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Silencing of cytosolic NADP+-dependent isocitrate dehydrogenase gene enhances ethanol-induced toxicity in HepG2 cells.
Arch Pharm Res. 2010 Jul; 33(7):1065-71.AP

Abstract

It has been shown that acute and chronic alcohol administrations increase the production of reactive oxygen species, lower cellular antioxidant levels and enhance oxidative stress in many tissues. We recently reported that cytosolic NADP(+)-dependent isocitrate dehydrogenase (IDPc) functions as an antioxidant enzyme by supplying NADPH to the cytosol. Upon exposure to ethanol, IDPc was susceptible to the loss of its enzyme activity in HepG2 cells. Transfection of HepG2 cells with an IDPc small interfering RNA noticeably downregulated IDPc and enhanced the cells' vulnerability to ethanol-induced cytotoxicity. Our results suggest that suppressing the expression of IDPc enhances ethanol-induced toxicity in HepG2 cells by further disruption of the cellular redox status.

Authors+Show Affiliations

Kyungpook National University, Taegu, Korea.No affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

20661717

Citation

Yang, Eun Sun, et al. "Silencing of Cytosolic NADP+-dependent Isocitrate Dehydrogenase Gene Enhances Ethanol-induced Toxicity in HepG2 Cells." Archives of Pharmacal Research, vol. 33, no. 7, 2010, pp. 1065-71.
Yang ES, Lee SM, Park JW. Silencing of cytosolic NADP+-dependent isocitrate dehydrogenase gene enhances ethanol-induced toxicity in HepG2 cells. Arch Pharm Res. 2010;33(7):1065-71.
Yang, E. S., Lee, S. M., & Park, J. W. (2010). Silencing of cytosolic NADP+-dependent isocitrate dehydrogenase gene enhances ethanol-induced toxicity in HepG2 cells. Archives of Pharmacal Research, 33(7), 1065-71. https://doi.org/10.1007/s12272-010-0713-4
Yang ES, Lee SM, Park JW. Silencing of Cytosolic NADP+-dependent Isocitrate Dehydrogenase Gene Enhances Ethanol-induced Toxicity in HepG2 Cells. Arch Pharm Res. 2010;33(7):1065-71. PubMed PMID: 20661717.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Silencing of cytosolic NADP+-dependent isocitrate dehydrogenase gene enhances ethanol-induced toxicity in HepG2 cells. AU - Yang,Eun Sun, AU - Lee,Su-Min, AU - Park,Jeen-Woo, Y1 - 2010/07/27/ PY - 2009/09/24/received PY - 2010/04/14/accepted PY - 2010/03/03/revised PY - 2010/7/28/entrez PY - 2010/7/28/pubmed PY - 2011/4/19/medline SP - 1065 EP - 71 JF - Archives of pharmacal research JO - Arch Pharm Res VL - 33 IS - 7 N2 - It has been shown that acute and chronic alcohol administrations increase the production of reactive oxygen species, lower cellular antioxidant levels and enhance oxidative stress in many tissues. We recently reported that cytosolic NADP(+)-dependent isocitrate dehydrogenase (IDPc) functions as an antioxidant enzyme by supplying NADPH to the cytosol. Upon exposure to ethanol, IDPc was susceptible to the loss of its enzyme activity in HepG2 cells. Transfection of HepG2 cells with an IDPc small interfering RNA noticeably downregulated IDPc and enhanced the cells' vulnerability to ethanol-induced cytotoxicity. Our results suggest that suppressing the expression of IDPc enhances ethanol-induced toxicity in HepG2 cells by further disruption of the cellular redox status. SN - 0253-6269 UR - https://www.unboundmedicine.com/medline/citation/20661717/Silencing_of_cytosolic_NADP+_dependent_isocitrate_dehydrogenase_gene_enhances_ethanol_induced_toxicity_in_HepG2_cells_ L2 - https://dx.doi.org/10.1007/s12272-010-0713-4 DB - PRIME DP - Unbound Medicine ER -