Antimycin-insensitive oxidation of succinate and reduced nicotinamide-adenine dinucleotide in electron-transport particles I. pH dependency and hydrogen peroxide formation

Jensen, P.K.

doi:10.1016/0926-6593(66)90057-9

Cited by 129 publications

(59 citation statements)

References 15 publications

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“…It has now been about 50 years since it was showed that electron transfer along mitochondrial respiratory chain leads to ROS formation (Jensen 1966, Loschen et al 1974. The primary reactive species generated within mitochondria by univalent auto-oxidation of electron carriers is O 2…”

Section: Mitochondria-derived H 2 Omentioning

confidence: 99%

Skeletal muscle insulin resistance: role of mitochondria and other ROS sources

Meo

Iossa

Venditti

2017

Journal of Endocrinology

228

103

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At present, obesity is one of the most important public health problems in the world because it causes several diseases and reduces life expectancy. Although it is well known that insulin resistance plays a pivotal role in the development of type 2 diabetes mellitus (the more frequent disease in obese people) the link between obesity and insulin resistance is yet a matter of debate. One of the most deleterious effects of obesity is the deposition of lipids in non-adipose tissues when the capacity of adipose tissue is overwhelmed. During the last decade, reduced mitochondrial function has been considered as an important contributor to 'toxic' lipid metabolite accumulation and consequent insulin resistance. More recent reports suggest that mitochondrial dysfunction is not an early event in the development of insulin resistance, but rather a complication of the hyperlipidemia-induced reactive oxygen species (ROS) production in skeletal muscle, which might promote mitochondrial alterations, lipid accumulation and inhibition of insulin action. Here, we review the literature dealing with the mitochondria-centered mechanisms proposed to explain the onset of obesity-linked IR in skeletal muscle. We conclude that the different pathways leading to insulin resistance may act synergistically because ROS production by mitochondria and other sources can result in mitochondrial dysfunction, which in turn can further increase ROS production leading to the establishment of a harmful positive feedback loop.

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Section: Mitochondria-derived H 2 Omentioning

confidence: 99%

Skeletal muscle insulin resistance: role of mitochondria and other ROS sources

Meo

Iossa

Venditti

2017

Journal of Endocrinology

228

103

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“…Mitochondrial superoxide steady state concentration is 5 to 10 times more than that detected in the nucleus and cytoplasm. Both submitochondrial particles and intact mitochondria contribute to hydrogen peroxide production (Jensen et al, 1966, Hinkle et al, 1967, Chance et al, 1971, Boveris et al, 1972, and Loschen et al, 1975. It was suggested that the whole amount of mitochondrial hydrogen peroxide is due to dismutation of superoxide (Boveris Mitochondrion is one of the major cellular sources and targets of ROS.…”

Section: Mitochondria As a Source Of Rosmentioning

confidence: 99%

Mitochondrial dysfunction in rabies virus infection of neurons

et al. 2013

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“…According to that theory, interventions that lessen the generation or enhance the detoxification of reactive oxygen molecules in an organism should lessen the manifestations of aging and enhance longevity. This "oxygen radical theory of aging" evolved into the "mitochondrial theory of aging" after it was recognized that the mitochondrial electron transport chain is an important source of superoxide generation in the cell (Jensen 1966a).…”

Section: Mitochondrial Hypothesis Of Agingmentioning

confidence: 99%

Physiological Phenotype and Vulnerability in Parkinson's Disease

Surmeier

Guzmán²,

Sánchez³

et al. 2012

Cold Spring Harbor Perspectives in Medicine

102

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This review will focus on the principles underlying the hypothesis that neuronal physiological phenotype-how a neuron generates and regulates action potentials-makes a significant contribution to its vulnerability in Parkinson's disease (PD) and aging. A cornerstone of this hypothesis is that the maintenance of ionic gradients underlying excitability can pose a significant energetic burden for neurons, particularly those that have sustained residence times at depolarized membrane potentials, broad action potentials, prominent Ca 2þ entry, and modest intrinsic Ca 2þ buffering capacity. This energetic burden is shouldered in neurons primarily by mitochondria, the sites of cellular respiration. Mitochondrial respiration increases the production of damaging superoxide and other reactive oxygen species (ROS) that have widely been postulated to contribute to cellular aging and PD. Many of the genetic mutations and toxins associated with PD compromise mitochondrial function, providing a mechanistic linkage between known risk factors and cellular physiology that could explain the pattern of pathology in PD. Because much of the mitochondrial burden created by this atrisk phenotype is created by Ca 2þ entry through L-type voltage-dependent channels for which there are antagonists approved for human use, a neuroprotective strategy to reduce this burden is feasible.

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Antimycin-insensitive oxidation of succinate and reduced nicotinamide-adenine dinucleotide in electron-transport particles I. pH dependency and hydrogen peroxide formation

Cited by 129 publications

References 15 publications

Skeletal muscle insulin resistance: role of mitochondria and other ROS sources

Skeletal muscle insulin resistance: role of mitochondria and other ROS sources

Mitochondrial dysfunction in rabies virus infection of neurons

Physiological Phenotype and Vulnerability in Parkinson's Disease

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