Modulation of the Permeability Transition Pore by Inhibition of the Mitochondrial KATP Channel in Liver vs. Brain Mitochondria

2007 ◽  
Vol 215 (2-3) ◽  
pp. 69-74 ◽  
Author(s):  
K. Kupsch ◽  
S. Parvez ◽  
D. Siemen ◽  
G. Wolf
Keyword(s):  
Katp Channel ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Brain Mitochondria ◽  
Mitochondrial Katp Channel

scholarly journals Mild Hypoxemia during Initial Reperfusion Alleviates the Severity of Secondary Energy Failure and Protects Brain in Neonatal Mice with Hypoxic-Ischemic Injury

2011 ◽  
Vol 32 (2) ◽  
pp. 232-241 ◽  
Author(s):  
Zoya V Niatsetskaya ◽  
Pradeep Charlagorla ◽  
Dzmitry A Matsukevich ◽  
Sergey A Sosunov ◽  
Korapat Mayurasakorn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Oxygen Saturation ◽  
Infarct Volume ◽  
Birth Asphyxia ◽  
Permeability Transition Pore ◽  
Oxidative Injury ◽  
Permeability Transition ◽  
Brain Mitochondria ◽  
Mptp Opening

Reperfusion triggers an oxidative stress. We hypothesized that mild hypoxemia in reperfusion attenuates oxidative brain injury following hypoxia-ischemia (HI). In neonatal HI-mice, the reperfusion was initiated by reoxygenation with room air (RA) followed by the exposure to 100%, 21%, 18%, 15% oxygen for 60 minutes. Systemic oxygen saturation (SaO2), cerebral blood flow (CBF), brain mitochondrial respiration and permeability transition pore (mPTP) opening, markers of oxidative injury, and cerebral infarcts were assessed. Compared with RA-littermates, HI-mice exposed to 18% oxygen exhibited significantly decreased infarct volume, oxidative injury in the brain mitochondria and tissue. This was coupled with improved mitochondrial tolerance to mPTP opening. Oxygen saturation maintained during reperfusion at 85% to 95% was associated ( r=0.57) with the best neurologic outcome. Exposure to 100% or 15% oxygen significantly exacerbated brain injury and oxidative stress. Compared with RA-mice, hyperoxia dramatically increased reperfusion CBF, but exposure to 15% oxygen significantly reduced CBF to values observed during the HI-insult. Mild hypoxemia during initial reperfusion alleviates the severity of HI-brain injury by limiting the reperfusion-driven oxidative stress to the mitochondria and mPTP opening. This suggests that at the initial stage of reperfusion, a slightly decreased systemic oxygenation (SaO2 85% to 95%) may be beneficial for infants with birth asphyxia.

scholarly journals Amyloid β-Peptide Promotes Permeability Transition Pore in Brain Mitochondria

2001 ◽  
Vol 21 (6) ◽  
pp. 789-800 ◽  
Author(s):  
Paula I. Moreira ◽  
Maria S. Santos ◽  
António Moreno ◽  
Catarina Oliveira
Keyword(s):  
Transmembrane Potential ◽  
Mitochondrial Permeability Transition Pore ◽  
Mitochondrial Permeability Transition ◽  
Amyloid Β ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Brain Mitochondria ◽  
Amyloid Β Peptide ◽  
Mitochondrial Permeability ◽  
Pre Treatment

In this work the effect of the neurotoxic amino acid sequence, Aβ25–35, on brain mitochondrial permeability transition pore (PTP) was studied. For the purpose, the mitochondrial transmembrane potential (ΔΨm), mitochondrial respiration and the calcium fluxes were examined. It was observed that Aβ25–35, in the presence of Ca2+, decreased the ΔΨm, the capacity of brain mitochondria to accumulate calcium and led to a complete uncoupling of the respiration. However, the reverse sequence of the peptide Aβ25–35 (Aβ35–25) did not promote the PTP. The alterations promoted by Aβ35–25 and/or Ca2+ could be reversed when Ca2+ was removed by EGTA or when ADP plus oligomycin were present. The pre-treatment with CsA or ADP plus oligomycin prevented the ΔΨm drop and preserved the capacity of mitochondria to accumulate Ca2+. These results suggest that Aβ25–35 can promote the PTP induced by Ca2+.

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