Chat with AIExam 5: Aerobic Respiration and the Mitochondrion
A preparation of submitochondrial particles is made.The particles are able to oxidize substrates,generate a proton gradient and make ATP.If the particles are treated with urea,what happens? If DNP is added,what happens? How does DNP make the inner mitochondrial membrane permeable to protons?
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VerifiedUrea treatment removes the F1 spheres from ATP synthase.As a result,the membrane is no longer able to maintain the proton gradient.Protons leak out of the F0 base piece in an uncontrolled fashion when the headpiece is removed and ATP cannot be made because the headpiece that makes it is gone.DNP also uncouples ATP production from electron transport.It causes the membrane to become permeable to protons and thus dissipates the proton gradient,making ATP production by ATP synthase impossible.DNP combines with protons and,because of its lipid solubility,carries the protons across the inner mitochondrial membrane down their electrochemical gradient.
Why does the DNA in mitochondria exhibit about 10 times the mutation rate seen in nuclear DNA and what is the possible effect of this on disease processes?
(33) VerifiedBecause of its proximity to electron-transport processes,which lead to the release of mutagenic oxygen radicals,mtDNA is thought to come under a much greater level of attack than nuclear DNA.In addition,nuclear DNA is better protected from persistent damage by the presence of a greater variety of DNA repair systems.Thus,damage inflicted upon nuclear DNA can be repaired,while damage to mitochondrial DNA cannot be repaired as effectively.These factors explain the greater than 10-fold higher mutation rate of mtDNA.Thus,mutations are particularly likely to accumulate in the mitochondria of cells that remain in the body for long periods of time (nerves and muscle tissue).The degenerative changes in mitochondrial functions are thought to contribute to a number of common neurological diseases with adult-onset,most notably Parkinson's disease (PD).
___________ exhibit lower electron affinity.
(36) VerifiedC
Observations of two different cell types indicate a couple of differences in their mitochondria.Cell type 1 has 2-3 times the mitochondria of Cell Type 2.The mitochondria in Cell Type 1 are also larger,contain more cristae and the cristae extend farther across the mitochondria than in Cell Type 2.Which cell type is likely to have more extensive energy requirements?
(36) What energy source other than ATP hydrolysis do mitochondria,unlike most other organelles,routinely use to power their activities?
(43) You treat some cells with DNP and discover that ATP production ceases.Upon closer examination,you also note that the number of calcium ions sequestered in the mitochondrion decreases.Please explain.
(41) What causes Zellweger's syndrome? What do the peroxisomes of ZS patients look like?
(33) When fission of mitochondria becomes more frequent than fusion,the mitochondria tend to become __________.
(37) The presence of Ca2+ ion transport molecules in the inner mitochondrial membrane is consistent with the mitochondrion's role in _______.
(38) How is the energy used to make ATP via the electron transport chain generated?
(28) What are the structural features of electron-transport complexes that allow them to function as proton pumps?
(37) What happens to the mtDNA of mice that are homozygous for the mutant gene called Polg? How do the "mutator" mice differ from their normal littermates? How do mice that are heterozygous for the Polg mutation differ from those that are homozygous for the Polg mutation? What should have happened to the life span of mice heterozygous for the Polg gene,if mtDNA mutations were a major contributor to the normal aging process? What do the above results of studies of the Polg mutation suggest about the relationship between mtDNA mutations and premature aging in animals?
(31) Why must the process by which cytochrome oxidase works be efficient?
(38) Which activity below is not thought to be driven by the proton-motive force?
(29) Which mitochondrial genes when mutated or experiencing deletions cause the most serious disorders?
(26) A patient who has abnormal mitochondria has the following symptoms: long-term fatigue and muscle weakness,elevated metabolic rate and body temperature.Studies indicate that the mitochondria have been released from their normal respiratory control.How does this explain the elevated temperature? Why are most disorders that have been traced to mitochondrial dysfunction characterized by degeneration of muscle or brain tissue? What are the characteristics of some of the conditions that result from dysfunctional mitochondria?
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