HCV/Oxidative Stress and Liver Disease

by K. Okita (Editor)

Overview

Since the discovery of superoxide dismutase more than three decades ago, there has been rapid growth in the knowledge of oxidative stress and disease. This volume containing the proceedings of the 13th Yamaguchi Symposium on Liver Disease includes discussion of the direct cellular effects of hepatitis C virus (HCV) proteins on hepaytes and reviews evidence that oxidative stress caused primarily by the HCV core protein plays a key role in disease pathogenesis. Also included are chapters on new aspects of oxidative stress and liver disease such as carbon monoxide as a regulator of liver microcirculation, hepatic iron accumulation and the incidence of hepaellular carcinoma, and oxidative stress in the absence of inflammation in hepaarcinogenesis. This collection of papers from the Yamaguchi Symposium creates a valuable reference resource for physicians and hepatologists.

Product Details

ISBN-13:	9784431703242
Publisher:	Springer Japan
Publication date:	12/13/2002
Series:	Frontiers in Hepatology
Pages:	107
Product dimensions:	6.10(w) x 9.25(h) x 0.20(d)

Table of Contents

Alcohol-HCV Interactions in Transgenic Mice Expressing Viral Proteins in the Liver.- Role of Core Protein-Induced Oxidative Stress in the Pathogenesis of Hepatitis C.- Hepatitis C Virus Core-Mediated Alteration of Gene Expression and Signal Transduction in the Host Cell.- Signals Induced by HCV Proteins.- Role of Hepatitis C Virus in Hepaarcinogenesis: Oxidative Stress in the Absence of Inflammation.- Reduced Chemical Hepaarcinogenesis in Interferon-β Receptor Knockout Mice.- Fewer Somatic Mutations of Mihondrial DNA in Noncancerous Liver Tissue Patients with Hepaellular Carcinoma Respond to Interferon Therapy.- Hepatic Iron Staining in Chronic Hepatitis C Patients with Low HCV RNA Levels as a Predictive Marker for Interferon Therapy.- Hepatic Iron Accumulation and Incidence of Hepaellular Carcinoma in Patients with Chronic Hepatitis C.- Carbon Monoxide as a Gaseous Regulator of Liver Microcirculation.- Tamoxifen-Induced Nonalcoholic Steatohepatitis.

Editorial Reviews

Reviewer: Steven I. Shedlofsky, MD (University of Kentucky College of Medicine)
Description: This book represents the proceedings of the Yamaguchi University Symposium on Liver Disease that was held sometime in 2001. However, there are only 11 papers reproduced in a small 104-page presentation and only eight of the papers have anything to do with hepatitis C and hepatic oxidative stress.
Purpose: The important role of hepatic oxidative stress in mediating the injury caused by hepatitis C was apparently the subject of Yamaguchi liver symposium. The preface of the book does not give much information about the symposium or the qualifications of its participants. However, there was only one non-Japanese member included in the group and thus the purpose of the publication might loosely be construed as a vehicle to present the work of Japanese investigators in the area of hepatitis C, oxidative stress and/or liver disease. However, the book does not provide any coherent or organized theme.
Audience: The information includes reviews and some original data of interest to basic and clinical investigators working on hepatitis C-induced liver injury. The editor, K. Okita, is the Chair of the Hepatology Division at Yamaguchi University, but Dr. Okita himself did not participate in any of the scientific studies presented.
Features: The 11 papers represent a diverse group of studies; but only eight of the papers deal with hepatitis C and oxidative stress. Original data may be present in five of the papers and the rest are brief reviews of the authors' work that reference previously published articles. Therefore, there is not much new information. The most interesting papers deal with the hepatitis C core protein, either expressed in transgenic mice or expressed in mouse or human cell lines. The core protein is shown to increase steatosis, increase measures of oxidative stress, alter signal transduction pathways, block apoptosis, and predispose mice to hepatocellular carcinoma. Two papers deal with hepatic iron as a source of oxidative stress. But one paper with minimal data suggests that a high hepatic iron in humans who have a low viral load is associated with an unbelievable 75 percent sustained viral response with interferon monotherapy. The quality and depth of each of the papers varies considerably.
Assessment: This publication is not a very useful one, even for investigators interested in hepatitis C and oxidative stress. Most of the information is available in other published peer-reviewed journals where the data are probably presented and discussed in greater depth. Furthermore, because the symposium proceedings are not organized around any particular themes and the work presented is not comprehensive, there is too much missing from the book to make it worth acquiring.

Doody's Review Service