Evaluation of Oxidative Stress and DNA Damage in Benign Prostatic Hyperplasia Patients and Comparison with Controls

Abstract

In the present study, oxidative stress and lymphocytic DNA damage in both pre-op and post-op benign prostrate hyperplasia (BPH) patients with age >50 years was evaluated and compared with normal healthy subjects (controls- without any evidence of disease) of the same sex and age group. From December 2007 to November 2009, oxidative stress in 45 BPH patients were evaluated both before (pre-op patients) and after 7 days of surgery (post-op patients) in terms of measurements of plasma levels of (1) various anti-oxidative enzymes, (2) non-enzymatic antioxidants and (3) malondialdehyde which is a product of lipid peroxidation. The lymphocyte DNA damage was also evaluated by single cell alkaline gel electrophoresis in terms of tail length migration in these patients. These values were compared with their respective control subjects of similar sex and age group. The activities of antioxidant enzymes and the levels of antioxidant, reduced glutathione were found significantly decreased (p < 0.05) in serum samples of pre-operative group of BPH patients as compared to the controls. These altered parameters increased significantly (p < 0.05) and returned to their near normal control values, but not up to baseline values, in post operative patients i.e. after the cancer load was decreased by surgery. Lymphocytic DNA damage was found to be significantly increased in pre-op group as compared to controls and was reduced after surgery in post-op group. The present study therefore, shows significantly increased levels of oxidative stress and DNA damage in BPH patients which were reduced after removal of tumour load. Thus oxidative damage plays an important role in prostate tumourogenesis and timely management of oxidative stress can be of importance in preventing the occurrence of BPH.

Oxidative Stress in Benign Prostatic Hyperplasia: A Systematic Review

“…It is an extremely common disease of ageing men and carries a distressingly high morbidity because of its irritative and obstructive symptoms. The etiology and pathogenesis of BPH are not well understood [2] . …”

Antioxidant defense system in prostate adenocarcinoma and benign prostate hyperplasia of elderly patients

“…However, Yilmaz et al [25] observed the decreased activities of SOD in the erythrocytes of PC and BPH patients when compared with healthy men. Similarly, Ahmed et al [33] found the decreased plasma activities of SOD and GST in BPH group. The observed lack of alterations in the EC-SOD and GST activities in the PC and the BPH patients may suggest that the increased ROS generation plays a more important role in the prostate pathogenic processes than weakened antixidant defense system.…”

“…Some authors demonstrated the decreases of GPx activities in plasma or erythrocytes of cancer patients [25], whereas the others did not observe any significant differences in GPx-3 activities between patients with cancer and healthy people [32]. Yilmaz et al [25] and Ahmed et al [33] observed the most decreased activities of GPx-1 in the erythrocytes of BPH patients. In the study performed by Yilmaz et al [25] the erythrocyte GPx-1 activities in PC patients were also lower than in healthy men.…”

Effects of low-frequency ultrasound combined with microbubbles on benign prostate hyperplasia

“…21 The cause of enhanced oxidative stress could be overproduction of free radicals or decrease in the activities of free radical scavenging enzymes like SOD. 22 Peroxidation-antioxidant balance may be used to treat BPH to alter the overproduction of free radicals. In the present study, the SOD significantly increased in the G2 and G3 groups after treatment; this was especially obvious in the G3 group.…”