New extension of the Mitchell Theory for oxidative phosphorylation in mitochondria of living organisms
The Mitchell Theory implies the proton motive force Δp across the inner mitochondrial membrane as the energy-rich intermediate of oxidative phosphorylation. Δp is composed mainly of an electrical (ΔΨ m) and a chemical part (ΔpH) and generated by the respiratory chain complexes I, III and IV. It is c...
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| Published in | Biochimica et biophysica acta Vol. 1800; no. 3; pp. 205 - 212 |
|---|---|
| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
| Published |
Netherlands
Elsevier B.V
01.03.2010
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| Subjects | |
| Online Access | Get full text |
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| Abstract | The Mitchell Theory implies the proton motive force Δp across the inner mitochondrial membrane as the energy-rich intermediate of oxidative phosphorylation. Δp is composed mainly of an electrical (ΔΨ
m) and a chemical part (ΔpH) and generated by the respiratory chain complexes I, III and IV. It is consumed mostly by the ATP synthase (complex V) to produce ATP. The free energy of electron transport within the proton pumps is sufficient to generate Δp of about 240 mV. The proton permeability of biological membranes, however, increases exponentially above 130 mV leading to a waste of energy at high values (ΔΨ
m
>
140 mV). In addition, at ΔΨ
m
>
140 mV, the production of the superoxide radical anion O
2
−
at complexes I, II and III increases exponentially with increasing ΔΨ
m. O
2
−
and its neutral product H
2O
2 (=
ROS, reactive oxygen species) induce oxidative stress which participates in aging and in the generation of degenerative diseases. Here we describe a new mechanism which acts independently of the Mitchell Theory and keeps ΔΨ
m at low values through feedback inhibition of complex IV (cytochrome
c oxidase) at high ATP/ADP ratios, thus preventing the formation of ROS and maintaining high efficiency of oxidative phosphorylation. |
|---|---|
| AbstractList | The Mitchell Theory implies the proton motive force Deltap across the inner mitochondrial membrane as the energy-rich intermediate of oxidative phosphorylation. Deltap is composed mainly of an electrical (DeltaPsi(m)) and a chemical part (DeltapH) and generated by the respiratory chain complexes I, III and IV. It is consumed mostly by the ATP synthase (complex V) to produce ATP. The free energy of electron transport within the proton pumps is sufficient to generate Deltap of about 240 mV. The proton permeability of biological membranes, however, increases exponentially above 130 mV leading to a waste of energy at high values (DeltaPsi(m)>140 mV). In addition, at DeltaPsi(m)>140 mV, the production of the superoxide radical anion O(2)(-) at complexes I, II and III increases exponentially with increasing DeltaPsi(m). O(2)(-) and its neutral product H(2)O(2) (=ROS, reactive oxygen species) induce oxidative stress which participates in aging and in the generation of degenerative diseases. Here we describe a new mechanism which acts independently of the Mitchell Theory and keeps DeltaPsi(m) at low values through feedback inhibition of complex IV (cytochrome c oxidase) at high ATP/ADP ratios, thus preventing the formation of ROS and maintaining high efficiency of oxidative phosphorylation. The Mitchell Theory implies the proton motive force Deltap across the inner mitochondrial membrane as the energy-rich intermediate of oxidative phosphorylation. Deltap is composed mainly of an electrical (DeltaPsi(m)) and a chemical part (DeltapH) and generated by the respiratory chain complexes I, III and IV. It is consumed mostly by the ATP synthase (complex V) to produce ATP. The free energy of electron transport within the proton pumps is sufficient to generate Deltap of about 240 mV. The proton permeability of biological membranes, however, increases exponentially above 130 mV leading to a waste of energy at high values (DeltaPsi(m)>140 mV). In addition, at DeltaPsi(m)>140 mV, the production of the superoxide radical anion O(2)(-) at complexes I, II and III increases exponentially with increasing DeltaPsi(m). O(2)(-) and its neutral product H(2)O(2) (=ROS, reactive oxygen species) induce oxidative stress which participates in aging and in the generation of degenerative diseases. Here we describe a new mechanism which acts independently of the Mitchell Theory and keeps DeltaPsi(m) at low values through feedback inhibition of complex IV (cytochrome c oxidase) at high ATP/ADP ratios, thus preventing the formation of ROS and maintaining high efficiency of oxidative phosphorylation.The Mitchell Theory implies the proton motive force Deltap across the inner mitochondrial membrane as the energy-rich intermediate of oxidative phosphorylation. Deltap is composed mainly of an electrical (DeltaPsi(m)) and a chemical part (DeltapH) and generated by the respiratory chain complexes I, III and IV. It is consumed mostly by the ATP synthase (complex V) to produce ATP. The free energy of electron transport within the proton pumps is sufficient to generate Deltap of about 240 mV. The proton permeability of biological membranes, however, increases exponentially above 130 mV leading to a waste of energy at high values (DeltaPsi(m)>140 mV). In addition, at DeltaPsi(m)>140 mV, the production of the superoxide radical anion O(2)(-) at complexes I, II and III increases exponentially with increasing DeltaPsi(m). O(2)(-) and its neutral product H(2)O(2) (=ROS, reactive oxygen species) induce oxidative stress which participates in aging and in the generation of degenerative diseases. Here we describe a new mechanism which acts independently of the Mitchell Theory and keeps DeltaPsi(m) at low values through feedback inhibition of complex IV (cytochrome c oxidase) at high ATP/ADP ratios, thus preventing the formation of ROS and maintaining high efficiency of oxidative phosphorylation. The Mitchell Theory implies the proton motive force Δp across the inner mitochondrial membrane as the energy-rich intermediate of oxidative phosphorylation. Δp is composed mainly of an electrical (ΔΨ m) and a chemical part (ΔpH) and generated by the respiratory chain complexes I, III and IV. It is consumed mostly by the ATP synthase (complex V) to produce ATP. The free energy of electron transport within the proton pumps is sufficient to generate Δp of about 240 mV. The proton permeability of biological membranes, however, increases exponentially above 130 mV leading to a waste of energy at high values (ΔΨ m > 140 mV). In addition, at ΔΨ m > 140 mV, the production of the superoxide radical anion O 2 − at complexes I, II and III increases exponentially with increasing ΔΨ m. O 2 − and its neutral product H 2O 2 (= ROS, reactive oxygen species) induce oxidative stress which participates in aging and in the generation of degenerative diseases. Here we describe a new mechanism which acts independently of the Mitchell Theory and keeps ΔΨ m at low values through feedback inhibition of complex IV (cytochrome c oxidase) at high ATP/ADP ratios, thus preventing the formation of ROS and maintaining high efficiency of oxidative phosphorylation. |
| Author | Kadenbach, Bernhard Ramzan, Rabia Wen, Li Vogt, Sebastian |
| Author_xml | – sequence: 1 givenname: Bernhard surname: Kadenbach fullname: Kadenbach, Bernhard organization: Fachbereich Chemie, Cardiovascular Laboratory, Philipps-University, D-35032 Marburg, Germany – sequence: 2 givenname: Rabia surname: Ramzan fullname: Ramzan, Rabia organization: Fachbereich Chemie, Cardiovascular Laboratory, Philipps-University, D-35032 Marburg, Germany – sequence: 3 givenname: Li surname: Wen fullname: Wen, Li email: kadenbach@staff.uni-marburg.de organization: Biomedical Research Center, Cardiovascular Laboratory, Philipps-University, D-35032 Marburg, Germany – sequence: 4 givenname: Sebastian surname: Vogt fullname: Vogt, Sebastian organization: Biomedical Research Center, Cardiovascular Laboratory, Philipps-University, D-35032 Marburg, Germany |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/19409964$$D View this record in MEDLINE/PubMed |
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| Keywords | Cytochrome c oxidase Oxidative stress Degenerative disease Protein phosphorylation Mitchell Theory Hyperpolarization Mitochondrial membrane potential |
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| Snippet | The Mitchell Theory implies the proton motive force Δp across the inner mitochondrial membrane as the energy-rich intermediate of oxidative phosphorylation. Δp... The Mitchell Theory implies the proton motive force Deltap across the inner mitochondrial membrane as the energy-rich intermediate of oxidative... |
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| SubjectTerms | Adenosine Diphosphate - metabolism Adenosine Triphosphate - metabolism Animals Apoptosis Cytochrome c oxidase Degenerative disease Disease Humans Hyperpolarization Mitchell Theory Mitochondria - metabolism Mitochondrial membrane potential Mitochondrial Membranes - metabolism Models, Theoretical Oxidative Phosphorylation Oxidative Stress Oxygen Consumption Protein Kinases - metabolism Protein phosphorylation Protein Subunits - metabolism Proton Pumps Reactive Oxygen Species - metabolism |
| Title | New extension of the Mitchell Theory for oxidative phosphorylation in mitochondria of living organisms |
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