GAP is the only molecule that continues in the glycolytic pathway. At this point there are two molecules of GAP, the next steps are to fully convert to pyruvate. The phosphate group then attacks the GAP molecule and releases it from the enzyme to yield 1,3 bisphosphoglycerate, NADH, and a hydrogen atom. Phosphoglycerate kinase PGK with the help of magnesium converts 1,3 bisphosphoglycerate to 3-phosphoglycerate by removing a phosphate group.
Phosphoglycerate mutase rearranges the position of the phosphate group on 3-phosphoglycerate allowing it to become 2-phosphoglycerate. Enolase dehydrates 2 phosphoglycerate molecules by removing water. In aerobic respiration, the transition reaction occurs in the mitochondria. Pyruvate moves out of the cytoplasm and into the mitochondrial matrix. In anaerobic conditions, pyruvate will stay in the cytoplasm and be used in lactic acid fermentation instead.
The Krebs cycle, or also known as the citric acid cycle was discovered by Hans Adolf Krebs in It can be described as a metabolic pathway that generates energy.
This process happens in the mitochondrial matrix, where pyruvate has been imported following glycolysis. These products are generated per single molecule of pyruvate. The products of the Krebs cycle power the electron transport chain and oxidative phosphorylation. Acetyl CoA enters the Krebs cycle after the transition reaction has taken place conversion of pyruvate to acetyl CoA. See figure 9. There are 8 steps in the Krebs cycle. Below reviews some of the principal parts of these steps and the products of Krebs cycle:.
Acetyl CoA joins with oxaloacetate releasing the CoA group and producing citrate, a six-carbon molecule. The enzyme involved in this process is citrate synthase. Citrate is converted to isocitrate by the enzyme aconitase. This involves the removal then the addition of water. The ketone is then decarboxylated i. CO 2 removed by isocitrate dehydrogenase leaving behind alpha-ketoglutarate which is a 5-carbon molecule.
Isocitrate dehydrogenase, is central in regulating the speed of the Krebs cycle citric acid cycle. Oxidative decarboxylation takes place by alpha-ketoglutarate dehydrogenase. Succinyl-CoA is converted to succinyl phosphate, and then succinate. Succinate thiokinase other names include succinate synthase and Succinyl coenzyme A synthetase , converts succinyl-CoA to succinate, and free coenzyme A.
Firstly, the coenzyme A at the succinyl group is substituted by a hydrogen phosphate ion. Succinyl phosphate then transfers its phosphoric acid residue to guanosine diphosphate GDP so that GTP and succinate are produced. Succinate is oxidized to fumarate by succinate dehydrogenase. Flavin adenine dinucleotide FAD is the coenzyme bound to succinate dehydrogenase.
FADH 2 is formed by the removal of 2 hydrogen atoms from succinate. This releases energy that is sufficient to reduce FAD. FADH remains bound to succinate dehydrogenase and transfers electrons directly to the electron transport chain. Succinate dehydrogenase performs this process inside the mitochondrial inner membrane which allows this direct transfer of the electrons. L-malate is formed by the hydration of fumarate.
The enzyme involved in this reaction is fumarase. In the final step, L-malate is oxidized to form oxaloacetate by malate dehydrogenase. Where is oxygen used in cellular respiration? It is in the stage involving the electron transport chain.
The electron transport chain is the final stage in cellular respiration. It occurs on the inner mitochondrial membrane and consists of several electron carriers. The purpose of the electron transport chain is to form a gradient of protons that produces ATP. It moves electrons from NADH to FADH 2 to molecular oxygen by pumping protons from the mitochondrial matrix to the intermembrane space resulting in the reduction of oxygen to water.
Therefore, the role of oxygen in cellular respiration is the final electron acceptor. It is worth noting that the electron transport chain of prokaryotes may not require oxygen. Other chemicals including sulfate can be used as electron acceptors in the replacement of oxygen. Four protein complexes are involved in the electron transport chain.
These electrons are then shuttled down the remaining complexes and proteins. They are passed into the inner mitochondrial membrane which slowly releases energy. The electron transport chain uses the decrease in free energy to pump hydrogen ions from the matrix to the intermembrane space in the mitochondrial membranes.
This creates an electrochemical gradient for hydrogen ions. Overall, the end products of the electron transport chain are ATP and water. See figure The process described above in the electron transport chain in which a hydrogen ion gradient is formed by the electron transport chain is known as chemiosmosis.
After the gradient is established, protons diffuse down the gradient through ATP synthase. Chemiosmosis was discovered by the British Biochemist, Peter Mitchell.
In fact, he was awarded the Nobel prize for Chemistry in for his work in this area and ATP synthesis. How much ATP is produced in aerobic respiration? What are the products of the electron transport chain? Glycolysis provides 4 molecules of ATP per molecule of glucose; however, 2 are used in the investment phase resulting in a net of 2 ATP molecules.
Finally, 34 molecules of ATP are produced in the electron transport chain figure Only 2 molecules of ATP are produced in fermentation. This occurs in the glycolysis phase of respiration. Therefore, it is much less efficient than aerobic respiration; it is, however, a much quicker process. And so essentially, this is how in cellular respiration, energy is converted from glucose to ATP. And by glucose oxidation via the aerobic pathway, more ATPs are relatively produced.
What are the products of cellular respiration? The biochemical processes of cellular respiration can be reviewed to summarise the final products at each stage. Mitochondrial dysfunction can lead to problems during oxidative phosphorylation reactions. These mutations can lead to protein deficiencies. For example, complex I mitochondrial disease is characterized by a shortage of complex I within the inner mitochondrial membrane.
This leads to problems with brain function and movement for the individual affected. People with this condition are also prone to having high levels of lactic acid build-up in the blood which can be life-threatening. Complex I mitochondrial disease is the most common mitochondrial disease in children.
To date, more than different mitochondrial dysfunction syndromes have been described as related to problems with the oxidative phosphorylation process.
Furthermore, there have been over different point mutations in mitochondrial DNA as well as DNA rearrangements that are thought to be involved in various human diseases. There are many different studies ongoing by various research groups around the world looking into the different mutations of mitochondrial genes to give us a better understanding of conditions related to dysfunctional mitochondria. What is the purpose of cellular respiration? Different organisms have adapted their biological processes to carry out cellular respiration processes either aerobically or anaerobically dependent on their environmental conditions.
The reactions involved in cellular respiration are incredibly complex involving an intricate set of biochemical reactions within the cells of the organisms.
All organisms begin with the process of glycolysis in the cell cytoplasm, then either move into the mitochondria in aerobic metabolism to continue with the Krebs cycle and the electron transport chain or stay in the cytoplasm in anaerobic respiration to continue with fermentation Figure The ratio of fatty-acid carbons to glycerol carbons in a triglyceride provides an indication of how aerobically demanding triglyceride oxidation is.
Considering that the cytosolic NADH can be effectively reoxidized aerobically via the malate-aspartate shuttle or the glycerolphosphate shuttle and that the glycerol-derived pyruvate can also be oxidized in mitochondria, complete oxidation of a typical triglyceride can demand sufficient oxygen to reoxidize approximately mitochondrial NADH and FADH 2 equivalents.
See also: Lipid ; Lipid metabolism ; Triglyceride triacylglycerol. It should also be pointed out that amino acid oxidation is intermediate in its O 2 requirement between glycolysis and mitochondrial fatty-acid oxidation because some reduced cofactors are produced in the cytosol and others are produced in the mitochondria.
See also: Amino acid ; Amino acid metabolism. The other consideration that guides the magnitude of a cellular O 2 requirement is the degree to which a cell is busy with reactions that demand the hydride carried on NADH and NADPH and whether reducing equivalents can be produced cytosolically.
Unlike a fireplace, whose purpose is to combust fuel fully to generate heat Fig. Thus, the logic of life is such that the relatively low energy electrons carried on cytochrome C in the inner mitochondrial membrane have much less power to do meaningful work than the electrons carried on cytosolic NADPH. The former can donate to O 2 to generate water, having already generated a proton gradient in the descent from the high-energy state in NADH to the low-energy state in reduced cytochrome C.
The latter can donate electrons to beta-keto groups and alkenes to perform reductive biosynthesis. Therefore, it would be illogical for cells to let electrons flow downhill too far if they are needed for biosynthetic reactions. One of the best examples of a set of metabolic pathways that minimizes respiration occurs in white adipocytes fat-storing cells , which are specialized to convert glucose to triglycerides Fig.
This begins with import of glucose and conversion to pyruvate in the cytosol. In the mitochondria, pyruvate is converted to oxaloacetate and Ac-CoA by pyruvate carboxykinase and pyruvate dehydrogenase. These products are condensed to form citrate, which is then exported to the cytosol for conversion to cytosolic Ac-CoA and oxaloacetate. The glucose-derived Ac-CoA is not oxidized to CO 2 in the citric acid cycle, but rather is effectively exported to the cytosol to produce fat.
Moreover, because the adipocyte cytoplasm can produce NADPH by running the oxidative and nonoxidative phases of the pentose phosphate pathway and by converting oxaloacetate to malate and then malate to pyruvate, it has a system to capture most of glucose's available electrons into fat synthesis without a high oxygen demand. Although it is beyond the scope of this article to cover cell replicative and anabolic pathways, it is important to consider that every cell and tissue make everything in the human body from food using metabolic transformations whose biosynthetic complexities greatly exceed the catabolic complexities of breaking down carbohydrates, fats, and proteins.
Gluconeogenesis, ketogenesis, amino acid synthesis, nucleic acid synthesis, and steroid synthesis depend on reduced cofactors. See also: Fat and oil ; Nucleic acid ; Steroid. Like de novo lipogenesis, cytosolic ROS detoxification depends on NADPH that can be produced in the cytosol by nonaerobic processes, including the pentose phosphate pathway. Similarly, in brown adipocytes, which express high levels of the proton pore—forming uncoupling protein, high levels of oxygen consumption are linked to heat production rather than ATP formation Fig.
In summary, cellular respiration encompasses the oxygen-dependent and electron transport chain—dependent processes by which coenzymes reduced by fuel oxidation are reoxidized. It is linked to mitochondrial ROS production and detoxification, generation of electrochemical gradients across membranes, thermogenesis, and oxidative phosphorylation. It is minimized by cells performing high levels of reductive biosynthesis, despite their ongoing fuel oxidation.
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