Please use this identifier to cite or link to this item:
http://scholarbank.nus.edu.sg/handle/10635/28907
Title: | Reduced mitochondrial coenzyme Q10 levels in HepG2 cells treated with high-dose simvastatin: A possible role in statin-induced hepatotoxicity? |
Authors: | Tavintharan, S. Lim, S.C. Ong, C.N. Jeyaseelan, K. Sivakumar, M. Sum, C.F. |
Keywords: | Hepatotoxicity Oxidative stress Statins Transaminitis Ubiquinone |
Issue Date: | 2007 |
Citation: | Tavintharan, S., Lim, S.C., Ong, C.N., Jeyaseelan, K., Sivakumar, M., Sum, C.F. (2007). Reduced mitochondrial coenzyme Q10 levels in HepG2 cells treated with high-dose simvastatin: A possible role in statin-induced hepatotoxicity?. Toxicology and Applied Pharmacology 223 (2) : 173-179. ScholarBank@NUS Repository. |
Abstract: | Lowering of low-density lipoprotein cholesterol is well achieved by 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins). Statins inhibit the conversion of HMG-CoA to mevalonate, a precursor for cholesterol and coenzyme Q10 (CoQ10). In HepG2 cells, simvastatin decreased mitochondrial CoQ10 levels, and at higher concentrations was associated with a moderately higher degree of cell death, increased DNA oxidative damage and a reduction in ATP synthesis. Supplementation of CoQ10, reduced cell death and DNA oxidative stress, and increased ATP synthesis. It is suggested that CoQ10 deficiency plays an important role in statin-induced hepatopathy, and that CoQ10 supplementation protects HepG2 cells from this complication. © 2007 Elsevier Inc. All rights reserved. |
Source Title: | Toxicology and Applied Pharmacology |
URI: | http://scholarbank.nus.edu.sg/handle/10635/28907 |
ISSN: | 0041008X 10960333 |
Appears in Collections: | Staff Publications |
Show full item record
Files in This Item:
There are no files associated with this item.
SCOPUSTM
Citations
41
checked on Feb 27, 2018
WEB OF SCIENCETM
Citations
40
checked on Dec 19, 2018
Page view(s)
131
checked on Dec 30, 2018
Google ScholarTM
Check
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.