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Silencing of mitochondrial NADP+-dependent isocitrate dehydrogenase gene enhances selenite-induced apoptosis.
Free Radic Res. 2010 Mar; 44(3):332-9.FR

Abstract

Selenium has been shown to play a chemopreventive role in human cancer, presumably by inducing tumour cell apoptosis. Selenite is thought to induce oxidative stress by the generation of the superoxide anion and catalysing the oxidation of thiol groups. It has previously been reported that control of the mitochondrial redox balance is a primary function of mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDPm) by supplying NADPH for antioxidant systems. When investigating whether IDPm would be a vulnerable target of selenite, the loss of enzyme activity was observed. Transfection of HeLa cells with an IDPm small interfering RNA (siRNA) markedly decreased activity of IDPm and enhanced cells' susceptibility of selenite-induced apoptosis, as indicated by morphological evidence of apoptosis, DNA fragmentation and the modulation of mitochondrial function and apoptotic marker proteins. These results suggest that IDPm siRNA sensitizes HeLa cells to selenite-induced apoptotic cell death, presumably through the perturbation of the cellular redox status.

Authors+Show Affiliations

School of Life Sciences and Biotechnology, College of Natural Sciences, Kyungpook National University, Taegu 702-701, South Korea.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20088709

Citation

Kil, In Sup, et al. "Silencing of Mitochondrial NADP+-dependent Isocitrate Dehydrogenase Gene Enhances Selenite-induced Apoptosis." Free Radical Research, vol. 44, no. 3, 2010, pp. 332-9.
Kil IS, Chung KH, Park JW. Silencing of mitochondrial NADP+-dependent isocitrate dehydrogenase gene enhances selenite-induced apoptosis. Free Radic Res. 2010;44(3):332-9.
Kil, I. S., Chung, K. H., & Park, J. W. (2010). Silencing of mitochondrial NADP+-dependent isocitrate dehydrogenase gene enhances selenite-induced apoptosis. Free Radical Research, 44(3), 332-9. https://doi.org/10.3109/10715760903494184
Kil IS, Chung KH, Park JW. Silencing of Mitochondrial NADP+-dependent Isocitrate Dehydrogenase Gene Enhances Selenite-induced Apoptosis. Free Radic Res. 2010;44(3):332-9. PubMed PMID: 20088709.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Silencing of mitochondrial NADP+-dependent isocitrate dehydrogenase gene enhances selenite-induced apoptosis. AU - Kil,In Sup, AU - Chung,Kyu Ho, AU - Park,Jeen-Woo, PY - 2010/1/22/entrez PY - 2010/1/22/pubmed PY - 2010/5/12/medline SP - 332 EP - 9 JF - Free radical research JO - Free Radic Res VL - 44 IS - 3 N2 - Selenium has been shown to play a chemopreventive role in human cancer, presumably by inducing tumour cell apoptosis. Selenite is thought to induce oxidative stress by the generation of the superoxide anion and catalysing the oxidation of thiol groups. It has previously been reported that control of the mitochondrial redox balance is a primary function of mitochondrial NADP(+)-dependent isocitrate dehydrogenase (IDPm) by supplying NADPH for antioxidant systems. When investigating whether IDPm would be a vulnerable target of selenite, the loss of enzyme activity was observed. Transfection of HeLa cells with an IDPm small interfering RNA (siRNA) markedly decreased activity of IDPm and enhanced cells' susceptibility of selenite-induced apoptosis, as indicated by morphological evidence of apoptosis, DNA fragmentation and the modulation of mitochondrial function and apoptotic marker proteins. These results suggest that IDPm siRNA sensitizes HeLa cells to selenite-induced apoptotic cell death, presumably through the perturbation of the cellular redox status. SN - 1029-2470 UR - https://www.unboundmedicine.com/medline/citation/20088709/Silencing_of_mitochondrial_NADP+_dependent_isocitrate_dehydrogenase_gene_enhances_selenite_induced_apoptosis_ L2 - https://www.tandfonline.com/doi/full/10.3109/10715760903494184 DB - PRIME DP - Unbound Medicine ER -