The Roles of Telomerase Activity and Oxidative/Nitrosative Stress in HBV-Related Hepatocellular Carcinoma: Associations with AFP, LDH, and Liver Function Parameters
摘要
Elucidating the molecular mechanisms underlying disease progression is crucial for developing treatments for hepatitis B (HBV) infection and hepatocellular carcinoma (HCC). This study investigated telomerase activity, oxidative/nitrosative stress, and DNA oxidation levels in HBV- and HCC-related liver pathogenesis and evaluated their relationships with disease progression.
MethodsTelomerase enzyme activity and h-TERT were evaluated to determine the relationship between developing hepatitis and cancer in the liver and cellular aging processes. Oxidative/Nitrosative Stress was evaluated by measuring total oxidant levels (TOS), oxidative stress index (OSI), 8-hydroxy-2’-deoxyguanosine (8-OHdG), inducible nitric oxide synthase (iNOS), nitric oxide (NO), and 3-nitrotyrosine (3-NT).
ResultsA significant increase in TOS, OSI, 8-OHdG, and NO levels was observed in HBV and HCC patients, parallel with increased telomerase enzyme activity and hTERT expression. 3-nitrotyrosine (3-NT) and iNOS levels, markers of nitrosative stress, were also significantly increased in the patient groups compared with the control group, with the highest levels observed in the HBV group.
ConclusionOur findings suggest that oxidation and nitrosylation of cellular macromolecules, as well as increased telomerase activity, play critical roles in the pathogenesis of viral hepatitis and hepatocellular carcinogenesis. Future therapeutic approaches focusing on telomerase activation and modulation of oxidative/nitrosative stress may be considered a potential strategy to prevent disease progression in HBV and HCC patients.