Harper 2018 MiPschool Tromso D1: Difference between revisions
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|editor=[[Beno M]], [[Plangger M]], | |editor=[[Beno M]], [[Plangger M]], | ||
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== Affiliations == | |||
::::Mitochondrial Bioenergetics Lab, Dept Biochemistry, Microbiology Immunology, Fac Medicine, Univ Ottawa, ON, Canada. | |||
{{Labeling | {{Labeling | ||
|injuries=Oxidative stress;RONS | |injuries=Oxidative stress;RONS | ||
|tissues=Heart, Skeletal muscle | |tissues=Heart, Skeletal muscle | ||
|couplingstates=LEAK | |couplingstates=LEAK | ||
|event=D1, Oral | |||
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Latest revision as of 15:33, 16 October 2018
OXPHOS efficiency in skeletal and cardiac muscles: Proton leaks, ROS and glutathione redox. |
Link: MitoEAGLE
Harper ME (2018)
Event: MiPschool Tromso-Bergen 2018
Oxidative phosphorylation (OXPHOS) is estimated to account for roughly 90% of cellular ATP production, though this can vary between cell types, metabolic conditions, and disease states. The efficiency of ATP production by OXPHOS is highly variable, and efficiency can be expressed as units ATP produced per unit of substrate oxidized, or as units ATP produced per unit of oxygen consumed. Efficiency of OXPHOS is affected by site of electron entry into the electron transport system. It also is greatly affected by proton leak uncoupling, and other routes of proton return to the mitochondrial matrix. Proton leak has poorly understood mechanisms, but includes the uncoupling proteins and the adenine nucleotide translocator (ANT). Beyond decreasing the efficiency of OXPHOS, proton leak decreases emission of reactive oxygen species (ROS) from the electron transport system by lowering protonmotive force. High levels of ROS can cause damage to cellular lipids, proteins, DNA and RNA. However low levels of ROS are important in cell signaling processes. Glutathione is the major non-protein antioxidant in cells and in mitochondria. It also plays important roles in the post-translational modification of protein thiols, and this can protect the proteins from further damage, and can modify the function of the proteins. The latter concepts will be covered in this lecture, and experimental findings from studies of skeletal and cardiac muscles will be presented.
• Bioblast editor: Beno M, Plangger M
Affiliations
- Mitochondrial Bioenergetics Lab, Dept Biochemistry, Microbiology Immunology, Fac Medicine, Univ Ottawa, ON, Canada.
Labels:
Stress:Oxidative stress;RONS
Tissue;cell: Heart, Skeletal muscle
Coupling state: LEAK
Event: D1, Oral