Mitochondrial Oxidative Phosphorylation

Kadenbach, Bernhard

doi:10.1007/978-1-4614-3573-0

Cited by 17 publications

(4 citation statements)

References 689 publications

(1,060 reference statements)

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“…This study also finds evidence to suggest that electrons from ubiquinol (QH 2 ) generated by succinate oxidation at CII can be transferred in both the forward direction to CIII and the reverse direction to CI (RET) [38,57]. This was indicated by both the increased efficiency of the CII-dependent rate of ATP synthesis and the higher rate of H 2 O 2 production, when measured in the presence of the CI inhibitor rotenone.…”

Section: Discussionmentioning

confidence: 68%

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Neuronal and astrocyte dysfunction diverges from embryonic fibroblasts in theNdufs4fky/fkymouse

et al. 2014

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Mitochondrial dysfunction causes a range of early-onset neurological diseases and contributes to neurodegenerative conditions. The mechanisms of neurological damage however are poorly understood, as accessing relevant tissue from patients is difficult, and appropriate models are limited. Hence, we assessed mitochondrial function in neurologically relevant primary cell lines from a CI (complex I) deficient Ndufs4 KO (knockout) mouse (Ndufs4fky/fky) modelling aspects of the mitochondrial disease LS (Leigh syndrome), as well as MEFs (mouse embryonic fibroblasts). Although CI structure and function were compromised in all Ndufs4fky/fky cell types, the mitochondrial membrane potential was selectively impaired in the MEFs, correlating with decreased CI-dependent ATP synthesis. In addition, increased ROS (reactive oxygen species) generation and altered sensitivity to cell death were only observed in Ndufs4fky/fky primary MEFs. In contrast, Ndufs4fky/fky primary isocortical neurons and primary isocortical astrocytes displayed only impaired ATP generation without mitochondrial membrane potential changes. Therefore the neurological dysfunction in the Ndufs4fky/fky mouse may partly originate from a more severe ATP depletion in neurons and astrocytes, even at the expense of maintaining the mitochondrial membrane potential. This may provide protection from cell death, but would ultimately compromise cell functionality in neurons and astrocytes. Furthermore, RET (reverse electron transfer) from complex II to CI appears more prominent in neurons than MEFs or astrocytes, and is attenuated in Ndufs4fky/fky cells.

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Section: Discussionmentioning

confidence: 68%

“…Together these data imply that RET (reverse electron transfer) may occur in all primary cell types examined. The term RET describes the process in which ubiquinol generated by CII donates electrons to a reverse CI reaction rather than to the forward CIII reaction [38]. RET is blocked by rotenone inhibition of CI.…”

Section: Resultsmentioning

confidence: 99%

Neuronal and astrocyte dysfunction diverges from embryonic fibroblasts in theNdufs4fky/fkymouse

et al. 2014

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“…Drp1 inhibition under these conditions likely rebalanced the regulatory machinery of mitochondrial dynamics. Altogether, it suggests that the balance in mitochondrial dynamics is essential for the regulation of skeletal muscle quality and function (Ferree & Shirihai, 2012). Second, our study used a pharmacological inhibitor that inhibited Drp1 translocation without total Drp1 content reduction in mice.…”

Section: Discussionmentioning

confidence: 89%

“…Mitochondria are highly dynamic organelles that continually fuse (fusion) and divide (fission; Ferree & Shirihai, 2012). The orchestrated balance of fusion and fission is crucial in maintaining mitochondrial morphology, quality, and function (Wai & Langer, 2016).…”

Section: Introductionmentioning

confidence: 99%

Pharmacological inhibition of dynamin‐related protein 1 attenuates skeletal muscle insulin resistance in obesity

et al. 2021

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Toxic effects of hydrogen sulfide donor NaHS induced liver apoptosis is regulated by complex IV subunits and reactive oxygen species generation in rats

Feng

Zhang

Shi

et al. 2019

Environmental Toxicology

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In recent years, the protective effect of hydrogensulfide donor sodium hydrosulfide (NaHS) on multiple organs has been widely reported. The study aimed to explorethe effect of commonly used concentration of NaHS on theliver and its potential damage mechanism. Rats divided into 4 groups: control, NaHS I (1 mg/kg), II (3 mg/kg) and III (5 mg/kg) groups, and each group is divided into four-timepoints (2, 6, 12, and 24 hours). Results showed that H2S concentration increased, mitochondrial complex IV activity inhibited, the COX I and IV subunits and mitochondrial apoptosis pathwayrelated proteins expression increased in atime-and dose-dependent manner. We confirmed that 1 mg/kg NaHS had no injuryeffect on the liver, 3 and 5 mg/kg NaHS inhibitsthe activity of mitochondrial complex IV by promoting COX I and IV subunits expression, leading to the increase in ROS and ultimately inducing apoptosis and liver injury.apoptosis, COX I and COX IV subunits, hepatotoxicity, hydrogen sulfide, reactive oxygen species

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Mitochondrial Oxidative Phosphorylation

Cited by 17 publications

References 689 publications

Neuronal and astrocyte dysfunction diverges from embryonic fibroblasts in theNdufs4fky/fkymouse

Neuronal and astrocyte dysfunction diverges from embryonic fibroblasts in theNdufs4fky/fkymouse

Pharmacological inhibition of dynamin‐related protein 1 attenuates skeletal muscle insulin resistance in obesity

Toxic effects of hydrogen sulfide donor NaHS induced liver apoptosis is regulated by complex IV subunits and reactive oxygen species generation in rats

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