Literature summary for 7.1.1.9 extracted from

Racay, P.; Tatarkova, Z.; Drgova, A.; Kaplan, P.; Dobrota, D.
Ischemia-reperfusion induces inhibition of mitochondrial protein synthesis and cytochrome C oxidase activity in rat hippocampus (2008), Physiol. Res., 58, 127-138.

Search for more literature for 7.1.1.9

Application

Application	Comment	Organism
additional information	inhibition of COX activity is rather caused by ischemia-induced modification of COX polypeptides than by inhibition of mitochondrial translation	Rattus norvegicus

Inhibitors

Inhibitors	Comment	Organism	Structure
additional information	15 min of global ischemia leads to the inhibition of COXI synthesis to 56% of control. After 1, 3 and 24 hours of reperfusion, COXI synthesis is inhibited to 46, 50 and 72% of control, respectively. Extent COXIII and COXII/ATPase6 synthesis inhibition is comparable to the extent of COXI synthesis inhibition. No significant changes in COXI mRNA and in both COXI and COXII protein level after ischemia, thus ischemia-reperfusion affects directly mitochondrial translation machinery. Ischemia in duration of 15 min and consequent 1, 3 and 24 hours of reperfusion leads to the inhibition of COX activity to 90.3, 80.3, 81.9 and 83.5% of control, respectively	Rattus norvegicus

Localization

Localization	Comment	Organism	GeneOntology No.	Textmining
mitochondrion	-	Rattus norvegicus	5739	-

Organism

Organism	UniProt	Comment	Textmining
Rattus norvegicus	-	-	-

Source Tissue

Source Tissue	Comment	Organism	Textmining
brain	-	Rattus norvegicus	-
hippocampus	-	Rattus norvegicus	-

Substrates and Products (Substrate)

Substrates	Comment Substrates	Organism	Products	Comment (Products)	Rev.	Reac.
reduced cytochrome c + O2 + H+	-	Rattus norvegicus	oxidized cytochrome c + H2O	-	?

Synonyms

Synonyms	Comment	Organism
COX	-	Rattus norvegicus
COX subunit I	-	Rattus norvegicus
COXI	-	Rattus norvegicus
COXII	-	Rattus norvegicus
COXIII	-	Rattus norvegicus
cytochrome c oxidase	-	Rattus norvegicus

Use of this online version of BRENDA is free under the CC BY 4.0 license. See terms of use for full details.

Release 2023.1 (January 2023)