Dias 2022 Free Radic Biol Med: Difference between revisions
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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 | |info=Free Radic Biol Med 193:779-86. [https://www.ncbi.nlm.nih.gov/pubmed/36403737 PMID: 36403737 Open Access] | ||
|authors=Dias C, | |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 ( | |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]] | ||
|mipnetlab=PT Coimbra Laranjinha J | |||
}} | }} | ||
{{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
| 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
