2009 Volume 48 Issue 18 Pages 1585-1593
Aim Hepatocyte apoptosis is involved in the pathogenesis of liver diseases, while at the same time oxidative stress plays an important role in liver cell damage. This prompted us to evaluate the possible relationship between hepatocyte apoptosis and oxidative stress in patients with chronic hepatitis B.
Methods CHB patients were placed in groups A (ALT >40 IU/L) and B (ALT ≤40 IU/L). Healthy controls were considered as group C (all ALT ≤40 IU/L). Serum concentrations of α-tocopherol, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) were determined and liver cell apoptosis was evaluated by using terminal deoxynucleotydil transferase-mediated d-UTP biotin nick-end labeling (TUNEL).
Results SOD, GSH-Px, and MDA did not differ between groups. α-Tocopherol was significantly decreased in groups A (p<0.01) and B (p<0.05) when compared with group C and it was negatively correlated with the apoptosis index (r=-0.575, p<0.01).
Conclusion Only the plasma concentration of α-tocopherol rather than the other oxidative stress markers changed significantly in patients with normal alanine aminotransferase levels (ALT <40 IU/L) when compared with healthy controls and correlated significantly with the apoptosis index, suggesting that α-tocopherol may be a possible marker to reflect liver cell damage, especially in the absence of serum aminotransferase elevation.