ACUTE ETHANOL EXPOSURE INCREASES THE ACTIVITY OF MITOCHONDRIA-ASSOCIATED GLYCOGEN SYNTHASE KINASE-3 BETA (GSK-3Î’): ROLE IN PHOSPHORYLATION OF MITOCHONDRIAL PROTEINS

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T. A. I. O. Y. B. E. H. Vera Teplova, Arshad Jahangir, “ACUTE ETHANOL EXPOSURE INCREASES THE ACTIVITY OF MITOCHONDRIA-ASSOCIATED GLYCOGEN SYNTHASE KINASE-3 BETA (GSK-3Î’): ROLE IN PHOSPHORYLATION OF MITOCHONDRIAL PROTEINS”, ijmhs, vol. 3, no. 4, Oct. 2013.
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Abstract

Background: Ethanol oxidation alters mitochondrial metabolism that may be consequence of the closing of mitochondrial voltage dependent anion channels (VDAC) and decrease outer membrane permeability. Phosphorylation of VDAC by cytosolic kinases modulates outer membrane permeability. This study examines how acute ethanol treatment of rats affects the activity of glycogen synthase kinase-3 beta (GSK-3β) associated with liver mitochondria and the level of phosphorylation of several mitochondrial proteins, specifically porins, forming VDAC in the outer membrane of mitochondria.
Results: The level of protein phosphorylation in mitochondria, isolated from ethanol treated animals is differed from that in mitochondria of rats which were not subjected to ethanol treatment. It was found that ethanol treatment increased the activity of GSK-3β activity in isolated mitochondria and increased the rate of incorporation of 32P from [γ-32P] ATP into mitochondrial proteins of 63 kDa, 32 kDa, 25 kDa and 3.5 kDa. Enhanced level of VDAC (32 kDa band) phosphorylation correlated with increased content of phosphotyrosine residues determined in the same 32 kDa band. Additionally, it was found that levels of total GSK-3β kinase as well as phosphorylated forms of this enzyme were decreased in mitochondria isolated from ethanol treated animals as compared with mitochondria from controls. Changes in phosphorylation of mitochondrial porins/VDAC and GSK-3β in ethanol-exposed rats paralleled with decreased Ca2+-retention capacity of isolated mitochondria with accelerated opening of Ca2+-dependent mitochondrial permeability transition pore.
Conclusions: The results of this study conclude that acute ethanol exposure of rats decrease both, the total GSK-3β associated with liver mitochondria and the level of Ser9-phosphorylation of this kinase. It is reported that acute ethanol treatment of animals modulates the activity of mitochondria-associated GSK-3β, enhances phosphorylation of mitochondrial porins/VDAC, probably, due to tyrosine-specific phosphorylation and thus, modulates the permeability of the outer mitochondrial membrane after ethanol exposure

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