Mitochondrial energetic metabolism—some general principles

Mazat, Jean‐Pierre; Ransac, Stéphane; Heiske, Margit; Devin, Anne; Rigoulet, Michel

doi:10.1002/iub.1138

Cited by 38 publications

(30 citation statements)

References 60 publications

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“…The enzyme activity of MRC proteins, which is essential for maintenance of the mitochondrial membrane potential (ΔΨm), is critical for ATP synthesis. Loss of the ΔΨm leads to a reduction in energy production, an increase in the permeability of the mitochondrial membrane, and the release of apoptotic factors such as cytochrome c , apoptosis‐inducing factor, and procaspases from the mitochondria into the cytoplasm …”

Section: Mitochondrial Activity In Oamentioning

confidence: 99%

Apoptosis signaling pathways in osteoarthritis and possible protective role of melatonin

Hosseinzadeh

Kamrava

Joghataei

et al. 2016

Journal of Pineal Research

292

172

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Osteoarthritis (OA) is a degenerative joint disease characterized by progressive erosion of articular cartilage. As chondrocytes are the only cell type forming the articular cartilage, their gradual loss is the main cause of OA. There is a substantial body of published research that suggests reactive oxygen species (ROS) are major causative factors for chondrocyte damage and OA development. Oxidative stress elicited by ROS is capable of oxidizing and subsequently disrupting cartilage homeostasis, promoting catabolism via induction of cell death and damaging numerous components of the joint. IL-1β and TNF-α are crucial inflammatory factors that play pivotal roles in the pathogenesis of OA. In this process, the mitochondria are the major source of ROS production in cells, suggesting a role of mitochondrial dysfunction in this type of arthritis. This may also be promoted by inflammatory cytokines such as IL-1β and TNF-α which contribute to chondrocyte death. In patients with OA, the expression of endoplasmic reticulum (ER) stress-associated molecules is positively correlated with cartilage degeneration. Melatonin and its metabolites are broadspectrum antioxidants and free radical scavengers which regulate a variety of molecular pathways such as inflammation, proliferation, apoptosis, and metastasis in different pathophysiological situations. Herein, we review the effects of melatonin on OA, focusing on its ability to regulate apoptotic processes and ER and mitochondrial activity. We also evaluate likely protective effects of melatonin on OA pathogenesis. K E Y W O R D Sapoptosis, endoplasmic reticulum, inflammation, melatonin, mitochondria, molecular actions, osteoarthritis, oxidative stress

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Section: Mitochondrial Activity In Oamentioning

confidence: 99%

Apoptosis signaling pathways in osteoarthritis and possible protective role of melatonin

Hosseinzadeh

Kamrava

Joghataei

et al. 2016

Journal of Pineal Research

292

172

View full text Add to dashboard Cite

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“…More importantly, although there is a direct stoichiometry between the oxidation of a substrate molecule and the production of NADHCH C and FADH 2 , NADHCH C can be reoxidised in reactions other than Complex I of the ETC and the proton motive force generated by the ETC can be dissipated by processes other than ATP synthesis (e.g. counter-ion transport and uncoupling protein activity) (Mazat et al 2013). The concepts of efficiency and plasticity in the coupling of substrate oxidation to energy conservation (ATP synthesis) have been expanded on in several authoritative review articles (Harper et al 2008, Mazat et al 2013.…”

Section: Fuel For Energy Productionmentioning

confidence: 99%

“…counter-ion transport and uncoupling protein activity) (Mazat et al 2013). The concepts of efficiency and plasticity in the coupling of substrate oxidation to energy conservation (ATP synthesis) have been expanded on in several authoritative review articles (Harper et al 2008, Mazat et al 2013. These review articles have highlighted the presence of a significant and variable basal proton leak in mitochondria (20-25%) of most tissues and reported that in perfused rat muscle systems futile proton cycling may contribute as much as 50% to the respiration rate (Rolfe & Brand 1996), although other methodologies have suggested that this could be as little as 10% (Marcinek et al 2004, Conley et al 2007.…”

Section: Fuel For Energy Productionmentioning

confidence: 99%

Fatty acid metabolism, energy expenditure and insulin resistance in muscle

Turner¹,

Cooney²,

Kraegen³

et al. 2013

Journal of Endocrinology

167

120

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Fatty acids (FAs) are essential elements of all cells and have significant roles as energy substrates, components of cellular structure and signalling molecules. The storage of excess energy intake as fat in adipose tissue is an evolutionary advantage aimed at protecting against starvation, but in much of today's world, humans are faced with an unlimited availability of food, and the excessive accumulation of fat is now a major risk for human health, especially the development of type 2 diabetes (T2D). Since the first recognition of the association between fat accumulation, reduced insulin action and increased risk of T2D, several mechanisms have been proposed to link excess FA availability to reduced insulin action, with some of them being competing or contradictory. This review summarises the evidence for these mechanisms in the context of excess dietary FAs generating insulin resistance in muscle, the major tissue involved in insulin-stimulated disposal of blood glucose. It also outlines potential problems with models and measurements that may hinder as well as help improve our understanding of the links between FAs and insulin action. (C:18:0), oleic acid (C18:1n-9), linoleic acid (C18:2n-6) and, particularly in smaller mammals, arachidonic acid (20:4n-6) and docosahexaenoic acid (22:6n-3). These FAs are the major components of storage triglycerides and cellular membranes, and although C16-C18 FAs are also components of some of the FA-derived signalling molecules (diacylglycerols (DAGs) and ceramides), many of the major lipid signalling molecules (prostaglandins and leukotrienes) are synthesised from very-long-chain, unsaturated FAs (e.g. arachidonic and docosahexaenoic acids) ( Kruger et al. 2010).In the context of the links between excessive lipid storage (obesity) and reduced insulin action (insulin Journal of EndocrinologyThematic Review N TURNER and others Fatty acids and insulin action 220:2 T61-T79

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“…However, despite detailed crystallographic information, the precise mechanisms involved in this coupling remain unclear (Mazat et al, 2013). The unusual arrangement in terms of the biochemical synthesis being indirectly linked to the generation of potential and proton movement makes the system appear inexact and thereby to violate chemical principles (Wilson and Forman, 1982).…”

Section: Oxidative Phosphorylationmentioning

confidence: 98%

“…This gives a total of 10 potential protons pumped per NADH fed into the electron transport chain. The chemiosmotic mechanism provides a mechanism for connecting the energy derived from the flow of electrons down the respiratory electron transport chain to ATP synthase (or as it is sometimes referred to, complex V) (Mazat et al, 2013).…”

Section: Oxidative Phosphorylationmentioning

confidence: 99%