Regulation of singlet oxygen-induced apoptosis by cytosolic NADP⁺-dependent isocitrate dehydrogenase

Singlet oxygen is a highly reactive form of molecular oxygen that may harm living systems by oxidizing critical cellular macromolecules and it also promotes deleterious processes such as cell death. Recently, we demonstrated that the control of redox balance and the cellular defense against oxidativ...

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Bibliographic Details
Published in:Molecular and cellular biochemistry 2007-08, Vol.302 (1-2), p.27-34
Main Authors: Kim, Sun Yee, Lee, Su Min, Tak, Jean Kyoung, Choi, Kyeong Sook, Kwon, Taeg Kyu, Park, Jeen-Woo
Format: Article
Language:English
Subjects:
Animals
Antioxidant enzyme
Apoptosis
Apoptosis - drug effects
Apoptosis Regulatory Proteins - metabolism
Cytosol - drug effects
Cytosol - enzymology
Dehydrogenase
HL-60
HL-60 Cells
Humans
Immunoblotting
isocitrate dehydrogenase
Isocitrate Dehydrogenase - metabolism
Membrane Potential, Mitochondrial - drug effects
Mice
Oxidation-Reduction - drug effects
Oxygen
Regulation
singlet oxygen
Singlet Oxygen - pharmacology
Transfection
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Summary:Singlet oxygen is a highly reactive form of molecular oxygen that may harm living systems by oxidizing critical cellular macromolecules and it also promotes deleterious processes such as cell death. Recently, we demonstrated that the control of redox balance and the cellular defense against oxidative damage are the primary functions of cytosolic NADP⁺-dependent isocitrate dehydrogenase (IDPc) through supplying NADPH for antioxidant systems. In this report, we demonstrate that modulation of IDPc activity in HL-60 cells regulates singlet oxygen-induced apoptosis. When we examined the protective role of IDPc against singlet oxygen-induced apoptosis with HL-60 cells transfected with the cDNA for mouse IDPc in sense and antisense orientations, a clear inverse relationship was observed between the amount of IDPc expressed in target cells and their susceptibility to apoptosis. The results suggest that IDPc plays an important protective role in apoptosis of HL-60 cells induced by singlet oxygen.
ISSN:0300-8177
1573-4919
DOI:10.1007/s11010-007-9421-x