Mitochondrial nitric oxide production supported by reverse electron transfer

Bombicino, Silvina Sonia; Iglesias, Darío E.; Zaobornyj, Tamara; Boveris, Alberto; Valdez, Laura B.

doi:10.1016/j.abb.2016.08.010

Cited by 20 publications

(9 citation statements)

References 66 publications

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“…Dysfunction of complex I is found in clinical conditions such as Parkinson's disease, [18][19][20][21] ischemiareperfusion, 22,23 endotoxic shock 24 and aging; [25][26][27] and it is usually accompanied by changes in mtNOS activity, 20,[22][23][24][25] increases in H 2 O 2 and ONOO − production rates and oxidative and/or nitrosative damage. This finding agrees with the reported functional interaction between complex I and mtNOS [28][29][30][31] and with the dependence of mitochondrial NO production on membrane potential. 30,32,33 Many studies have shown that polyphenols attenuate the progression of diseases associated with oxidative stress and mitochondrial dysfunction.…”

Section: Introductionsupporting

confidence: 92%

“…The effect of 3 and 10 nM of (+)-catechin was tested. 31 In order to consider the NOS inhibitor-sensitive HbO 2 oxidation, control experiments adding 2 mM N ω -monometil-Larginine (L-NMMA) were performed. The absorbance changes that were inhibited by L-NMMA were expressed as nmol NO per min per mg protein or nmol NO per min per U.…”

Section: Mitochondrial Complex I Activitymentioning

confidence: 99%

“…Taking into account the reported functional interaction between complex I and mtNOS activities, 28,31 and the regulation of mitochondrial NO production by membrane potential, 30,32,33 mtNOS activity was measured and the effect of 1.0-25 nM (+)-catechin was studied. This concentration range was selected according to the effects of that flavonoid on complex I activity and mitochondrial membrane potential.…”

Section: Mitochondrial Membrane Potentialmentioning

confidence: 99%

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(+)-Catechin inhibits heart mitochondrial complex I and nitric oxide synthase: functional consequences on membrane potential and hydrogen peroxide production

et al. 2019

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Section: Introductionsupporting

confidence: 92%

Section: Mitochondrial Complex I Activitymentioning

confidence: 99%

Section: Mitochondrial Membrane Potentialmentioning

confidence: 99%

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(+)-Catechin inhibits heart mitochondrial complex I and nitric oxide synthase: functional consequences on membrane potential and hydrogen peroxide production

et al. 2019

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“…Parihar and colleagues suggested that the respiratory chain Complex I regulates mitochondrial NOS activity by showing mitochondrial NOS activity associated to Complex I in isolated rat liver and brain mitochondria (42). Furthermore, the study of heart mitochondrial preparations demonstrated that Complex I enriched fractions had higher mitochondrial NOS (nNOS-alpha isoform), suggesting that mitochodrial NOS is physically close to Complex I (43). …”

Section: A Mitochondrial Nos?mentioning

confidence: 99%

NO control of mitochondrial function in normal and transformed cells

Tengan¹,

Moraes²

2017

Biochimica et Biophysica Acta (BBA) - Bioenergetics

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Nitric oxide (NO) is a signaling molecule with multiple facets and involved in numerous pathological process, including cancer. Among the different pathways where NO has a functionally relevant participation, is the control of mitochondrial respiration and biogenesis. NO is able to inhibit the electron transport chain, mainly at Complex IV, regulating oxygen consumption and ATP generation, but at the same time, can also induce increase in reactive oxygen and nitrogen species. The presence of reactive species can induce oxidative damage or participate in redox signaling. In this review, we discuss how NO affects mitochondrial respiration and mitochondrial biogenesis, and how it influences the development of mitochondrial deficiency and cancer.

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“…Due to positive clinical responses in stroke-like episodes, L-ARG supplementation has been recommended to patients with MELAS, especially in the acute phase of the disease [27,28]. The pathogenesis of stroke-like episodes is attributed to the co-existence of mitochondrial cytopathy and mitochondrial angiopathy, causing impairment in oxidative phosphorylation and vasodilation, respectively [28]. However, we still do not know how L-ARG impacts mitochondrial function in these cases.…”

Section: Discussionmentioning

confidence: 99%

L-Arginine Reduces Nitro-Oxidative Stress in Cultured Cells with Mitochondrial Deficiency

et al. 2021

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L-Arginine (L-ARG) supplementation has been suggested as a therapeutic option in several diseases, including Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like syndrome (MELAS), arguably the most common mitochondrial disease. It is suggested that L-ARG, a nitric oxide (NO) precursor, can restore NO levels in blood vessels, improving cerebral blood flow. However, NO also participates in mitochondrial processes, such as mitochondrial biogenesis, the regulation of the respiratory chain, and oxidative stress. This study investigated the effects of L-ARG on mitochondrial function, nitric oxide synthesis, and nitro-oxidative stress in cell lines harboring the MELAS mitochondrial DNA (mtDNA) mutation (m.3243A>G). We evaluated mitochondrial enzyme activity, mitochondrial mass, NO concentration, and nitro-oxidative stress. Our results showed that m.3243A>G cells had increased NO levels and protein nitration at basal conditions. Treatment with L-ARG did not affect the mitochondrial function and mass but reduced the intracellular NO concentration and nitrated proteins in m.3243A>G cells. The same treatment led to opposite effects in control cells. In conclusion, we showed that the main effect of L-ARG was on protein nitration. Lowering protein nitration is probably involved in the mechanism related to L-ARG supplementation benefits in MELAS patients.

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Mitochondrial nitric oxide production supported by reverse electron transfer

Cited by 20 publications

References 66 publications

(+)-Catechin inhibits heart mitochondrial complex I and nitric oxide synthase: functional consequences on membrane potential and hydrogen peroxide production

(+)-Catechin inhibits heart mitochondrial complex I and nitric oxide synthase: functional consequences on membrane potential and hydrogen peroxide production

NO control of mitochondrial function in normal and transformed cells

L-Arginine Reduces Nitro-Oxidative Stress in Cultured Cells with Mitochondrial Deficiency

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