Possible relations between oxidative damage and apoptosis in benign prostate hyperplasia and prostate cancer patients.

Cancer has been described as the twentieth century plague, and is a very common health problem. It has been reported that ROS and ROS products play a key role in cancer and that oxidative damage is effective in apoptosis initiation. In this study we aimed to evaluate the relationship between MDA (malondialdehyde), DNA damage (8-hydroxyguanine, 8-OH-dG), and caspase-3 in BHP and prostate cancer patients. Twenty male patients with prostate cancer and 20 male patients with benign prostate hyperplasia were included into this study. The MDA (nanomole), DNA damage (nanograms per millilitre), and caspase-3 (nanograms per millilitre) levels were measured in prostate cancer and benign prostate hyperplasia using Elisa kits (Millipore Corporation, Billerica, MA, USA). In the prostate cancer group, serum MDA (30.96 ± 9.25) and DNA damage (4.42 ± 0.36) levels were significantly raised (p < 0.05) when compared to the benign prostate hyperplasia group (24.05 ± 8.06, 3.99 ± 0.54). However, in the prostate cancer group, serum caspase-3 (2.36 ± 0.82) levels were statistically significantly lowered (p < 0.05) compared with the benign prostate hyperplasia group (3.15 ± 1.04). We observed that altered prooxidant, DNA damage levels may lead to an increase in oxidative damage and may consequently play an important role in prostate carcinogenesis. These findings indicate that, although the triggering of these changes is unknown, changes in the levels of MDA, DNA damage, and caspase-3 in the blood are related to prostatic carcinoma development. In addition, it would be appropriate to conduct new studies with a large number of patients at different stages.