Dias 2019 MiPschool Coimbra: Difference between revisions
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{{Abstract | {{Abstract | ||
|title=[[Image: | |title=[[Image:Picture CandidaDias.jpg|left|90px|Candida Dias]] Protective effect of nitrite in brain ischemia/reperfusion via modulation of mitochondrial respiration. | ||
|info=[[MitoEAGLE]] | |info=[[MitoEAGLE]] | ||
|authors= ย | |authors=Dias C, Lourenco CF, Barbosa RM, Ledo A, Laranjinha J | ||
|year=2019 | |year=2019 | ||
|event=MiPschool Coimbra 2019 | |event=MiPschool Coimbra 2019 | ||
|abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoeagle.org/index.php/MitoEAGLE|COST Action MitoEAGLE]] | |abstract=[[Image:MITOEAGLE-logo.jpg|left|100px|link=http://www.mitoeagle.org/index.php/MitoEAGLE|COST Action MitoEAGLE]] | ||
Nitrite, once considered an inert metabolic endpoint of nitric oxide (โขNO), has more recently emerged as a metabolic precursor of โขNO ''in vivo''. This alternative source of โขNO may play a critical role in the brain under emergency conditions such as ischemia, when enzymatic โขNO production is hindered due to lack of oxygen. Evidence shows that nitrite is protective in situations of ischemia/reperfusion and appears to be beneficial in aging and neurodegeneration. Most relevantly, nitrite concentration ''in vivo'' can be modulated by diet through the ingestion of nitrate rich foods, being generally associated with increased longevity and lower incidence of cardiovascular disease. | |||
One putative target for nitriteยดs protective bioactivity in ischemia is through modulation of mitochondrial respiration. We used high-resolution respirometry to determine the effects of nitrite on brain tissue respiration in conditions of ischemia/ reperfusion. We applied an ''in vitro'' ischemia/reperfusion protocol to permeabilized rat hippocampal tissue and determined the differences of complex I supported respiration in the presence and absence of nitrite. | |||
While under control (no nitrite) conditions, a significant increase in the respiration rate is observed upon re-oxygenation (โoxidative burstโ), in the presence of nitrite (10 ฮผM), this burst is abolished. This inhibition may prevent the increased production of reactive oxygen species associated with this oxidative burst and may be one of the mechanisms through which nitrite is protective during brain ischemia. | |||
Future studies are focused on confirming nitrite reduction to โขNO as a requirement for the inhibition of the oxidative burst as well as pin-pointing the site of nitrite/โขNO bioactivity within the mitochondrial respiratory chain. | |||
|editor=[[Plangger M]], | |editor=[[Plangger M]], | ||
|mipnetlab=PT Coimbra Laranjinha J | |||
}} | |||
{{Labeling | |||
|area=Respiration, Exercise physiology;nutrition;life style, Pharmacology;toxicology | |||
|injuries=Ischemia-reperfusion | |||
|organism=Rat | |||
|tissues=Nervous system | |||
|preparations=Permeabilized tissue | |||
|instruments=Oxygraph-2k | |||
}} | }} | ||
== Affiliations and support == | == Affiliations and support == | ||
::::Dias C(1,2), Lourenรงo CF(1,2), Barbosa RM(1,2), Ledo A(1,2), Laranjinha J(1,2) | |||
::::#Center Neuroscience Cell Biology | |||
::::#Fac Pharmacy; Univ Coimbra, Portugal. - [email protected] | |||
::::Funding: FEDER through COMPETE and FCT under the projects UID/NEU/04539/2019, POCI-01-0145-FEDER-029099, CENTRO-01-0145-FEDER-000012-HealthyAging2020 by the Centro 2020 Regional Operational Program, and PD/BD/114371/2016. | |||
ย | |||
Revision as of 10:33, 24 June 2019
 |
Link: MitoEAGLE
Dias C, Lourenco CF, Barbosa RM, Ledo A, Laranjinha J (2019)
Event: MiPschool Coimbra 2019
Nitrite, once considered an inert metabolic endpoint of nitric oxide (โขNO), has more recently emerged as a metabolic precursor of โขNO in vivo. This alternative source of โขNO may play a critical role in the brain under emergency conditions such as ischemia, when enzymatic โขNO production is hindered due to lack of oxygen. Evidence shows that nitrite is protective in situations of ischemia/reperfusion and appears to be beneficial in aging and neurodegeneration. Most relevantly, nitrite concentration in vivo can be modulated by diet through the ingestion of nitrate rich foods, being generally associated with increased longevity and lower incidence of cardiovascular disease.
One putative target for nitriteยดs protective bioactivity in ischemia is through modulation of mitochondrial respiration. We used high-resolution respirometry to determine the effects of nitrite on brain tissue respiration in conditions of ischemia/ reperfusion. We applied an in vitro ischemia/reperfusion protocol to permeabilized rat hippocampal tissue and determined the differences of complex I supported respiration in the presence and absence of nitrite.
While under control (no nitrite) conditions, a significant increase in the respiration rate is observed upon re-oxygenation (โoxidative burstโ), in the presence of nitrite (10 ฮผM), this burst is abolished. This inhibition may prevent the increased production of reactive oxygen species associated with this oxidative burst and may be one of the mechanisms through which nitrite is protective during brain ischemia.
Future studies are focused on confirming nitrite reduction to โขNO as a requirement for the inhibition of the oxidative burst as well as pin-pointing the site of nitrite/โขNO bioactivity within the mitochondrial respiratory chain.
โข Bioblast editor: Plangger M
โข O2k-Network Lab: PT Coimbra Laranjinha J
Labels: MiParea: Respiration, Exercise physiology;nutrition;life style, Pharmacology;toxicology
Stress:Ischemia-reperfusion Organism: Rat Tissue;cell: Nervous system Preparation: Permeabilized tissue
HRR: Oxygraph-2k
Affiliations and support
- Dias C(1,2), Lourenรงo CF(1,2), Barbosa RM(1,2), Ledo A(1,2), Laranjinha J(1,2)
- Center Neuroscience Cell Biology
- Fac Pharmacy; Univ Coimbra, Portugal. - [email protected]
- Dias C(1,2), Lourenรงo CF(1,2), Barbosa RM(1,2), Ledo A(1,2), Laranjinha J(1,2)
- Funding: FEDER through COMPETE and FCT under the projects UID/NEU/04539/2019, POCI-01-0145-FEDER-029099, CENTRO-01-0145-FEDER-000012-HealthyAging2020 by the Centro 2020 Regional Operational Program, and PD/BD/114371/2016.
