The Mitochondrial Interplay of Ubiquinol and Nitric Oxide in Endotoxemia

Lisdero, Constanza; Carreras, Marı́a Cecilia; Meulemans, A.; Melani, Mariana; Aubier, Michel; Boczkowski, Jorge; Poderoso, Juan José

doi:10.1016/s0076-6879(04)82004-4

Cited by 25 publications

(17 citation statements)

References 28 publications

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“…In pathologic conditions, such as endotoxemia, we and others have shown that iNOS can also be present in mitochondria and contribute to mitochondrial damage observed in experimental sepsis models (20,21).…”

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confidence: 78%

Mitochondrial Nitric Oxide Synthase: A Masterpiece of Metabolic Adaptation, Cell Growth, Transformation, and Death

Finocchietto

Franco

Holod

et al. 2009

Exp Biol Med (Maywood)

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Mitochondria are specialized organelles that control energy metabolism and also activate a multiplicity of pathways that modulate cell proliferation and mitochondrial biogenesis or, conversely, promote cell arrest and programmed cell death by a limited number of oxidative or nitrative reactions. Nitric oxide (NO) regulates oxygen uptake by reversible inhibition of cytochrome oxidase and the production of superoxide anion from the mitochondrial electron transfer chain. In this sense, NO produced by mtNOS will set the oxygen uptake level and contribute to oxidation-reduction reaction (redox)-dependent cell signaling. Modulation of translocation and activation of neuronal nitric oxide synthase (mtNOS activity) under different physiologic or pathologic conditions represents an adaptive response properly modulated to adjust mitochondria to different cell challenges.

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confidence: 78%

Mitochondrial Nitric Oxide Synthase: A Masterpiece of Metabolic Adaptation, Cell Growth, Transformation, and Death

Finocchietto

Franco

Holod

et al. 2009

Exp Biol Med (Maywood)

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“…17 Once induced, iNOS may translocate from the cytosol to the mitochondria where it exhibits a characteristic, high, Ca 2+ independent activity and nitric oxide generation. [27][28][29][30] The localisation of iNOS primarily in the photoreceptor mitochondria, along with the localisation of reactive oxidants by DCF and the reduced form of MitoTracker (figs 6, 7) suggests that the observed mitochondrial oxidative stress in the mitochondria could be primarily due to peroxynitrite formation. As peroxynitrite formation requires nitric oxide and superoxide generation in proximity, and as both of these oxidants are increased markedly in the photoreceptor mitochondria on day 5 ONL IS Figure 4 Immunolocalisation of inducible nitric oxide synthase (iNOS) in the retina in day 5 post immunisation animals.…”

Section: Discussionmentioning

confidence: 99%

Photoreceptor mitochondrial oxidative stress in early experimental autoimmune uveoretinitis

Rajendram

Saraswathy

Rao³

2006

British Journal of Ophthalmology

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“…It was recently reported [41] that iNOS may translocate from the cytosol to mitochondria during sepsis. Our data agree with this finding, as we demonstrate that mtiNOS derives from iNOS and increases in sepsis.…”

Section: Discussionmentioning

confidence: 99%

Melatonin counteracts inducible mitochondrial nitric oxide synthase‐dependent mitochondrial dysfunction in skeletal muscle of septic mice

Escames

López

Tapias

et al. 2005

Journal of Pineal Research

134

160

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Mitochondrial nitric oxide synthase (mtNOS) produces nitric oxide (NO) to modulate mitochondrial respiration. Besides a constitutive mtNOS isoform it was recently suggested that mitochondria express an inducible isoform of the enzyme during sepsis. Thus, the mitochondrial respiratory inhibition and energy failure underlying skeletal muscle contractility failure observed in sepsis may reflect the high levels of NO produced by inducible mtNOS. The fact that mtNOS is induced during sepsis suggests its relation to inducible nitric oxide synthase (iNOS). Thus, we examined the changes in mtNOS activity and mitochondrial function in skeletal muscle of wild-type (iNOS(+/+)) and iNOS knockout (iNOS(-/-)) mice after sepsis. We also studied the effects of melatonin administration on mitochondrial damage in this experimental paradigm. After sepsis, iNOS(+/+) but no iNOS(-/-) mice showed an increase in mtNOS activity and NO production and a reduction in electron transport chain activity. These changes were accompanied by a pronounced oxidative stress reflected in changes in lipid peroxidation levels, oxidized glutathione/reduced glutathione ratio, and glutathione peroxidase and reductase activities. Melatonin treatment counteracted both the changes in mtNOS activity and rises in oxidative stress; the indole also restored mitochondrial respiratory chain in septic iNOS(+/+) mice. Mitochondria from iNOS(-/-) mice were unaffected by either sepsis or melatonin treatment. The data suggest that inducible mtNOS, which is coded by the same gene as that for iNOS, is responsible for mitochondrial dysfunction during sepsis. The results also suggest the use of melatonin for the protection against mtNOS-mediated mitochondrial failure.

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The Mitochondrial Interplay of Ubiquinol and Nitric Oxide in Endotoxemia

Cited by 25 publications

References 28 publications

Mitochondrial Nitric Oxide Synthase: A Masterpiece of Metabolic Adaptation, Cell Growth, Transformation, and Death

Mitochondrial Nitric Oxide Synthase: A Masterpiece of Metabolic Adaptation, Cell Growth, Transformation, and Death

Photoreceptor mitochondrial oxidative stress in early experimental autoimmune uveoretinitis

Melatonin counteracts inducible mitochondrial nitric oxide synthase‐dependent mitochondrial dysfunction in skeletal muscle of septic mice

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