1. Oxidative phosphorylation | Biology (article) - Khan Academy
The electron transport chain forms a proton gradient across the inner mitochondrial membrane, which drives the synthesis of ATP via chemiosmosis. Why do we need ...
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2. The Mitochondrion - Molecular Biology of the Cell - NCBI Bookshelf
In this process of oxidative phosphorylation, the inner mitochondrial membrane serves as a device that changes one form of chemical bond energy to another, ...
Mitochondria occupy a substantial portion of the cytoplasmic volume of eucaryotic cells, and they have been essential for the evolution of complex animals. Without mitochondria, present-day animal cells would be dependent on anaerobic glycolysis for all of their ATP. When glucose is converted to pyruvate by glycolysis, only a very small fraction of the total free energy potentially available from the glucose is released. In mitochondria, the metabolism of sugars is completed: the pyruvate is imported into the mitochondrion and oxidized by O2 to CO2 and H2O. This allows 15 times more ATP to be made than that produced by glycolysis alone.
3. Mitochondrial proton and electron leaks - PMC - NCBI
Mitochondrial proton and electron leak have a major impact on mitochondrial coupling efficiency and production of reactive oxygen species.
Mitochondrial proton and electron leak have a major impact on mitochondrial coupling efficiency and production of reactive oxygen species. In the first part of this chapter, we address the molecular nature of the basal and inducible proton leak pathways, ...
4. 5.2: Electron Transport and Oxidative Phosphorylation - Biology LibreTexts
Mar 6, 2021 · In eukaryotic cells, the vast majority of ATP synthesis occurs in the mitochondria in a process called oxidative phosphorylation.
See AlsoCountercurrent Exchange In The Fish Gill Helps To Maximize ________.Which Of The Following Is A Key Part Of The Formation Of Most Natural Bridges?Breaking Down Glucose Into PyruvateWhat Is The Correct Order Of Processes Involving The Movement Of Oxygen From The Environment To Mitochondria In Vertebrates?In eukaryotic cells, the vast majority of ATP synthesis occurs in the mitochondria in a process called oxidative phosphorylation. Even plants, which generate ATP by photophosphorylation in …
5. 4.3 Citric Acid Cycle and Oxidative Phosphorylation
Missing: cross predict
Chapter 4: Introduction to How Cells Obtain Energy
6. Thermodynamic efficiency, reversibility, and degree of coupling ...
Aug 18, 2020 · The protonmotive mitochondrial respiratory chain, comprising complexes I, III and IV, transduces free energy of the electron transfer ...
The protonmotive mitochondrial respiratory chain, comprising complexes I, III and IV, transduces free energy of the electron transfer reactions to an electrochemical proton gradient across the inner mitochondrial membrane. This gradient is used to drive synthesis of ATP and ion and metabolite transport. The efficiency of energy conversion is of interest from a physiological point of view, since the energy transduction mechanisms differ fundamentally between the three complexes. Here, we have chosen actively phosphorylating mitochondria as the focus of analysis. For all three complexes we find that the thermodynamic efficiency is about 80–90% and that the degree of coupling between the redox and proton translocation reactions is very high during active ATP synthesis. However, when net ATP synthesis stops at a high ATP/ADP.Pi ratio, and mitochondria reach “State 4” with an elevated proton gradient, the degree of coupling drops substantially. The mechanistic cause and the physiological implications of this effect are discussed. Wikström and Springett analyze the thermodynamic efficiency of redox reactions and proton translocation by the complexes of mitochondrial respiratory chain. They report that the thermodynamic efficiency is about 80–90% and that the degree of coupling between the redox and proton translocation reactions is very high during active ATP synthesis, but decreases when ATP synthesis stops.
7. Regulation of Oxidative Phosphorylation of Liver ... - MDPI
(1) The electron transport chain; (2) the uncoupling of oxidation from phosphorylation by leaking H+ across the inner mitochondrial membrane (Leak); and (3) ...
The link between liver dysfunction and decreased mitochondrial oxidative phosphorylation in sepsis has been clearly established in experimental models. Energy transduction is plastic: the efficiency of mitochondrial coupling collapses in the early stage of sepsis but is expected to increase during the recovery phases of sepsis. Among the mechanisms regulating the coupling efficiency of hepatic mitochondria, the slipping reactions at the cytochrome oxidase and ATP synthase seem to be a determining element, whereas other regulatory mechanisms such as those involving proton leakage across the mitochondrial membrane have not yet been formally proven in the context of sepsis. If the dysfunction of hepatic mitochondria is related to impaired cytochrome c oxidase and ATP synthase functions, we need to consider therapeutic avenues to restore their activities for recovery from sepsis. In this review, we discussed previous findings regarding the regulatory mechanism involved in changes in the oxidative phosphorylation of liver mitochondria in sepsis, and propose therapeutic avenues to improve the functions of cytochrome c oxidase and ATP synthase in sepsis.
8. Cellular Respiration | Biology for Majors I - Lumen Learning
... will not allow it to cross the hydrophobic interior of the ... This illustration shows the electron transport chain embedded in the inner mitochondrial membrane.
Now that we’ve learned how autotrophs like plants convert sunlight to sugars, let’s take a look at how all eukaryotes—which includes humans!—make use of those sugars.
9. What would happen to cellular respiration if H+ could freely move ...
Oct 23, 2019 · If protons (H+) were able to freely move across the mitochondrial membrane, cellular respiration will not occur.
What would happen to cellular respiration if H+ could freely move across the mitochondrial membranes?
10. A radical shift in perspective: mitochondria as regulators of ...
Apr 1, 2017 · ADP activates the mitochondrial ATP synthase, thus allowing protons to return to the matrix side of the inner mitochondrial membrane, and ...
Summary: Mitochondria are often considered to be a source of harmful reactive oxygen species. Here, we explain how they may behave as regulators of hydrogen peroxide, an important ROS in cellular function.
11. and H+-Fluxes Drive ATP Synthesis and Enable Mitochondrial K+ ...
Finally, that part of the proton gradient and energy not being directly dissipated via ATP synthase because of the equivalent movement of charge as K+ would ...
Abstract. ATP synthase (F1Fo) synthesizes daily our body's weight in ATP, whose production-rate can be transiently increased several-fold to meet changes in ene
12. Prescription drugs and mitochondrial metabolism - Portland Press
Mitochondria are central to the physiology and survival of nearly all eukaryotic cells and house diverse metabolic processes including oxidative ...
Abstract. Mitochondria are central to the physiology and survival of nearly all eukaryotic cells and house diverse metabolic processes including oxidative phosphorylation, reactive oxygen species buffering, metabolite synthesis/exchange, and Ca2+ sequestration. Mitochondria are phenotypically heterogeneous and this variation is essential to the complexity of physiological function among cells, tissues, and organ systems. As a consequence of mitochondrial integration with so many physiological processes, small molecules that modulate mitochondrial metabolism induce complex systemic effects. In the case of many commonly prescribed drugs, these interactions may contribute to drug therapeutic mechanisms, induce adverse drug reactions, or both. The purpose of this article is to review historical and recent advances in the understanding of the effects of prescription drugs on mitochondrial metabolism. Specific ‘modes’ of xenobiotic–mitochondria interactions are discussed to provide a set of qualitative models that aid in conceptualizing how the mitochondrial energy transduction system may be affected. Findings of recent in vitro high-throughput screening studies are reviewed, and a few candidate drug classes are chosen for additional brief discussion (i.e. antihyperglycemics, antidepressants, antibiotics, and antihyperlipidemics). Finally, recent improvements in pharmacokinetics models that aid in quantifying systemic effects of drug–mitochondria interactions are briefly considered.
