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| {{EAGLE
| | #REDIRECT [[Dias Candida]] |
| |COST=Member
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| |COST WG1=WG1
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| |COST WG3=WG3}}
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| {{Person
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| |lastname=Dias
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| |firstname=Cândida
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| |title=PhD student
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| |institution=[[File:Picture CandidaDias.jpg|right|180px|Candida D]] Redox Biology and Brain Sensing,
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| Center for Neuroscience and Cell Biology,
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| University of Coimbra, PT
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| |address=Rua Larga - Faculdade de Medicina, Pólo 1, Piso 1
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| |area code=3004-504
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| |city=Coimbra
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| |country=Portugal
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| }}
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| {{Labelingperson}}
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| == MitoEAGLE Short-Term Scientific Mission ==
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| ****: [[Short-Term_Scientific_Missions_MitoEAGLE#STSM_Grant_Period_4 |STSM Grant Period 4]]
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| ::: '''Work Plan summary'''
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| :::: Nitrite, once considered an inert metabolic endpoint of nitric oxide (•NO), has more recently emerged as a metabolic precursor of •NO in vivo. This alternative source of •NO may play a critical role in the brain under emergency conditions such as ischemia, when enzymatic •NO 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, which are generally associated with increased longevity and lower incidence of cardiovascular disease. One putative target for nitrite´s protective bioactivity in ischemia is through modulation of mitochondrial respiration. In our previous work, we applied an in vitro ischemia/reperfusion protocol to permeabilised rat hippocampal tissue and determined the differences of NADH-linked respiration (supported by glutamate, pyruvate and malate) in the presence and absence of nitrite. Our preliminary results indicate that while under control conditions (no nitrite), a significant increase in the respiration rate is observed upon re-oxygenation (“oxidative burst”), in the presence of nitrite (10 µM) this burst is abolished. However, this effect is dose-dependent, as a higher concentration (100 µM) could not prevent the oxidative burst. 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. The aim of this STSM will be to determine the effects of nitrite on brain mitochondrial respiration and hydrogen peroxide production upon ischemia/reperfusion, using an identical protocol to what we previously did, to better correlate between measurements. The results could help to understand the mechanism through which nitrite appears to be protective in brain ischemia/reperfusion. Furthermore, it will include the evaluation of a jointly optimized tissue holder to extend SOPs from tissue homogenates, isolated mitochondria and permeabilized tissue to standardized and hormonized protocols and applications with tissue slices. Before starting this experimental plan, this mission will involve the participation in the “Oroboros O2k-Workshop” where an update on latest developments of high resolution respirometry, including fluorometry and TiP2k applications for evaluation of mitochondrial function, will be provided.
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| == Participated at ==
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| ::::* [[MiPschool Coimbra 2019|MiP/MitoEAGLE Training School 2019 Coimbra PT]]
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