Skip Navigation



Alcohol and Alcoholism Advance Access published online on March 7, 2005
Alcohol and Alcoholism, doi:10.1093/alcalc/agh142
This Article
Right arrow FREE Full Text (PDF) Freely available
Right arrow All Versions of this Article:
40/3/172    most recent
agh142v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by XU, Y.
Right arrow Articles by LIEBER, C. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by XU, Y.
Right arrow Articles by LIEBER, C. S.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Alcohol & Alcoholism © Medical Council on Alcohol 2005; all rights reserved
Received January 10, 2005
Accepted February 3, 2005

Article

DLPC ATTENUATES ALCOHOL-INDUCED CYTOTOXICITY IN HEPG2 CELLS EXPRESSING CYP2E1

YOUQING XU 1, MARIA A. LEO 2, and CHARLES S. LIEBER 2*

1 Liver Research Center, Beijing Friendship Hospital, Beijing, 100050, China
2 Section of Liver Disease and Nutrition, Alcohol Research and Treatment Center, Veterans Affairs Medical Center & Mt Sinai School of Medicine, 130 West Kingsbridge Road, Bronx, NY10468, USA

* To whom correspondence should be addressed.
CHARLES S. LIEBER, E-mail: liebercs{at}aol.com


  Abstract

Aims: Alcoholic liver injury was shown to result largely from oxidative stress generated by ethanol metabolism via cytochrome P4502E1 (CYP2E1). Our aim was to determine whether this could be overcome by using dilinoleoylphosphatidylcholine (DLPC), an innocuous antioxidant extracted from soybeans. Methods: To address this question, we determined whether DLPC protects against alcohol-induced cytotoxicity in HepG2 cells expressing CYP2E1. A HepG2 subclone (2E1) expressing CYP2E1 and a control subclone (Neo) were exposed for 2 h to DLPC (10 µM), and then 100 mM ethanol was added for 5 days. Results: Ethanol significantly decreased cell viability in the 2E1 cells and increased apoptosis. These alterations were attenuated by DLPC with the most significant effects in the 2E1 cells. This was accompanied by a reduction of the ethanol-induced oxidative stress, including diminished hydrogen peroxide production in the 2E1, but not in the Neo cells. The mitochondrial membrane potential was significantly diminished by ethanol in both cells. It was also improved after adding DLPC, but only in the 2E1 cells. In these cells, mitochondrial glutathione (GSH) was also partially restored by DLPC, which significantly inhibited the CYP2E1 induction by ethanol. Conclusion: DLPC opposes the cytotoxicity induced by alcohol in HepG2 cells expressing CYP2E1, a protective action due, at least in part, to an attenuation of the alcohol-induced oxidative stress and the alteration in the mitochondrial membrane potential. On account of these beneficial effects of DLPC and its innocuity, it is now germane to assess its therapeutic action in alcoholics.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Exp. Biol. Med.Home page
Z. Zhou, J. Liu, Z. Song, C. J. McClain, and Y. J. Kang
Zinc Supplementation Inhibits Hepatic Apoptosis in Mice Subjected to a Long-Term Ethanol Exposure
Experimental Biology and Medicine, May 1, 2008; 233(5): 540 - 548.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
G. Kroemer, L. Galluzzi, and C. Brenner
Mitochondrial Membrane Permeabilization in Cell Death
Physiol Rev, January 1, 2007; 87(1): 99 - 163.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.