Borutaite 2014 Abstract MiP2014: Difference between revisions
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{{Abstract | {{Abstract | ||
|title=Controversies regarding cytochrome c test for mitochondrial membrane integrity. | |title=Controversies regarding cytochrome ''c'' test for mitochondrial membrane integrity. | ||
|info=[[File:Borutaite_V.jpg|150px|right|Borutaite V]] [[Laner 2014 Mitochondr Physiol Network MiP2014|Mitochondr Physiol Network 19.13]] - [http://www.mitophysiology.org/index.php?mip2014 MiP2014] | |||
|authors=Borutaite V, Arandarcikaite O, Skemiene K | |authors=Borutaite V, Arandarcikaite O, Skemiene K | ||
|year=2014 | |year=2014 | ||
|event=MiP2014 | |event=MiP2014 | ||
|abstract=Cytochrome ''c'' is a small soluble protein which has two main functions: transfer of electrons within the mitochondrial respiratory system and formation of apoptosomes when released into cytosol. Under normal conditions, the outer mitochondrial (mt) membrane is not permeable to cytochrome ''c''. Therefore, stimulation of mitochondrial respiration by exogenous cytochrome ''c'' is widely used as a test for outer mt-membrane damage. Using this test, we and others have shown that heart ischemia causes rapid permeabilization of the outer mt-membrane, resulting in loss of cytochrome ''c'' from mitochondria and subsequent inhibition of mitochondrial respiration. In contrast, addition of exogenous cytochrome ''c'' to mitochondria isolated from ischemia-damaged brains does not stimulate mitochondrial respiration, suggesting that during brain ischemia the outer mt-membrane remains intact. We also found that in the presence of certain polyphenolic plant compounds (anthocyanins), addition of cytochrome ''c'' to isolated mitochondria results in acute stimulation of mitochondrial respiration. This effect is not linked to the permeabilization of the outer mt-membrane, as these anthocyanins can directly reduce cytochrome ''c'', thus facilitating electron transfer to cytochrome ''c'' oxidase. | |||
Certain anthocyanins, such as delphinidin-3-O-glucoside or cyaniding-3-O-glucoside, can serve as electron acceptors at Complex I of the mitochondrial respiratory system and, therefore, in pathological conditions related to inhibition of Complex I, facilitate an alternative electron transfer from Complex I to cytochrome ''c'' and cytochrome ''c'' oxidase. | |||
Supported by European Social Fund under the Global grant measure; project No VP1-3.1-SMM-07-K-01-130. | |||
|mipnetlab=LT Kaunas Borutaite V | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration, mt-Membrane | |area=Respiration, mt-Membrane | ||
| | |organism=Rat | ||
| | |tissues=Heart, Nervous system | ||
|injuries=Ischemia- | |preparations=Isolated mitochondria | ||
|injuries=Ischemia-reperfusion, Permeability transition | |||
|topics=Cyt c | |||
|instruments=Oxygraph-2k | |||
|event=C2, Oral | |||
|additional=MiP2014 | |||
}} | }} | ||
== Affiliation == | |||
Inst Neurosc, Lithuanian Univ Health Sc, Kaunas, Lithuania. - [email protected] | Inst Neurosc, Lithuanian Univ Health Sc, Kaunas, Lithuania. - [email protected] |
Latest revision as of 08:23, 16 June 2015
Controversies regarding cytochrome c test for mitochondrial membrane integrity. |
Link:
Mitochondr Physiol Network 19.13 - MiP2014
Borutaite V, Arandarcikaite O, Skemiene K (2014)
Event: MiP2014
Cytochrome c is a small soluble protein which has two main functions: transfer of electrons within the mitochondrial respiratory system and formation of apoptosomes when released into cytosol. Under normal conditions, the outer mitochondrial (mt) membrane is not permeable to cytochrome c. Therefore, stimulation of mitochondrial respiration by exogenous cytochrome c is widely used as a test for outer mt-membrane damage. Using this test, we and others have shown that heart ischemia causes rapid permeabilization of the outer mt-membrane, resulting in loss of cytochrome c from mitochondria and subsequent inhibition of mitochondrial respiration. In contrast, addition of exogenous cytochrome c to mitochondria isolated from ischemia-damaged brains does not stimulate mitochondrial respiration, suggesting that during brain ischemia the outer mt-membrane remains intact. We also found that in the presence of certain polyphenolic plant compounds (anthocyanins), addition of cytochrome c to isolated mitochondria results in acute stimulation of mitochondrial respiration. This effect is not linked to the permeabilization of the outer mt-membrane, as these anthocyanins can directly reduce cytochrome c, thus facilitating electron transfer to cytochrome c oxidase.
Certain anthocyanins, such as delphinidin-3-O-glucoside or cyaniding-3-O-glucoside, can serve as electron acceptors at Complex I of the mitochondrial respiratory system and, therefore, in pathological conditions related to inhibition of Complex I, facilitate an alternative electron transfer from Complex I to cytochrome c and cytochrome c oxidase.
Supported by European Social Fund under the Global grant measure; project No VP1-3.1-SMM-07-K-01-130.
• O2k-Network Lab: LT Kaunas Borutaite V
Labels: MiParea: Respiration, mt-Membrane
Stress:Ischemia-reperfusion, Permeability transition Organism: Rat Tissue;cell: Heart, Nervous system Preparation: Isolated mitochondria
Regulation: Cyt c
HRR: Oxygraph-2k
Event: C2, Oral
MiP2014
Affiliation
Inst Neurosc, Lithuanian Univ Health Sc, Kaunas, Lithuania. - [email protected]