Introduction

Historically, benign prostatic hyperplasia (BPH) has been a major focus of urologic practice and surgery. BPH assigns most of men after the age of 50 and represents the most common urologic disease among elderly males [ 1]. BPH is histologically

Department of Urology, Harran University Medical School, Arastirma Hospital, Meterorology Caddesi, Sanliurfa 63200, Turkey e-mail: [email protected]

A. Agarwal et al. (eds.), Studies on Men's Health and Fertility, Oxidative Stress 591

in Applied Basic Research and Clinical Practice, DOI 10.1007/978-1-61779-776-7_27, © Springer Science+Business Media, LLC 2012

defined as an overgrowth of the epithelial and stromal cells from the transition zone and periurethral area. Incidence of histological BPH could be over 70% at 60 years and over 90% at 70 years [2] . However, histological BPH doesn't always lead to clinical manifestations. BPH symptoms can range over a wide scale from minimal bother to urinary retention and renal failure. To date, we still have no precise knowledge of the cellular and molecular processes underlying the pathogenesis of BPH and leading to a symptomatic disease [3]. Although the influence of androgens and estrogens has been demonstrated, hormonal factors alone may not fully explain BPH development.

Hydroxyl radicals, peroxides, and superoxides are reactive oxygen species (ROS) that are generated during everyday metabolic processes in a normal cell. ROS, generated either endogenously (mitochondria, metabolic process, inflammation, etc.) or from external sources [4], play a vital role in regulating several biologic phenomena. While increased ROS generation has traditionally been associated with tissue injury or DNA damage which are general manifestations of pathological conditions associated with infection, aging, mitochondrial DNA mutations, and cellular proliferation, new and exciting information points to an essential role for increased ROS generation in several cellular processes associated with neoplastic transformation and aberrant growth and proliferation [5, 6]. Processes associated with proliferation, apoptosis, and senescence may be a result of the activation of signaling pathways in response to intracellular changes in ROS levels [7]. Thus, the excessive production of ROS or inadequacy in a normal cell's antioxidant defense system (or both) can cause the cell to experience oxidative stress. This oxidative stress may play a broader role in cellular processes associated with initiation and development of BPH.

The role of inflammation in prostate diseases is suggested by the presence of inflammatory cells within the BPH and Prostate Cancer (PC). On histologic examinations from patients with BPH, inflammatory aspects are present in approximately 40% of cases. The men with inflammatory aspects inside the prostate have a significantly higher risk for BPH progression and acute urinary retention (AUR). Evidence shows that a cyclooxygenase-2 (COX-2) inhibitor can increase the apoptotic activity in human BPH tissue. In vitro studies showed an overexpression of inflammatory markers in BPH and PC compared with a normal tissue. There are significant inflammatory markers differences between BPH and PC, which is more severe inflammation process in PC. Another basic difference was a gene polymorphism in PC. Targeting the microenvironment may represent a promising therapeutic approach for prostate disease. Many epidemiological studies showed a beneficial effect of drug that influences inflammation such as nonsteroidal anti-inflammatory drugs (NSAIDs), antioxidant compound in food or supplements, and vitamin D receptor (VDR) agonists. These drugs need more investigation to prove their efficacy as chemopreventive agents for prostatic disease.

This chapter presents recent evidence that suggests a link between oxidative stress and BPH. This review is aimed to explore the mechanism of inflammation and oxidative stress in prostate and the possibility of drug development against inflammation for prostatic disease prevention.

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