8-hydroxy-2'-deoxyguanosine and TP53 in Egyptian Patients with Hepatitis C Viral Chronic Liver Diseases: Insight into the Pathogenesis and Predictive Force

Hoda M. El-Emshaty, Somaia M. Osman , Fathy M. El-Taweel, Mohamed M. El-Hemaly, Hisham Ismail 3 Gastrointestinal Surgery Center, Faculty of Medicine, Mansoura University, Mansoura, Egypt Chemistry Dept., Faculty of Science, Damietta University, New Damietta, Egypt. Biochemistry Division, Chemistry Dept., Faculty of Science, Minia University, Minia, Egypt. Running title: Predictive force of serum 8-OHdG in HCV-chronic liver diseases *Corresponding Author: Dr. Hoda Mohamed El-Emshaty Professor of Biochemistry, Gastrointestinal Surgical Center, Faculty of Medicine, Mansoura University, Mansoura, Egypt E-mail: elemshaty_h@yahoo.com DOI: 10.21608/jbaar.2022.223518 Abstract Reactive oxygen species (ROS) is excessively generated during tumor development yielding the oxidatively modified products of proteins and DNA. These DNA alterations could contribute to the development of cancer through the activation of oncogenes and inactivating tumor suppressor genes (TSGs). Therefore, 8-OHdG DNA oxidative damage and TP53 protein expression were evaluated amongst HCV-Chronic liver disease patients to explore their possible role in hepatocarcinogenesis and to predict HCC development at early stages. A total of 141 patients with HCV-related liver diseases; 69 with hepatocellular carcinoma and 72 with liver cirrhosis were enrolled in this study in addition to 56 healthy subjects. Serum 8-OHdG and TP53 expression by ELISA were markedly elevated in HCC patients compared to LC and healthy individuals (p<0.0001). A significant correlation was noted for 8-OHdG and TP53 with disease progression and tumor differentiation but not with tumor site. 8-OHdG and TP53 were highly (p<0.05) predicting for HCC at early stages and the diagnostic performance for discriminating HCC from LC by ROC curve showed the best AUC was recorded for 8-OHdG (0.745) followed by TP53 (0.667) with accuracy (87.2% and 82% respectively). Therefore, HCV-induced oxidative DNA damage could increase the carcinogenic potential of HCC development through the activation of TP53.