Oxidative stress in prostate hyperplasia and carcinogenesis

Abstract

Prostatic hyperplasia (PH) is a common urologic disease that affects mostly elderly men. PH can be classified as benign prostatic hyperplasia (BPH), or prostate cancer (PCa) based on its severity. Oxidative stress (OS) is known to influence the activities of inflammatory mediators and other cellular processes involved in the initiation, promotion and progression of human neoplasms including prostate cancer. Scientific evidence also suggests that micronutrient supplementation may restore the antioxidant status and hence improve the clinical outcomes for patients with BPH and PCa. This review highlights the recent studies on prostate hyperplasia and carcinogenesis, and examines the role of OS on the molecular pathology of prostate cancer progression and treatment.

Keywords: Antioxidants; Cancer treatment; Oxidative stress; Prostate cancer.

Fig. 1

Gleason’s Pattern of Prostate Carcinogenesis: Gleason’s score is the standard used to stage prostate cancer. It helps to determine the treatment strategy to be employed

Fig. 2

Prostate Cancer and Predisposing Factors: This illustrates the relationship between oxidative stress, antioxidant agents and other predisposing factors such as age, sex, race, and family history in prostate cancer

Fig. 3

The NIH Consensus Classification of Prostatitis Syndromes [54, 56, 57, 150]

Fig. 4

Prostate Carcinogenesis Model: This illustrates what happens at the cellular level as prostate hyperplasia progresses from asymptomatic to metastatic stage

Fig. 5

Oxidative Linked Genes Involved in Prostate Cancer: These genes have been linked to oxidative stress and their expression was aberrant in prostate cancer [26, 151]

Fig. 6

Gene Involved in the signaling pathways which contribute to the development and progression (including invasion, metastasis, and relapse) of PCa: The genes that maintain hemostasis receive attack from pro-oxidative stress genes and genes that are involved in metastasis. DNA damage leads to suppression of antioxidant pro-gene and this gives way to the over-expression of cancer promoting genes