Introduction: Oxidative damage is an important factor contributing to ageing and many degenerative dis- eases. It can be detected by the DNA base damage, which is formation of 8-oxo-7,8-dihydro-2’deoxygua- nosine (8-oxodG). The 8-oxodG is an important indicator of oxidative stress and has been competent- ly specified as a recognized initiator of the carcinogenic process and premutagenic injury in mammalian cells. Aims: In this preliminary study, we investigated the possible association of oxidative DNA damage in hepa- tocellular carcinoma (HCC) patients in comparison with Malaysian healthy controls taking into account the dif- ferent races and genders in both groups. Method: DNA of peripheral white blood cells was isolated from 91 HCC patients and 304 controls. The level of oxidative DNA damage was determined by ELISA procedure. Results: Quantitative measurement of 8-oxodG was higher in HCC patients at mean value of 3.30 ± 2.32 ng/ml. In controls, the average value is 1.57 ± 1.92 ng/ml. Comparison between gender showed that there was a significant difference observed in the level of 8-oxodG between male and female in controls, where p = 0.003. The level of 8-oxodG was higher in male than in female controls. There was a significant difference in the average value of 8-ox- odG level between the controls and HCC patients where p
Replicative senescence of human diploid fibroblasts (HDFs) occurs when cells lose their capacity to proliferate and enter a phase of irreversible growth arrest. Stress-induced premature senescence (SIPS) on the other hand is caused by subcytotoxic concentrations of various oxidants which trigger accelerated cellular senescence. In this study, a SIPS model was established by exposing human diploid fibroblasts (HDFs) to 20 μM H2O2 for 2 weeks. A proteomic comparison between young, senescent and SIPS cells was done using two dimensional gel electrophoresis (2DGE) to elucidate the changes in protein expression associated with cellular aging. Our analysis showed that 28 protein spots were differentially expressed in senescent cells whereas 10 protein spots were differentially expressed in SIPS as compared to young cells. Three similar protein spots were differentially expressed in both senescent and SIPS cells when compared to the young cells. These results indicate that a difference in protein expression exists between senescent cells and SIPS cells compared to young cells.