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Difference between revisions of "Dias 2022 Free Radic Biol Med"

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{{Publication
{{Publication
|title=Dias C, Lourenço CF, Laranjinha J, Ledo A (2022) Modulation of oxidative neurometabolism in ischemia/reperfusion by nitrite. https://doi.org/10.1016/j.freeradbiomed.2022.11.021
|title=Dias C, Lourenço CF, Laranjinha J, Ledo A (2022) Modulation of oxidative neurometabolism in ischemia/reperfusion by nitrite. https://doi.org/10.1016/j.freeradbiomed.2022.11.021
|info=Free Radic Biol Med [Epub ahead of print]. [https://www.ncbi.nlm.nih.gov/pubmed/36403737 PMID: 36403737 Open Access]
|info=Free Radic Biol Med 193:779-86. [https://www.ncbi.nlm.nih.gov/pubmed/36403737 PMID: 36403737 Open Access]
|authors=Dias C, Lourenco CF, Laranjinha J, Ledo A
|authors=Dias C, Lourenco CF, Laranjinha J, Ledo A
|year=2022
|year=2022
|journal=Free Radic Biol Med
|journal=Free Radic Biol Med
|abstract=Nitrite has been viewed in the past essentially as an inert metabolic endpoint of nitric oxide (•NO). However, it has become evident that, under certain conditions, nitrite can be a source of •NO. In the brain, this alternative source of •NO production independent of nitric oxide synthase activity may be particularly relevant in ischemia/reperfusion (I/R), where low oxygen availability limits enzymatic production of •NO. Notably, in vivo concentration of nitrite can be easily increased with diet, through the ingestion of nitrate-rich foods, opening the window for a therapeutic intervention based on diet. Considering the modulation of mitochondrial respiration by •NO, we have hypothesized that the protective action of nitrite in I/R may also result from modulation of mitochondrial function. We used high-resolution respirometry to evaluate the effects of nitrite in two in vitro models of I/R. In both cases, an increase in oxygen flux was observed following reoxygenation, a phenomenon that has been coined "oxidative burst". The amplitude of this "oxidative burst" was decreased by nitrite in a concentration-dependent manner. Additionally, a pilot in vivo study in which animals received a nitrate-rich diet as a strategy to increase circulating and tissue levels of nitrite also revealed that the "oxidative burst" was decreased in the nitrate-treated animals. These results may provide mechanistic support to the observation of a protective effect of nitrite in situations of brain ischemia.
|abstract=Nitrite has been viewed in the past essentially as an inert metabolic endpoint of nitric oxide (<sup>•</sup>NO). However, it has become evident that, under certain conditions, nitrite can be a source of <sup>•</sup>NO. In the brain, this alternative source of <sup>•</sup>NO production independent of nitric oxide synthase activity may be particularly relevant in ischemia/reperfusion (I/R), where low oxygen availability limits enzymatic production of <sup>•</sup>NO. Notably, ''in vivo'' concentration of nitrite can be easily increased with diet, through the ingestion of nitrate-rich foods, opening the window for a therapeutic intervention based on diet. Considering the modulation of mitochondrial respiration by <sup>•</sup>NO, we have hypothesized that the protective action of nitrite in I/R may also result from modulation of mitochondrial function. We used high-resolution respirometry to evaluate the effects of nitrite in two ''in vitro'' models of I/R. In both cases, an increase in oxygen flux was observed following reoxygenation, a phenomenon that has been coined "oxidative burst". The amplitude of this "oxidative burst" was decreased by nitrite in a concentration-dependent manner. Additionally, a pilot ''in vivo'' study in which animals received a nitrate-rich diet as a strategy to increase circulating and tissue levels of nitrite also revealed that the "oxidative burst" was decreased in the nitrate-treated animals. These results may provide mechanistic support to the observation of a protective effect of nitrite in situations of brain ischemia.
|keywords=Hippocampus, Ischemia-reperfusion, Nitric oxide, Nitrite, Oxidative burst, Respirometry
|keywords=Hippocampus, Ischemia-reperfusion, Nitric oxide, Nitrite, Oxidative burst, Respirometry
|editor=[[Plangger M]]
|editor=[[Plangger M]]
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}}
}}
{{Labeling
{{Labeling
|area=Respiration
|area=Respiration, Exercise physiology;nutrition;life style
|injuries=Ischemia-reperfusion
|organism=Rat
|tissues=Nervous system
|preparations=Permeabilized tissue, Intact cells
|couplingstates=ROUTINE, OXPHOS, ET
|pathways=N, S, ROX
|instruments=Oxygraph-2k
|instruments=Oxygraph-2k
|additional=2022-11
|additional=2022-11
}}
}}

Latest revision as of 19:19, 24 February 2023

Publications in the MiPMap
Dias C, Lourenço CF, Laranjinha J, Ledo A (2022) Modulation of oxidative neurometabolism in ischemia/reperfusion by nitrite. https://doi.org/10.1016/j.freeradbiomed.2022.11.021

» Free Radic Biol Med 193:779-86. PMID: 36403737 Open Access

Dias C, Lourenco CF, Laranjinha J, Ledo A (2022) Free Radic Biol Med

Abstract: Nitrite has been viewed in the past essentially as an inert metabolic endpoint of nitric oxide (NO). However, it has become evident that, under certain conditions, nitrite can be a source of NO. In the brain, this alternative source of NO production independent of nitric oxide synthase activity may be particularly relevant in ischemia/reperfusion (I/R), where low oxygen availability limits enzymatic production of NO. Notably, in vivo concentration of nitrite can be easily increased with diet, through the ingestion of nitrate-rich foods, opening the window for a therapeutic intervention based on diet. Considering the modulation of mitochondrial respiration by NO, we have hypothesized that the protective action of nitrite in I/R may also result from modulation of mitochondrial function. We used high-resolution respirometry to evaluate the effects of nitrite in two in vitro models of I/R. In both cases, an increase in oxygen flux was observed following reoxygenation, a phenomenon that has been coined "oxidative burst". The amplitude of this "oxidative burst" was decreased by nitrite in a concentration-dependent manner. Additionally, a pilot in vivo study in which animals received a nitrate-rich diet as a strategy to increase circulating and tissue levels of nitrite also revealed that the "oxidative burst" was decreased in the nitrate-treated animals. These results may provide mechanistic support to the observation of a protective effect of nitrite in situations of brain ischemia. Keywords: Hippocampus, Ischemia-reperfusion, Nitric oxide, Nitrite, Oxidative burst, Respirometry Bioblast editor: Plangger M O2k-Network Lab: PT Coimbra Laranjinha J


Labels: MiParea: Respiration, Exercise physiology;nutrition;life style 

Stress:Ischemia-reperfusion  Organism: Rat  Tissue;cell: Nervous system  Preparation: Permeabilized tissue, Intact cells 


Coupling state: ROUTINE, OXPHOS, ET  Pathway: N, S, ROX  HRR: Oxygraph-2k 

2022-11