This research was supported by a Grant-in-Aid for Scientific Research from the Japanese Ministry of Education, Science, and Culture of Japan, and by a grant from Keio University, School of Medicine.
Ethanol-Induced Apoptosis and Oxidative Stress in Hepatocytes
Version of Record online: 11 APR 2006
Alcoholism: Clinical and Experimental Research
Volume 20, Issue Supplement s9, pages 340A–346A, December 1996
How to Cite
Higuchi, H., Kurose, I., Kato, S., Miura, S. and Ishii, H. (1996), Ethanol-Induced Apoptosis and Oxidative Stress in Hepatocytes. Alcoholism: Clinical and Experimental Research, 20: 340A–346A. doi: 10.1111/j.1530-0277.1996.tb01804.x
A part of the data and discussion in this review was presented in 16th Annual Conference of the Japanese Society for Biomedical Research on Alcohol 1996.
- Issue online: 11 APR 2006
- Version of Record online: 11 APR 2006
- Nick End Labeling;
- Hoechst 33342;
- Laser Scanning Confocal Microscope
This short review focuses on ethanol-induced oxidative stress and hepatocyte apoptosis. Apoptosis is increasingly recognized as a fundamental biological process that impacts on an early development, maturation, and acquisition of disease states of multicellular organisms. Although the occurrence of apoptosis has been identified for many decades, relatively recent acceptance of this principle is evidenced by remarkable increases in special conferences and presentations on this topic as well as its rapidly expanding volume of scientific literature. Oxidative stress is well recognized to be a key step in the pathogenesis of ethanol-associated liver injury. Ethanol administration induces an increase in lipid peroxidation either by enhancing the production of oxygen reactive species and/or by decreasing the level of endogenous antioxidants. Studies in our laboratory using a confocal laser scanning microscopic system strongly suggest that agents which inhibit ethanol-induced oxidative stress effectively attenuate hepatocyte death, i.e., apoptosis and necrosis. In addition, our investigations demonstrated that inhibitors of intracellular antioxidants exaggerate ethanol-associated hepatocyte apoptosis. Although the detailed mechanism still remains unknown, it is conceivable that an oxidant-dependent mechanism is largely involved in the process for ethanol-induced hepatocyte apoptosis.