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

Authors
Kim, SY; Lee, SM; Tak, JK; Choi, KS; Kwon, TK; Park, JW
Citation
Molecular and cellular biochemistry, 302(1-2):27-34, 2007
Journal Title
Molecular and cellular biochemistry
ISSN
0300-81771573-4919
Abstract
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.
MeSH terms
AnimalsApoptosis/drug effects*Apoptosis Regulatory Proteins/metabolismCytosol/drug effects*Cytosol/enzymology*HL-60 CellsHumansImmunoblottingIsocitrate Dehydrogenase/metabolism*Membrane Potential, Mitochondrial/drug effectsMiceOxidation-Reduction/drug effectsSinglet Oxygen/pharmacology*Transfection
DOI
10.1007/s11010-007-9421-x
PMID
17646934
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Biochemistry & Molecular Biology
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