Mitochondrial reactive oxygen species production and elimination

Nickel, Alexander; Kohlhaas, M; Maack, Christoph

doi:10.1016/j.yjmcc.2014.03.011

Cited by 269 publications

(226 citation statements)

References 153 publications

Supporting

Mentioning

211

Contrasting

Unclassified

Order By: Relevance

“…Reactive oxygen species were initially considered to be toxic molecules but a growing body of evidence suggests that oxidative stress, which is the result of a balance between the formation of ROS and their scavenging by antioxidant defenses, is regulated and participates to the maintenance of redox homeostasis and various cellular signaling pathways. In normal cells, the cellular and mitochondrial levels of ROS are safe and participate to the vital activity of the cell (Angelova & Abramov, 2016; Bae, Oh, Rhee, & Yoo, 2011; Dröge, 2002; Nickel, Kohlhaas, & Maack, 2014). However, under acute and chronic cellular stress conditions (e.g., acute ischemia and neurodegenerative diseases, respectively), the production of ROS is no longer regulated and becomes detrimental for the cell.…”

Section: Regulating Factors Of Mptp and Agingmentioning

confidence: 99%

Mitochondria and aging: A role for the mitochondrial transition pore?

2018

View full text Add to dashboard Cite

SummaryThe cellular mechanisms responsible for aging are poorly understood. Aging is considered as a degenerative process induced by the accumulation of cellular lesions leading progressively to organ dysfunction and death. The free radical theory of aging has long been considered the most relevant to explain the mechanisms of aging. As the mitochondrion is an important source of reactive oxygen species (ROS), this organelle is regarded as a key intracellular player in this process and a large amount of data supports the role of mitochondrial ROS production during aging. Thus, mitochondrial ROS, oxidative damage, aging, and aging‐dependent diseases are strongly connected. However, other features of mitochondrial physiology and dysfunction have been recently implicated in the development of the aging process. Here, we examine the potential role of the mitochondrial permeability transition pore (mPTP) in normal aging and in aging‐associated diseases.

show abstract

Section: Regulating Factors Of Mptp and Agingmentioning

confidence: 99%

Mitochondria and aging: A role for the mitochondrial transition pore?

2018

View full text Add to dashboard Cite

show abstract

“…In addition, it is becoming increasingly clear that mitochondria can act as dynamic receivers, integrators, and transmitters of oxidative stress derived from various sources (Nickel et al, 2014). We and others have shown that also disturbances in peroxisomal redox metabolism have an immediate impact on mitochondrial ROS production, both in cellulo (Walton and Pizzitelli, 2012;Wang et al, 2013b) and in vivo (López-Erauskin et al, 2013;Peeters et al, 2015).…”

Section: Physiological Significancementioning

confidence: 98%

Molecular Mechanisms and Physiological Significance of Organelle Interactions and Cooperation

2017

Frontiers Research Topics

View full text Add to dashboard Cite

“…ROS are considered the main cause of development of degenerative diseases 25, for damaging the heart after ischaemia 26, and in development and progression of heart failure (Box 3) 27, 28, 29, 30, 31, 32.…”

Section: Introductionmentioning

confidence: 99%

Revisiting Kadenbach: Electron flux rate through cytochrome c‐oxidase determines the ATP‐inhibitory effect and subsequent production of ROS

et al. 2016

View full text Add to dashboard Cite

Mitochondrial respiration is the predominant source of ATP. Excessive rates of electron transport cause a higher production of harmful reactive oxygen species (ROS). There are two regulatory mechanisms known. The first, according to Mitchel, is dependent on the mitochondrial membrane potential that drives ATP synthase for ATP production, and the second, the Kadenbach mechanism, is focussed on the binding of ATP to Cytochrome c Oxidase (CytOx) at high ATP/ADP ratios, which results in an allosteric conformational change to CytOx, causing inhibition. In times of stress, ATP‐dependent inhibition is switched off and the activity of CytOx is exclusively determined by the membrane potential, leading to an increase in ROS production. The second mechanism for respiratory control depends on the quantity of electron transfer to the Heme aa3 of CytOx. When ATP is bound to CytOx the enzyme is inhibited, and ROS formation is decreased, although the mitochondrial membrane potential is increased.

show abstract

Mitochondrial reactive oxygen species production and elimination

Cited by 269 publications

References 153 publications

Mitochondria and aging: A role for the mitochondrial transition pore?

Mitochondria and aging: A role for the mitochondrial transition pore?

Molecular Mechanisms and Physiological Significance of Organelle Interactions and Cooperation

Revisiting Kadenbach: Electron flux rate through cytochrome c‐oxidase determines the ATP‐inhibitory effect and subsequent production of ROS

Contact Info

Product

Resources

About