ArticleNeurochemical research2012
Ischemia-induced inhibition of mitochondrial complex I in rat brain: effect of permeabilization method and electron acceptor.
Article in Neurochemical research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 20 citations in OpenAlex.
- Vagus Nerve Stimulation Improves Mitochondrial Dysfunction in Post-cardiac Arrest Syndrome in the Asphyxial Cardiac Arrest Model in Rats.Frontiers in neuroscience · 2022Article
- Heterogeneity of GRIM-19 Expression in the Adult Mouse Brain.Cellular and molecular neurobiology · 2019Article
- Deactivation of mitochondrial complex I after hypoxia-ischemia in the immature brain.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019Article
- Comparison of the anti-apoptotic effects of 15- and 35-minute suspended moxibustion after focal cerebral ischemia/reperfusion injury.Neural regeneration research · 2018Article
- Diabetes-induced abnormalities of mitochondrial function in rat brain cortex: the effect of n-3 fatty acid diet.Molecular and cellular biochemistry · 2017Article
- The Effect of Aging on Mitochondrial Complex I and the Extent of Oxidative Stress in the Rat Brain Cortex.Neurochemical research · 2016Article
- Reperfusion injury and reactive oxygen species: The evolution of a concept.Redox biology · 2015Review
- Protective effects of dietary avocado oil on impaired electron transport chain function and exacerbated oxidative stress in liver mitochondria from diabetic rats.Journal of bioenergetics and biomembranes · 2015Article
- Avocado Oil Improves Mitochondrial Function and Decreases Oxidative Stress in Brain of Diabetic Rats.Journal of diabetes research · 2015Article
- Possible contribution of proteins of Bcl-2 family in neuronal death following transient global brain ischemia.Cellular and molecular neurobiology · 2015Article
- Microcirculatory, mitochondrial, and histological changes following cerebral ischemia in swine.BMC neuroscience · 2014Article
- Conformational change of mitochondrial complex I increases ROS sensitivity during ischemia.Antioxidants & redox signaling · 2013Article
- Molecular mechanisms of ischemia-reperfusion injury in brain: pivotal role of the mitochondrial membrane potential in reactive oxygen species generation.Molecular neurobiology · 2013Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study we have examined the effect of global brain ischemia/reperfusion on biochemical properties of the mitochondrial respiratory complex I (CI) in rat hippocampus and cortex. Since the inner mitochondrial membrane forms the permeability barrier for NADH, the methodology of enzymatic activity determinations employs membrane permeabilization methods. This action affects the basic character of electrostatic and hydrophobic interactions inside the membrane and might influence functional properties of membrane embedded proteins. Therefore we have performed the comparative analysis of two permeabilization methods (sonication, detergent) and their impact on CI enzymatic activities under global brain ischemic-reperfusion conditions. We have observed that ischemia led to significant decrease of CI activities using both permeabilization methods in both brain areas. However, significant differencies in enzymatic activities were registered during reperfusion intervals according to used permeabilization method. We have also tested the effect of electron acceptors (decylubiquinone, potassium ferricyanide, nitrotetrazolium blue) on CI activities during I/R. Based on our results we assume that the critical site where ischemia affects CI activities is electron transfer to electron acceptor. Further, the observed mitochondrial dysfunction was analyzed by means of one and 2-dimensional BN PAGE/SDS PAGE with the focus on 3-nitrotyrosine immunodetection as a marker of oxidative damage to proteins. Add to this, initialization of p53 mitochondrial apoptosis through p53, Bax, Bcl-X(L) proteins and a possible involvement of GRIM-19, the CI structural subunit, in apoptotic processes were also studied.
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