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Modulation of NADP(+)-dependent isocitrate dehydrogenase in aging.
Redox Rep. 2004; 9(5):271-7.RR

Abstract

NADPH is an important cofactor in many biosynthesis pathways and the regeneration of reduced glutathione, critically important in cellular defense against oxidative damage. It is mainly produced by glucose-6-phosphate dehydrogenase, malic enzyme, and NADP(+)-specific isocitrate dehydrogenases (ICDHs). Here, we investigated age-related changes in ICDH activity and protein expression in IMR-90 human diploid fibroblast cells and tissues from Fischer 344 rats. We found that in IMR-90 cells the activity of cytosolic ICDH (IDPc) gradually increased with age up to the 46-48 population doubling level (PDL) and then gradually decreased at later PDL. 2',7'-Dichloro-fluorescein fluorescence which reflects intracellular ROS generation was increased with aging in IMR-90 cells. In ad libitum-fed rats, we noted age-related, tissue-specific modulations of IDPc and mitochondrial ICDH (IDPm) activities and protein expression in the liver, kidney and testes. In contrast, ICDH activities and protein expression were not significantly modulated in diet-restricted rats. These data suggest that modulation of ICDH is an age-dependent and a tissue-specific phenomenon.

Authors+Show Affiliations

Department of Biochemistry, College of Natural Sciences, Kyungpook National University, Taegu, Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

15606980

Citation

Kil, In Sup, et al. "Modulation of NADP(+)-dependent Isocitrate Dehydrogenase in Aging." Redox Report : Communications in Free Radical Research, vol. 9, no. 5, 2004, pp. 271-7.
Kil IS, Lee YS, Bae YS, et al. Modulation of NADP(+)-dependent isocitrate dehydrogenase in aging. Redox Rep. 2004;9(5):271-7.
Kil, I. S., Lee, Y. S., Bae, Y. S., Huh, T. L., & Park, J. W. (2004). Modulation of NADP(+)-dependent isocitrate dehydrogenase in aging. Redox Report : Communications in Free Radical Research, 9(5), 271-7.
Kil IS, et al. Modulation of NADP(+)-dependent Isocitrate Dehydrogenase in Aging. Redox Rep. 2004;9(5):271-7. PubMed PMID: 15606980.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Modulation of NADP(+)-dependent isocitrate dehydrogenase in aging. AU - Kil,In Sup, AU - Lee,Young Sup, AU - Bae,Young Seuk, AU - Huh,Tae Lin, AU - Park,Jeen-Woo, PY - 2004/12/21/pubmed PY - 2005/5/13/medline PY - 2004/12/21/entrez SP - 271 EP - 7 JF - Redox report : communications in free radical research JO - Redox Rep VL - 9 IS - 5 N2 - NADPH is an important cofactor in many biosynthesis pathways and the regeneration of reduced glutathione, critically important in cellular defense against oxidative damage. It is mainly produced by glucose-6-phosphate dehydrogenase, malic enzyme, and NADP(+)-specific isocitrate dehydrogenases (ICDHs). Here, we investigated age-related changes in ICDH activity and protein expression in IMR-90 human diploid fibroblast cells and tissues from Fischer 344 rats. We found that in IMR-90 cells the activity of cytosolic ICDH (IDPc) gradually increased with age up to the 46-48 population doubling level (PDL) and then gradually decreased at later PDL. 2',7'-Dichloro-fluorescein fluorescence which reflects intracellular ROS generation was increased with aging in IMR-90 cells. In ad libitum-fed rats, we noted age-related, tissue-specific modulations of IDPc and mitochondrial ICDH (IDPm) activities and protein expression in the liver, kidney and testes. In contrast, ICDH activities and protein expression were not significantly modulated in diet-restricted rats. These data suggest that modulation of ICDH is an age-dependent and a tissue-specific phenomenon. SN - 1351-0002 UR - https://www.unboundmedicine.com/medline/citation/15606980/Modulation_of_NADP_+__dependent_isocitrate_dehydrogenase_in_aging_ L2 - https://www.tandfonline.com/doi/full/10.1179/135100004225006056 DB - PRIME DP - Unbound Medicine ER -