory reactions direclty involved in the conversion of glucose to carbon dioxide-glycolysis, the conversion of pyruvate to acetyl-CoA, and the Krebs cycle-oxidize organic substrates and reduce coenzymes.

Following glycolysis is a reaction in which pyruvate is oxidized, producing the two carbon molecule acetyl-CoA and one molecule of CO2. The acetyl-CoA enters the Krebs cycle where, in a complex series of reactions, it too is converted to CO2. These reactions release energy used to produce more ATP and in the process reduce many coenzymes.

If respiration were to end at this point, the cell would lose its ability to oxidize glucose because of a relative shortage of oxidized coenzymes. However, cells perform another set of reactions celled the electron transport Chain where reduced coenzymes donate electrons to molecules that pass them down a chain of other molecules in a series of oxidation-reduction reactions to an inorganic molecule called the final (or terminal) electron acceptor. When the final electron acceptor is oxygen, the respiration is aerobic. When the final electron acceptor is an inorganic molecule other than oxygen (e.g., sulfate or nitrate) the respiration is anaerobic.

In contrast to respiration, fermentation is the metabolic process where the electrons stripped from glucose ultimately are accepted by one or more of its organic products. Reduced carbon compounds in the form of acids and organic solvents, as well as CO2, are the typical end products of fermentation. This substrate-level phosphorylation releases much less energy and produces less ATP.

Glycolysis

Glycolysis is the anaerobic breakdown of glucose to lactic acid. Glycolysis provided a mechanisms by which the energy in preformed organic molecules (e.g., glucose) conould be converted to ATP, which could then be used as a source of energy to drive other metabolic reactions. (Cooper, “The origin and evolution of cells” NCBI Bookshelf, “The cell: a molecular approach, 2nd edition, Sunderland (MA), Sinauer Associates, 2000).

Glycolysis is the anaerobic conversion of glucose to pyruvate with a net gain of 2 molecules of ATP for every glucose molecule that is broken down.

One main rate limiting reaction that occurs early in glycolysisis the phosphorylation of fructose 6 phosphate(F-6-P) to fructose 1,6 bisphosphate (F-1,k-BP), catalyzed by phosphofructokinase (PFK1). The enzyme, PFK1 is allosterically activated by fructose 2, 6 bisphosphate (F-2,6-BP). F-2,6-BP is also a product of the phosphorylation of F-6-F but in a reaction that is catalyzed by phosphofructokinase2 (PFK2).

Another rate limiting reaction that occurs at the end of glycolysis is the transfer of a phosphate group fromphosphoenolypyruvate to ADP to yield Pyruvate and ATP. This reaction is catalysed by pyruvate kinase which can exist in 1) a less activated phosphorylated form or 2) in a more active dephosphorylated form. Pyruvate kinase is slowed down by the phosporylating hormone, glycogen, and activated by the dephosphyrlating hormone, insulin.

In certain animal tissues like muscle when inadequate oxygen is present, pyruvate is converted into lactate. In this process, the NADH produced by glycolysis gives up its electrons and is converted into NAD+.

Gluconeogenesis:

Gluconeogenesis is the biosynthesis of glucose which occurs predominantly in the liver by a process that is essentially a reversal of glycolysis. Lactate which is producing during anaerobic glycolysis in muscle is a predominate source of carbon atoms for glucose synthesis by gluconeogenesis. The lactate that is produced in the muscle is released to the blood stream and transported to the liver where it is converted to glucose. The glucose is then returned by the blood for use by muscle as an energy source and to replenish glycogen stores. This cycle is termed the Cori cycle.

Because gluconeogenesis is essentially a reversal of glycolysis, the positive and negative effectors of glycolysis have reverse roles in gluconeogenesis. For example, unlike the first rate limiting reaction in glycolysis where PFK1 is stimulated by 2,6,-bisphosphate, the enzyme, fructose 1,6, bisphosphatase (F-6,6-BPase), which catalyzes the conversion of 1,6,-bisphoshate to fructose 6-phosphate in gluconeogenesis is decreased by high levels of 2,6-biosphosphate. Conversely, the presence of ATP which inhibits the glycolysis forward reaction stimulates fructose 1,6, bisphosphatase and the production of glucose.

The rate limiting reaction of the conversion of pyruvate to phosphoenolpyruvate in gluconeogenesis is catalyzed by the enzyme, phosphoenolpyruvate carboxylkinase (PEPCK). In contrast to the activity ofpyruvate kinase in glycolysis, PEPCK is induced in response to glucagon. The mechanism of action here is rather unique in that glucagon promotes transcription of a gene that encodes PEPCK through a kinase mediated signalling cascade (cAMP).

When thinking about the regulation of key enzymes in glycolysis and gluconeogenesis, the effectors make inherent sense. When blood glucose is high, insulin and the rate of glycolysis is up. When blood glucose is low, most cells go into an energy saving mode; glucagon and the rate of gluconeogenesis are up, PFK1 and PFK2 are off.

Citric Acid Cycle (Krebs Cycle):

The citric acid cycle is also known as the tricarboxylic acid cycle or the Krebs cycle. Each turn of the cytric acid cycle produces 3 molecules of NADH, 1 molecule of FADH2 and 1 molecule of GTP. The energy that is stored in the readily transferred high energy electrons of NADH and FADH2 is subsequently utilized for ATP production through a process called “oxidative phosphorylation” which is discussed below.

Before the citric acid cycle can start, both acetyl CoA and oxaloacetate are required. The 2 main precursors for precursors for acetyl CoA are pyruvate and fatty acids. Both of these fuel molecules are transported across the inner mitochondrial membrane and then converted to acetyl CoA by enzymes located in the mitochondrial matrix. In the case of pyruvate, acetyl CoA formation is catalyzed by a complex of 3 enzymes called the pyruvate dehydrogenase complex. Pyruvate is also a precursor for the formation of oxaloacetate through a reaction catalyzed by pyruvate carboxylase.

The citric acid starts off with the joining of the 4 C unit, oxaloacetate with the 2 C unit, acetyl CoA in a reaction catalyzed by citrate synthase to form citrate which is in turn isomerized into isocitrate in a reaction catalyzed by aconitase.

In the 1st of the 4 oxidation steps in the cycle, isocitrate + NAD is converted into alpha-ketoglutarate+ NADH in a reaction catalyzed by iscitrate dehydrogenase.

The second oxidation step comes when alpha ketoglutarate + NAD is converted into succinyl CoA + NADH in a reaction that is catalyzed by the alpha ketoglutarate dehydrogenase complex. This complex closely resembles the large enzyme complex, pyruvate dehydrogenase above which converted pyruvate to acetyl CoA.

Next, succinyl CoA + GDP is converted into succinate + GTP in a reaction catalyzed by succinyl CoA synthetase.

In the third oxidation step in the cycle, FAD removes 2 H atoms from succinate to form fumarate in a reaction catalyzed by succinate dehydrogenase. Fumarate is then converted into malate in a reaction catalyzed by fumarase.

In the last of 4 oxidation steps, malate + NAD yields oxaloacetate + NADH in a reaciton catalyzed by malate dehydrogenase. The regeneration of oxaloactetate allows the cycle to continue once again.

The citric acid cycle is not only important because is gnerates high energy electrons in the form of NADHwhich are passed to a membrane bound electron transport chain in oxydative phosphorylation which is discussed next, but also because many of the products above are intermediates for biosyntheses in other cycles as shown below.

Oxidative Phosphorylation (Eletron Transport Chain and Chemiosmosis):

The NADH and FADH produced at any stage in respiration converge on the electron transport chain. In eukaryoties, these membrane associated electron carriers are in the mitochondrial inner membrane and in prokaryotes in the plasma membrane. The redox reactions of the electron transport chain covert the energy in electrons to potential energy in  a protein gradient. The electron transport chain reaceives electrons from NADH and FADH2 and passes them down the cahin to oxygen. The protein complexes of the electron transport chain, in the inner membrane of mitochondria, use the energy from electron transfer to pump prtoins across the membrane, creating an electrochemical gradient. The enzyme ATP synthase uses this gradient to drive the endergonic reaction of phosphorylating ADP to ATP.

Oxidative phosphorylation produces about 2.5 molecules of ATP from the pair of electrons donated by NADH and 1.5 ATP molecules per electron pair from from FADH2. Without mitochondria where oxidative phosphorylation occurs, eucaryotes would be dependent on the relatively inefficient process of glycolysis for all of their ATP production.

Oxidative phosphorylation occurs in the inner mitochondrial membrane. NADH which is formed by glycolysis in the cytosol presents a problem since NADH can not diffuse across the inner mitochondrial membrane. The NADH that is generated during glycolysis is brought into the mitochondrial membrane using what is called the glycerol-3-phosphate shuttle. Another way that electrons from the cytosol enter the mitochondrial membrane is by the malate aspartate shuttle.

In oxidative phosphorylation, electron motive force is converted into proton motive force and then into phosphoryl potential. As electrons from reduced substrates flow through various complexes, protons are translocated across the inner mitochondrial membrane from the matrix to the intermembrane space. This creates a proton (H+) gradient which is negative on the matrix side and + on the cytosolic side of the inner mitochondrial membrane. As protons reenter the mitochondrial matrix due to this gradient, their reentry is coupled to the conversion of ADP and Pi to ATP. This conversion takes place in a complex known as the ATP synthase which is composed of 3 subunits. One unit called F- spans the inner membrane and serves as the proton channel of the complex. Another subunit, F1 contains the catalytic sties for ATP synthesis.

ATP and ADP do not freely diffuse across the inner membrane but must be transported using an ATP-ADP translocase. When this transport protein bind ADP, there is an eversion of the protein whereby ADP is transported in from the cytosolic side. Once inside the matrix, ADP is released. ATP then bind causing another eversion of the protein which transports ATP out to the cytosolic side.

Certain drugs can uncouple oxidative phosphorylation such as DNP and thermogenin.

Oxidation without O2:

Anaerobic Respiraction: In the presence of oxygen, cells can use oxygen to produce a alrge amount of ATP. But even when no oxygen is present to acept electrons, some organisms can still respire anaerobically, using inorganic molecules as final electron acceptors for an electron transport chain. For example, many prokaryotes use sulfur, nitrate, carbon dioxide or even inorganic metals as the final electron acceptor in place of oxygen. The free energy released by using these other molecuels as final electron acceptors is not as great as that using oxygen becasue they have a lower affinity for electrons. The amount of ATP rpoduced is less, but the process is still respirtation and not fermentation.

Among the heterotrophs that practice anaerobic respiration are Archaea such as thermophiles and methagnogens. Methanogens use carbon dioscide (CO2) as the electron acceptor, reducign CO2 to CH4 (methan). The hydrgoens are derived from organic molecuels produced by other organisms. Methanogens are found in diverse environments, including soil and the digestive systems of ruminants like cows.

The early sulfate reducers set the stage for the evolution of photosynthesis, creating an environment rich in H2S. The first form of photosynthesis obtained hydrogens from H2S using the energy of sunlight.

Fermentation: In the absence of oxygen, cells taht cannot utilize an alternative electrong acceptor for respration must rely exlusively on glycolysis to produce ATP. Bacterai carry out mroe than a dozen kinds of fermentation reactions, often using pyruvate or a derivative of pyrvate to accept the electrons form NADH. Organic molecuels other than pyruvate and its derivatives can be used as well.

Eukaryotic cells are capable of only a few types of fermentation. In one type, which accurs in yeast, the molecuels taht accepts electrons from NADH is derived from pyruvate, the end produce of glycolysis. Yeast enzymes remove a temrinal CO2 group form pyruvate through decarboxylation, producign a 2 carbon moelculed called acetaldehyde. The CO2, released causes break made with yeast to rise. This particular type of fermnentation is of great interest becasue it is the source of the ehtanol in wine and beer.

Muscle cells use the enzyme lactate dehydrogenase to transfer electrons form NADH back to the pyruvate that is produced by glycolysis. This reaction converts pyruvate into lactic acid and regenerates NAD+ form NADH.

Cholesterol and Lipoproteins

Cholesterol is an essential component of membranes. Elevated levels of cholesterol can also be very dangerous leading to such diseases as atherosclerosis. Statins (ex. fluvastatin) are commonly used to lower cholesterol levels.

The rate limiting reaction in the biosynthesis of cholesterol is the reduction (NADPH to NADP+) of 3-Hydroxy-3-methylglutaryl-CoA (HMG-CoA) to Mevalonate, catalyzed by the enzyme HMG-CoA Reductase. HMG-Co is a product which can also be cleaved to form the ketone body acetoacetate (see below). But that reaction occurs in the mitochondria whereas the reduction of HMG-CoA to mevalonate occurs in the cytosol. Other reactions after the product of mevalonate leading to the synthesis of cholesterol do occur in the mitochondria. The enzyme HMG-CoA reductase spans the ER membrane 3 times. Its active site, however, is actually on the cytoplasmic side of the ER membrane. HMG-CoA reductase is regulatedusing transcription mechanisms by 1. insuline (+) [after a meal, insulin levels increase which turns on cholesterol synthesis and in turn bile acid synthesis; 2. glucagon (-); 3. thyroid hormone (+), 4. statins (+) and bile acids (-) [if have enough bile acids no sense in making more cholesterol]. HMG-CoA reductase is regulated using translation mechanisms by 1. cholesterol which is the end product of the pathway.

Most of the cholesterol in our bodies is esterified using 1 of 2 different reactions. The 1. LCAT (lecithin cholesterol acyltransferase) reaction of 2. the ACAT (acyl CoA cholesterol acyltransferase) reaction.

Elimination of cholesterol from the bile requires bile acids. The rate limiting reaction in the biosynthesis of bile acids is the reduction (NADPH to NADP+) of cholesterol to 7?-hydroxycholesterol by the enzymecholesterol 7-?-hydroxylase. This rate limiting step occurs in the mitochondria of the liver. The next steps in the biosynthesis occur in peroxisomes of the liver and in the final steps, bile acids are conjugated with either glycine ortaurine in the cytosol. The enzyme cholesterol 7-?-hydroxylase is regulated by 1. thyroid hormone (+) 2. cholesterol (+) and 3. bile acids (-). Bile acids are returned to the liver via the enterohepatic circulation.

Cholesterol and triacylglycerols are transproted in the body in the form of lipoproteins.

Fatty Acid Degradation/Oxidation (Catabolism of fatty acids):

Fatty acids contain a long hydrocarbon chain and a terminal carboxylate group. They are stored in the body as triacyglycerols. The initial event in the utilization of fat as an energy source is the hydrolysis of triacyglycerol emulsion droplets (bile salts emulsify these triacyclycerols) by lipases into fatty acids. Lipase and co-lipase hydrolyze fatty acids in the intestine. lipoprotein lipase cleaves triglycerides in chylomicrons(transportors of lipids in the blood). lipoprotein lipase requires Apo C-II as an activator. Hormone sensitive lipase sometimes called “triacylglycerol lipase” cleaves triglycerides in adipose tissue. Epinephrine and glucogon induce this lipase by increasing cyclic cAMP which stimulates protein kinase which activates the lipase by phosphorylating it.

Fats are broken down into fatty acids plus glycerol. Long-chain fatty acids which contain C-H bonds provdie a rich harvest of energy. Fatty acids are oxidzed in the matrix of the mitochondrion. Enzymes remove the 2-carbon acetyl groups from the end of each fatty acid until the entire fatty acid is converted into acetyl groups. Each acetyl group is combined with coenzyme A to form acetyl-CoA. This process is known as beta-oxidation. This process is oxygen dependent, which explains why aerobic exercise burns fat, but anaerobic exercise does not. Many different metabolic processes generate acetyl-CoA. Not only does the oxidation of pyruvate produce it, but the metabolic breakdown of proteins, fats, and other lipids also generates acetyl-CoA. Indeed, almost all molecuels catabolized for energy are converted into acetyl-CoA.

Fatty acids are oxidzed in the mitochondrial matrix. However, before they can be oxidized, they are activated on the outer mitochondrial membrane and linked to coenzyme Ain a reaction catalyzed byacyl CoA synthetase. Since long chain acyl CoA molecules do not readily traverse the inner mitochondrial membrane, a special transporter carnitine is conjugated to them.

Carnitine palmitoyle transferase I (CPTI) catalyzes the rate limiting step in fatty acid oxidation. CPTI is regulated by malonyl CoA. (malonyl CoA is in turn regulated by the rate limiting step in the synthesis of fatty acids below in that if synthesis of fatty acids is high, [malonyl CoA] is also high which has a negative effect on CPTI. Conversely, in a fasted stated, [malonyl CoA] is low and the negative effect is removed).

The entry of acetyl CoA formed in fatty acid oxidation depends on the availability of oxaloacetate. If there are insufficient carboyhdrates, oxaloacetate will not be made. In such a case, acetyl CoA is diverted from the citric acid cycle to form what are known as “ketone bodies”. Ketone bodies are abnormatlly high in untreated diabetics or in people who fast because oxaloacetate is consumed to form glucose in the gluconeogenic pathway and hence is unavailable. The 3 ketone bodies formed are 1) acetoacetate, 2) acetone and 3) B-hydroxybutyrate. Ketone bodies are produced in the liver but used in extrahepatic tissues.

Fatty Acid Synthesis:

Whereas fatty acid degradation occurs in the mitochondrial matrix, synthesis of fatty acids occurs in the cytosol. Because fatty acid synthesis occurs in the cytosol whereas acetyl Cois formed from pyruvate in mitchondria, acetyl CoA must be transferred from the mitochondria to the cytosol. Since mitochondira are not readily permeable to acetyl CoA, acetyl CoA is condensed with oxaloacetate to form citrate which can pass to the cytosol.Thus citrate is used as a transporter. The citrate is then cleaved by ATP citrate lysase to reform the oxaloacetate and acetyl CoA.

Fatty acid synthesis starts off where fatty acid left off, namely, acetyl CoA. The rate limiting reaction is the carboxylation of acetyl CoA to malonyl CoA in a reaction catalyzed by acetyl CoA carboxylase which has a biotin prosthetic group. Phosphyrlation of acetyl CoA carboxylase results in inactivity whereas dephosphrylation results in activity so that as one might expect, glucogen has a negative regulatory affect and insulin a positive effect upon the activity of this enzyme.

The reductant used in fatty acid synthesis is NADPH whereas it is NAD+ and FAD in fatty acid breakdown. The major product of fatty acid synthesis is palmitate. In eukaryotes, longer fatty acids are actually formed by elongation reaction catalyzed by enzymes on the cytosolic face of the ER membrane through the use of something called the desaturase reaction.

Eicosanoid hormones are derived from polyunsaturated fatty acids. A precursor for eicosanoids isarachidonate which is a fatty acid derived from linoleate (an essential fatty acid) and is the major precursor of several classes of signal molecules – thromboxanes and prostaglandins.

Amino Acid Catabolism/Degradation:

10 of the 20 amino acids required for protein synthesis are essential and must be obtained through ingestion and digestion of dietary protein. Humans required a daily supply of these essential amino acids since there is no storage protein per se as with lipids (triglycerides) and carbohydrates (glycogen). However, in the fasting state, body proteins can be called on for glucose production.

Proteins are first borken down into their individual amino acids. The nitrogen-cotnaing side group (the amino group) is then removed from each amino acid in a process called deamination. A series of reactions converts the carbon chain thtat remains into a molecule that enters clycoysis or the citric acid cycle. For example, alanine is converted into pyruvate, glutamate into alpha-ketoglutarate, and aspartate into oxaloacetate. The reactions of glycolysis adn the citric acid cycle then extract the high energy electrons form these molecuels and put them to work making ATP.

One of the key early steps in amino acid catabolism are transamination reactions which involve the transferring amino acid nitrogen between amino acids in the body. One of the donor/acceptor pairs in transamination reaction is always glutamate and alpha-Ketoglutarate. The prostetic group of all aminotransferasesisPLP (pyridoxal phosphate) which is derived from vitamin B6.

Transamination reactions provide a mechanism for transfer of amino groups from various amino acids to glutamate which are then oxidatively deaminated via a key enzyme, glutamate dehydrogenase. The products of this reaction are alpha-Ketoglutarate and ammonia (NH4).

Ammonia is very toxic. The enzyme, glutamine synthetase catalyzes the conversion of NH4 to glutamine which is the major transport form of ammonia. In the liver, the reverse reaction is catalyzed by glutaminase, releasing free NH4+ which is then converted to urea, which is the major excreted form of excess nitrogen.

Amino Acid Synthesis: 

Non-essential amino acids can be synthesized from glycolytic or TCA cycle intermediates or from essential amino acids.

Amino acids are precursors to many important biomolecules. For example, tyrosine is a precursor forcatecholamines which are involved as hormones and neurotransmitors (such as epinephrine, norepinephrine, dopamine). Tryptophan is a precursor for serotonin. Catecholamines and serotein are sometimes called “biogenic amines.”

Arginine is a precursor for nitric oxide (NO) that is an important regulatory molecule. Arginine is also a precursor for plyamines which carry many + charges and complex with the – P on DNA during DNA replication.

Glutamate is a precursor for GABA and histidine is a precursor for histamine

Nucleotide Biosynthesis

When we think about nucleotides, we think of their necessity for the formation of nucleic acids (DNA & RNA). But nucleotides are also essential for energy metabolism (ATP), signaling and regulatory molecules. In addition, nucleotides are components of coenzymes and serve as activated intermediates. For example, S-adenosylmethionine (SAM) is an activated methyl group donor.

Nucleotide biosynthesis is typically divided into 1) purine biosynthesis and 2) pyrimidine biosynthesis. In both cases, amino acids are necessary.

Purine biosynthesis requires a purine ribose phosphate (PRPP) and glutamine. The reaction is catalyzed byPRPP-Amidotransferase. The reaction is highly regulated with PRPP itself being a + effector.

Pyrimidine biosynthesis also requires amino acids (glutamine as well as asparate). But first the purine ring is formed and only then is the ribose moiety added.

Because nucleotide biosynthesis is an energy consuming process, the body has developed pathways to reuse both purine and pyrimidine bases.

The enzymes ribonucleotide reductase and thymidylate synthase are important enzymes required for the formation of deoxyribunucletide precursors for DNA synthesis. Ribonucleotide reductase converts ribonucletoside diphosphates to deoxyribonucleoside diphosphates. Thymidylate synthesis converts dUMP to dTMP.

Nucleotide Degradation

Purine nucleotide degradation: The final step in purine degration is catalyzed by an enzyme called xanthine oxidase. The final product in this reaction is uric acid which has a limited solubility and can form crystals in tissues if the concentration is too high. This can result in a condition referred to as “gout”. Gout can be treated with allopurinol which inhibits uric acid production.

Since deoxyadenosine can only be degraded via the pathway involv. ing the enzyme adenosine deaminase, a deficiency involving adenosine deaminase results in the buildup of deoxyadenosine which can lead to immunodeficiencies.

Pyrimidine nucleotide degradation: Uracil and thymine are degraded via the same pathway of reactions, but the products are different. In the case of uracil, the product is ?-alanine and with thymine the product is ?-aminoisobutyrate. It is possible to estimate the turnover of DNA by measurement of ?-aminoisobutyrate . Levels are increased in patients undergoing chemotherapy or radiation therapy.

Photosyntehsis:

Phtosynthesis ocurs in a wide variety of organisms and it comes in different forms. These include a form of photosynthesis that does not produce oxygen (anoxygenic) and a form that does (oxygenic). Anoxygenic photosyntehsis is found in four different bacterial groups: purple bacteria, green sulfur bacteria, green nonsulfur bacteria and heliobacteria. oxygenic phtosyntehsis is found in cyanobacteria, seven groups of algae, and essentially all land plants. These two types of phtosynthesis share similariteis in the types of pigments they use to trap light energy, but they differ in the arrnagement and action of these pigments.

The overall equation for photsynthesis is the following: 6CO2 (carbon dioxide) + 12 H2O (water) + light —-C6H12O6 (glucose) + 6H2O (water) + 6O2 (oxygen).

This is the reverse of the recaction for respiration where glucose is oxidized to CO2 using O2 as the electron acceptor. In photosynthesis, CO2 is reduced to glucose using electrons gained from the oxdiation of water. The oxdiation of H2O and the reduction of CO2 requires energy that is provided by light.

Photosyntehsis requires light dependent reactions which use the energy in sunlgiht to make ATP and reduce the electron carreir NADP+ to NADPH. This also oxidzes water to provide electrons and produces O2. Photosyntehsis also requires light independent reactions that use this ATP and NADPH to power the syntehsis of organic molecules from CO2 in the air.

In plants, photosynthesis takes place in chloroplasts. The internal membrane of chloroplasts, called the thylakoid membrane, is a continous phospholipid bilayer organized into flattened sacs called thylakoid disks. These are stacked in columns called grana. This form three compartments: the thylakoid membrane itself, the spaces inside and ouside this membrane. The thylakoid membrane contains the enzmatic machinery to make ATP, and chlorophll and other photosynthetic pigments that capture lgiht energy. The compartment outside the thylakoid membrane system is called the stroma.

The thylakoid membrane contains the enzymatic machinery to make ATP, and chlorophyll and other photosynthetic pigments that capture light energy. In the thyladoid membrane, photosyntetic pigments, are orgnaized into photosystems that absorb light, which excites an electron that can be passed to an electorn carrier.

Carbohydrates contain many C-H bonds and are highly reduced compared with CO2. To build carbohydrates, cells use energy and a source of electrons produced by the light dependent reactions of the thylakoids.

The cycle of reactions that allow carbon fixation is called the Calvin cycle. The key step that makes the reduction of CO2 possible is the attachment of CO2 to a highly specilized organic molecule, ribulose 1,5-bisphosphate (RuBP). CO2 reacts with RuBP to form a transient 6 carbon intermediate that splits into two molecules. The overall reaction is called the carbon fixation reaction because inorgnaic carbon (CO2) is incorporated into an organic form. The enzyme that carries out this reaction, ribulose biphosphate carboxylase/oxygenase (rubisco), is a large, 16 subunt enzyme found int he chloroplast stroma. The Calvin cycle can be thought of as divided into 3 phases: (1) carbon fixation, (2) reduction and (3) regeneration of RuBP.

The carboxylation and oxidation of RuBP are catalyzed at the same active site on rubisco, and CO2 and O2 compete with each other at this site. Under normal conditions at 25C, the rate of the carboxylation reaction is fourt times that of the oxidation reaction, meaning that 20% of photosythetically fixed carbon is lost to photorespiration. This loss reises usbstantially as temperature increases, becasue under hot, arid conditions, specilized openings in the leaft called stomata close to conserve water. This cuts off the supply of CO2 entering the elaf and does not allow O2 to exit. As a result, the low CO2 and high O2 conditions within the leaf favor photorespiration which incorproates O2 into RuBP which undergoes additional reactions that actually release CO2.

The reduction in the yield of carbohydrate as a result of photorespiration is not trivial. C3 plants losoe between 25-50% of their photosynthetically fixed carbon in this way. The rate depends largely on temeprature. However, C4 plants include corn, sugarcane and other grasses can fix carbon using PEP carboxylase in mesophyll cells. This reaction produces the orgnic acid oxalacetate, which is coverted to malate and transported to bundle sheath cells that surround the leaft veins. Wihting the bundle sheath cells, malate is decarboxyalted to produce pyruvate and CO2. Becasue the bundle sheath cells are impemeable to CO2, the local level of CO2 is high and carbon fixation by rubisco and the Calvin cycle is efficient.

Chlorophylls absorb photons within anrrow energy ranges. Two kinds of chlorophyll in plants are chlorophill a and chlorophll b preferentially absorb violet blue and red light. Chlrophyll a is the main photosynthetic pigment in plans and cyanobacterai and is the only pigment that can act direclty to convert light energy to chemical energy. Chlorophyll b, acting as an accessory pigment, complements and adds to the lgiht absorption of chlorophyll a. Chlrophylls absorb photons by means of an excitation process analogous to the photoelectric effect. These pigments contain a complex ring structure, called a porphyrin ring, with alterating single and double bonds. At the center of the ring is a magnesium atom. Photons excite electrons in the porphyrin ring, which are then channeled away through the latenrating carbon single and double bond systems.