- Describe two features that make all enzymes catalysts.
Enzymes are catalysts that increase the rate of reaction between substances and remain unchanged in the reaction. Enzymes are vital to several bodily functions and make possible such processes like metabolism and catabolism. Two features that make enzymes catalysts is their ability to lower the activation energy and their inherent tendency to combine with coenzymes and cofactors. Activation energy is the minimum energy required to activate the molecules of reactants in order to initiate a chemical reaction. Some substrates have high activation energies that would need very high temperatures to activate the. However, such high temperatures would threaten the well-being of the body. Thus, enzymes are necessary to lower the activation energy, speeding up chemical reactions. Coenzymes and cofactors are components that bind with the enzymes in order to speed up the reaction by carrying electrons through the chemical reaction.
- Explain how enzymes act in the first two steps of fructose metabolism in the liver.
A biochemical process known as fructolysis facilitates the breakdown of fructose into simpler sugars necessary for energy production. This biochemical breakdown of fructose in the liver is as follows. Firstly, fructose is acted upon by the enzyme fructokinase in a process called fructolysis to produce fructose 1- phosphate as the product of this initial process. Secondly, aldolase B enzyme converts fructose 1- phosphate into dihydroxyacetone phosphate (DHAP) and glyceraldehyde. The body in energy production later utilizes these conversion products. (Ukessays.com)
- Provide an original, clearly labeled diagram, or series of diagrams, that illustrates the following:
The Lock and key model, as depicted in the diagram 1 below, suggests that the enzyme and the substrate possess specific and complementary geometric shapes that fit exactly into one another. Like a key into the lock, only a substrate with the correct size and shape of the substrate would fit the active site” (the lock) of the enzyme (Biology Online, 2008).
Diagram 1. The lock and key model of enzyme activity.
Diagram 2 depicting the activation energy of reaction in the presence and absence of an enzyme
In biochemical reactions, reactants require energy to interact with one another to create new substances. This requirement is necessary to cross a certain threshold, the activation energy, before the reaction can occur. Enzymes increase reaction rates and hasten the crossing of the activation energy threshold as shown above in diagram 2.
- Discuss the specific substrate acted on by aldolase B during the metabolism of fructose, including how the substrate is made.
Aldolase B enzyme acts on Fructose-1-Phosphate (F-1-P) during the metabolism of fructose. Fructose-1-phosphate is a byproduct of fructose. It mainly formed through fructolysis by the enzyme fructokinase. However, the small intestine and renal tubule produces F-1-P in small quantities.
- Explain the role of aldolase B in the metabolism of fructose, including the products of the reaction.
Fructolysis is the metabolism of fructose in the liver. During fructolysis, fructose is phosphorylated by fructokinase converting it to fructose 1-phosphate, using adenosine triphosphate (ATP) as a phosphate donor (Harvey, 2013). Fructose 1-phosphate is then cleaved by aldolase B to dihydroxyacetone phosphate (DHAP) and glyceraldehyde. Aldolase B enzyme acts on F-1-P in the final stages of fructose metabolism in the liver.
- Discuss how a deficiency in aldolase B is responsible for HFI.
HFI results from mutations in the aldolase B, fructose-bisphosphate (ALDOB) gene that replace amino acids in the aldolase B enzyme, and cause the production of an enzyme with reduced functionality. This mutation changes the shape of the enzyme making it difficult for the “enzymes to bind together and form tetramers” that metabolize fructose (Genetics Home Reference1, 2014).
A deficiency of functional aldolase B results in an accumulation of fructose-1-phosphate in liver cells. This buildup is toxic and results in the death of liver cells over time. Additionally, the breakdown products of fructose-1-phosphate, glyceraldehyde and DHAP are needed in the body for energy production and to maintain blood sugar levels. The combined effects of decreased cellular energy activities, low blood sugar, and liver cell death lead to hereditary fructose intolerance (HFI) (Genetics Home Reference2, 2014).
- Explore how mitochondrial disease can occur at multiple levels in different mitochondrial processes.
If the inter-conversion of the Cori cycle occurred and remain within a single cell then, it would cause the futile cycle. In this cycle, glucose is used by the cell and re-synthesized at the cost of ATP and guanosine triphosphate (GTP) hydrolysis resulting into a loss of 4 ATP during the futile cycle. In aerobic organisms, marks the final step of catabolism where acetyl-CoA is completely oxidized to carbon dioxide (CO2).
- Create an original dynamic diagram that shows how the citric acid cycle (CAC) is central to aerobic metabolism.
- Explain where in the CAC a hypothetical defect of an enzyme could occur that would decrease the overall ATP production of the mitochondria.
The citric acid cycle (CAC) releases a small amount of energy that causes the formation of a molecule of ATP. CO2 input from the Electron Transport Chain (ETC) also facilitates ATP formation. Therefore, any defect in ETC will prevent the conversion of ADP to ATP due to the existence of a gradient in the ETC used to produce the ATP. A special enzyme called ATP synthase produces ATP. Any defect in the ETC will, thus, prevent the conversion of ADP to ATP (Ukessays.com, n.d.). The Oxidative phosphorylation process converts the products of the Citric acid cycle into ATP in the mitochondria. The “NADH and succinate, which is the product of Krebs cycle, are oxidized to release energy” (Mitchell 1966, 1968 as cited in Medh, n.d.). This energy powers the enzyme ATP synthase that facilitates ATP production.
- Explain the specific role of coenzyme Q10 in the electron transport chain.
Co-enzyme Q10 is a substance existing in every cell whose specific role is energy production (Ernster & Dallner, 1995 as cited in Bhagavan & Chopra, 2007). It is necessary for the conversion of energy from carbohydrates and fats into ATP within the inner mitochondrial membrane. In this process, Co-enzyme Q10 accepts electrons produced during fatty acid and glucose metabolism and converts them to electron acceptors. Concurrently, it also transfers excess protons outside the mitochondrial membrane, causing the formation of a proton gradient across the membrane. The transfer process releases energy when the protons flow back into the mitochondrial interior, forming ATP.
- Describe the electron transport chain and oxidative phosphorylation.
The electron transport system has carrier molecules that transmit electrons from high-energy compounds to low-energy acceptors through the mitochondrial membrane. During these redox reactions, energy is released to produce ATP. In this process NADH or FADH2 pump electrons to this system, containing membrane-bound electron carriers that transfer free electrons from one membrane to another (reduction). During the reduction process, part of the energy released is used to pump hydrogen ions (H+) across the membrane and into the inter-membrane space (Michael, n.d.). Consequently, ATP synthase enzyme uses the osmotic gradient energy resulting from the concentration of H+ in the inter-membrane space to produce ATP. Osmotic pressure then moves the hydrogen ions into the matrix of the mitochondrion via the enzyme.
References
Bhagavan, H. N., & Chopra, R. K. (2007). Plasma coenzyme Q10 response to oral ingestion of coenzyme Q10 formulations. Elsevier B.V. and Mitochondria Research Society Review 7: 78-88. Retrieved from: https://www.grc.com/health/pdf/Plasma_coenzyme_Q10_response_to_oral_ingestion_of_coenzyme_Q10_formulations.pdf
Biology-Online.org. (2008). Lock-and-key model – definition. Retrieved from http://www.biology-online.org/dictionary/Lock-and-key_model
Genetics Home Reference1. (2014). ALDOB. Retrieved from http://ghr.nlm.nih.gov/gene/ALDOB
Genetics Home Reference2. (2014). Hereditary fructose intolerance. Retrieved from http://ghr.nlm.nih.gov/condition/hereditary-fructose-intolerance
Harvey, Richard A. (2013). Lippincott’s Illustrated Reviews: Biochemistry. In Wolters K. ed. 5th edition published by Wolters Kluwer. Retrieved from https://www.inkling.com/read/illustrated-reviews-biochemistry-harvey-5th/chapter-12/fructose-metabolism.
Medh, J. D. (n.d.). The Citric Acid Cycle: Central Role in Catabolism. Retrieved from http://www.csun.edu/~jm77307/Citric%20Acid%20Cycle.pdf
Michael, Gregory J. (n.d.). Cellular Respiration. Retrieved from http://faculty.clintoncc.suny.edu/faculty/Michael.Gregory/files/Bio%20101/Bio%20101%20Lectures/Cellular%20Respiration/cellular.htm
Ukessays.com. (n.d.). The Breakdown of Fructose. Retrieved from http://www.ukessays.com/essays/biology/the-breakdown-of-fructose-biology-essay.php
