Open AccessIschemia-reperfusion induces inhibition of mitochondrial protein synthesis and cytochrome c oxidase activity in rat hippocampus
Author(s) -
Peter Raçay,
Zuzana Tatarková,
A Drgová,
Peter Kaplán,
Dušan Dobrota
Publication year - 2009
Publication title -
physiological research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.647
H-Index - 70
eISSN - 1802-9973
pISSN - 0862-8408
DOI - 10.33549/physiolres.931383
Subject(s) - cytochrome c oxidase , ischemia , mitochondrion , cytochrome c , messenger rna , translation (biology) , microbiology and biotechnology , blot , oxidase test , chemistry , biology , biochemistry , pharmacology , enzyme , medicine , gene
Dysfunction of mitochondria induced by ischemia is considered tobe a key event triggering neuronal cell death after brainischemia. Here we report the effect of ischemia-reperfusion onmitochondrial protein synthesis and activity of cytochrome coxidase (EC 1.9.3.1, COX). By performing 4-vessel occlusionmodel of global brain ischemia, we have observed that 15 min ofglobal ischemia led to the inhibition of COX subunit I (COXI)synthesis to 56 % of control. After 1, 3 and 24 h of reperfusion,COXI synthesis was inhibited to 46, 50 and 72 % of control,respectively. Depressed synthesis of COXI was not a result ofeither diminished transcription of COXI gene or increasedproteolytic degradation of COXI, since both Northernhybridization and Western blotting did not show significantchanges in COXI mRNA and protein level. Thus, ischemiareperfusion affects directly mitochondrial translation machinery.In addition, ischemia in duration of 15 min and consequent 1, 3and 24 h of reperfusion led to the inhibition of COX activity to90.3, 80.3, 81.9 and 83.5 % of control, respectively. Based onour data, we suggest that inhibition of COX activity is rathercaused by ischemia-induced modification of COX polypeptidesthan by inhibition of mitochondrial translation.