ABSTRACT
Background: Oxidative stress plays a major pathogenic role in liver injury following chronic hepatitis B. Glutathione peroxidase [Gpx] has a central role in regulating the oxidative state. Hepatitis B virus [HBV] results in down-regulation of Gpx. On the other hand, iron homeostasis is disrupted in HBV infected patients. Therefore, the objective of this study was to assess the interplay of Gpx and serum iron on clinical and virological characteristics of patients with chronic HBV infection
Method: One hundred and fifty adult, treatment-naïve, patients with chronic hepatitis B were randomly selected from an ongoing cohort of patients with HBV. Plasma Gpx1 concentration and HBV DNA quantity were measured. Liver stiffness was measured by transient elastography
Results: Serum iron had a positive association with HBV DNA count in the total population. Serum iron was not associated with liver stiffness. However, HBV DNA was significantly associated with liver stiffness only in male patients. Serum Gpx was inversely associated with liver stiffness. Serum iron and Gpx had indirect effects on liver stiffness via HBV DNA count. We observed distinct effects of serum iron on HBV DNA and Gpx on liver stiffness in male and female patients
Conclusion: We identified interplay of serum iron and Gpx1 in relation to level of liver fibrosis in patients with chronic hepatitis B. Our results suggest that oxidative stress and serum iron are differentially implicated in the progression of chronic hepatitis B in male and female patients
ABSTRACT
There are hoarding documents for the biological importance of cyclooxygenase-2 [COX-2] in pancreatic carcinogenesis. We aimed to thoroughly investigate the DNA sequence variations of whole COX-2 exons in a large case- control study of pancreatic cancer by direct sequencing. The entire exonic regions of COX-2 including 10 exons were sequenced in the germline DNA of 96 patients with pancreatic cancer. Selected variants within exons six to seven [E6E7] amplicon from the test panel were genotyped in 96 controls. The COX-2 gene was demonstrated to be genetically conserved. Four missense mutations were found in three cases. However the common variant c.724-10_724-7deIATTT [rs20123141 1] that is located in intron 6, showed significant difference between cases and controls [21 [21.9%] vs 11 [%11.5], p=0.05]. This study determined that COX-2 has a conservative sequence, which is required for its enzymatic activity and supports the important role of this enzyme's expression in pancreatic cancer rather than any changes in its activity. The effect of intronic variant rs201231411 on COX-2 expression could be analyzed in future studies