Plasma glutathione concentration in patients with chronic hepatitis C virus infection

Authors

  • H. L. Lim,

    1. section of Hepatobmary Diseases, Division of Gastroenterology. Hepatology and Nutrition, University of Florida College of Medicine
    Search for more papers by this author
  • B. M. Myers,

    1. section of Hepatobmary Diseases, Division of Gastroenterology. Hepatology and Nutrition, University of Florida College of Medicine
    2. Gainesville VA Medical Center, Gainesville, Florida. USA
    Search for more papers by this author
  • B. A. Hamilton,

    1. section of Hepatobmary Diseases, Division of Gastroenterology. Hepatology and Nutrition, University of Florida College of Medicine
    Search for more papers by this author
  • G. L. Davis,

    1. section of Hepatobmary Diseases, Division of Gastroenterology. Hepatology and Nutrition, University of Florida College of Medicine
    Search for more papers by this author
  • J. Y. N. Lau

    Corresponding author
    1. section of Hepatobmary Diseases, Division of Gastroenterology. Hepatology and Nutrition, University of Florida College of Medicine
    Search for more papers by this author

Division of Gastroenterology. Hepatology and Nutrition, PO Box 100214, University of Florida. Gainesville, Florida 32610. USA.

Abstract

Summary. It has recently been proposed that a depletion of glutathione (GSH) may be a contributing factor to viral persistence and resistance to interferon-α (IFN-α) therapy in chronic hepatitis C virus (HCV) infection. The aim of this study was: (1) to compare plasma GSH levels in patients with chronic HCV infection and normal healthy controls; and (2) to correlate GSH levels with liver histology and serum HCV RNA levels. Twenty-four patients with compensated chronic hepatitis C and 2 7 healthy subjects were studied. Serum and heparinized plasma were prospectively prepared and frozen within 1 h of collection. Plasma glutathione and glutathione peroxidase (GP) levels were measured spectrophotometrically. The serum HCV RNA level was quantitated by the branched chain DNA signal-amplification assay. Plasma GSH levels were not decreased in patients with chronic HCV infection but were actually greater than in controls (control 1.2 7 ± 0.12 μg ml-1, HCV 1.62 ± 0.11 μg ml-1, P < 0.05). There was also no difference in plasma GP activity between these two groups (control 0.233 ± 0.007 U ml-1, HCV 0.230 ± 0.007 U ml-1). Among the patients with chronic HCV infection, there was no correlation between either plasma GSH or GP levels and the serum alanine aminotransferase (ALT) or aspartate aminotransferase (AST), serum HCV RNA level, or liver histology. This study demonstrates that chronic HCV infection does not decrease the plasma GSH and GP levels.

Ancillary