Ema
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"In modern biology mitochondria are considered to be much more than the powerhouse of the cell; they integrate multiple intracellular signals to regulate progression through the cell cycle and into apoptosis. Therefore it is vital that they maintain optimal functionality to prevent the development of abnormal cells," states co-author Jessica Beaudoin.
With this in vivo model, the research team uncovered evidence of distinct organellar perturbations in redox balance following inhibition of GSH synthesis with buthionine sulfoximine, demonstrating increased mitochondrial oxidation in response to GSH depletion compared to the cytosol. The effect was observed in multiple mammalian cell lines, including both normal and tumorigenic models. Taken together, these findings indicate different redox requirements for the glutathione thiol/disulfide redox couple within cytosol and mitochondria of resting cells and reveal distinct regulation of their redox poise in response to inhibition of glutathione biosynthesis.
Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology and Medicine, said "Kolossov et al have utilized a genetically-encoded redox probe that has the ability to determine oxidized/reduced glutathione levels within different cellular compartments of living cells. This will be an important approach for studying redox changes in disease states including cancer, neurodegenerative disorders, cardiovascular disease, sickle cell disease and many others which are known to involve oxidative stress."
"In modern biology mitochondria are considered to be much more than the powerhouse of the cell; they integrate multiple intracellular signals to regulate progression through the cell cycle and into apoptosis. Therefore it is vital that they maintain optimal functionality to prevent the development of abnormal cells," states co-author Jessica Beaudoin.
With this in vivo model, the research team uncovered evidence of distinct organellar perturbations in redox balance following inhibition of GSH synthesis with buthionine sulfoximine, demonstrating increased mitochondrial oxidation in response to GSH depletion compared to the cytosol. The effect was observed in multiple mammalian cell lines, including both normal and tumorigenic models. Taken together, these findings indicate different redox requirements for the glutathione thiol/disulfide redox couple within cytosol and mitochondria of resting cells and reveal distinct regulation of their redox poise in response to inhibition of glutathione biosynthesis.
Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology and Medicine, said "Kolossov et al have utilized a genetically-encoded redox probe that has the ability to determine oxidized/reduced glutathione levels within different cellular compartments of living cells. This will be an important approach for studying redox changes in disease states including cancer, neurodegenerative disorders, cardiovascular disease, sickle cell disease and many others which are known to involve oxidative stress."