Discussion Post
For this discussion we will use another case study from the National Center for Case Study Teaching in Science (NCCSTS) from the University at Buffalo. This case study explores the order and linkage of the biochemical processes involved in ATP synthesis in mitochondria (glycolysis, TCA cycle, electron transport chain, proton pumping, ATP synthase activity) and discusses how mitochondria may generate heat to maintain body temperature.
Use this link for a PDF of the case study:
As your read through the case study consider the following questions:
A. What are the consequences of a proton gradient and how could a gradient be used in the mitochondrion?
B. What must be an important characteristic of the inner membrane in order for this gradient to be established and maintained?
C. If you "poke a hole" in the inner membrane such that protons can freely move across it, what would happen:
a. To the proton distribution across the inner membrane?
b. To the amount of ATP produced by the mitochondria?
c. To the energy released in the movement of the protons?
D. Most ATP is consumed soon after its production. The cell has ways of detecting how much ATP is produced and needs to keep its supply constant. If you poke a hole through the inner membrane, what might the cell do to try to adapt to the change and reestablish previous levels of ATP? List all the possibilities.
E. What are the physiological effects that DNP has on the body (list as many as possible). Which of these effects are energy-related? Which linked processes do you think DNP is uncoupling taking into account the physiological effects you listed in Question 9?
F. Considering what you know about coupling, what would the effects be of blocking electron transport at each complex?
Original Post - Submit an original post based on the following questions:
A. Based on your understanding of the mechanism of action of DNP, how dangerous do you think DNP really is? For an athlete, what are the consequences of ATP depletion? Should Connor take DNP to lose weight?
B. Defects in electron transport and oxidative phosphorylation are responsible for a myriad of symptoms and diseases. The genetics of mitochondrial disease are complex due to the fact that mitochondrial proteins are encoded both by nuclear and mitochondrial DNA. Because mitochondria vary in number and in importance in different tissues, the outward symptoms are also complex and difficult to diagnose. The Online Mendelian Inheritance in Man® (OMIM®) is a comprehensive, authoritative compendium of human genes and genetic phenotypes that is freely available and updated daily. The full-text, referenced overviews in OMIM contain information on all known Mendelian disorders and over 12,000 genes. Go to https://omim.org/ and perform a search for mitochondrial diseases. Select one that you find interesting. What is the molecular basis of the disease you selected? What are the symptoms? Knowing what you know now about mitochondria, transport, and respiration, explain how the defect might affect respiration. Can you suggest a possible therapy for this disease?