Six Functions of Respiration: Isn't It Time to Take Control over ROS Production in Mitochondria, and Aging Along with It?

Autor(en): Skulachev, Vladimir P.
Vyssokikh, Mikhail Yu.
Chernyak, Boris V.
Mulkidjanian, Armen Y.
Skulachev, Maxim V.
Shilovsky, Gregory A.
Lyamzaev, Konstantin G.
Borisov, Vitaliy B.
Severin, Fedor F.
Sadovnichii, Victor A.
Stichwörter: adenosine diphosphate; adenosine triphosphate; aging; animal; animal experiment; animal model; Animals; autophagosome; biological functions; biosynthesis; brain mitochondrion; breathing; cardiolipin; cardiolipin oxidation; Cardiolipins; cell respiration; controlled study; depolarization; ion transport; lipid bilayer; macroautophagy; mammal; Mammals; membrane transport; mitochondria; mitochondrial membrane; mitochondrial membrane potential; mitochondrion; nonhuman; oxidative phosphorylation; Paracoccus denitrificans; phosphate; proton transport; rat; reaction analysis; reactive oxygen metabolite; reactive oxygen species; respiration; respiratory chain; Review; spermatogonium; whole cell
Erscheinungsdatum: 2023
Herausgeber: Multidisciplinary Digital Publishing Institute (MDPI)
Enthalten in: International Journal of Molecular Sciences
Band: 24
Ausgabe: 16
Zusammenfassung: 
Cellular respiration is associated with at least six distinct but intertwined biological functions. (1) biosynthesis of ATP from ADP and inorganic phosphate, (2) consumption of respiratory substrates, (3) support of membrane transport, (4) conversion of respiratory energy to heat, (5) removal of oxygen to prevent oxidative damage, and (6) generation of reactive oxygen species (ROS) as signaling molecules. Here we focus on function #6, which helps the organism control its mitochondria. The ROS bursts typically occur when the mitochondrial membrane potential (MMP) becomes too high, e.g., due to mitochondrial malfunction, leading to cardiolipin (CL) oxidation. Depending on the intensity of CL damage, specific programs for the elimination of damaged mitochondria (mitophagy), whole cells (apoptosis), or organisms (phenoptosis) can be activated. In particular, we consider those mechanisms that suppress ROS generation by enabling ATP synthesis at low MMP levels. We discuss evidence that the mild depolarization mechanism of direct ATP/ADP exchange across mammalian inner and outer mitochondrial membranes weakens with age. We review recent data showing that by protecting CL from oxidation, mitochondria-targeted antioxidants decrease lethality in response to many potentially deadly shock insults. Thus, targeting ROS- and CL-dependent pathways may prevent acute mortality and, hopefully, slow aging. © 2023 by the authors.
Beschreibung: 
Cited by: 0; All Open Access, Gold Open Access, Green Open Access
ISSN: 1661-6596
DOI: 10.3390/ijms241612540
Externe URL: https://www.scopus.com/inward/record.uri?eid=2-s2.0-85168714944&doi=10.3390%2fijms241612540&partnerID=40&md5=b10fc619f87f8211dcaed6eaafb994cb

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