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Oxidative stress in prostate hyperplasia and carcinogenesis

View Article: PubMed Central - PubMed

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.

No MeSH data available.


Related in: MedlinePlus

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
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Fig2: 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

Mentions: Several mechanisms for prostate hyperplasia development have been suggested and these include; oxidative stress (OS) [10–14], inflammatory mediators [3, 16–20], hormones (especially androgens whose increase in physiologic level can cause increase in oxidative stress and alterations in intracellular glutathione levels and the activity of other detoxification enzymes required for the maintenance of the cellular prooxidant-antioxidant balance such as gamma-glutamyl transpeptidase) [15], enzymatic factors, dietary factors [21–23], inflammatory genes [17, 24] and Gleason score grading system (Fig. 1) which is used to evaluate the prognosis of PCa [12]. Reactive nitrogen species (RNS) and ROS are byproducts of normal cellular metabolism which impact on cell signaling. Increase in the levels of ROS and RNS induces oxidative stress, causing the cells to activate a variety of mechanisms that allow them to cope with these changes [25]. It is known that OS contributes to the initiation and progression of PCa by regulating molecules such as DNA, transcription factors, and cell cycle regulators [12]. Other studies have shown that antioxidants and other molecules that protect cells against OS play a role in the prevention of PCa. The potential chemoprotective role of ROS regulators in the fight against PCa has been reported [26]. Chronic increases in ROS over time are known to induce somatic mutations and neoplastic transformation [27]. As shown in Fig. 2, several predisposing factors have been postulated to contribute to PCa initiation, promotion and progression. Age, race and family history play predominant roles however environmental factors such as chronic prostatitis, diet, medication and exposure radiation are associated with PCa. Cellular dysfunction including aberrant signaling, genotoxicity, gene mutation, DNA damage, cell cycle arrest, apoptosis and mitochondrial mutation also affect the PCa carcinogenesis and metastasis.Fig. 1


Oxidative stress in prostate hyperplasia and carcinogenesis
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
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC5017015&req=5

Fig2: 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
Mentions: Several mechanisms for prostate hyperplasia development have been suggested and these include; oxidative stress (OS) [10–14], inflammatory mediators [3, 16–20], hormones (especially androgens whose increase in physiologic level can cause increase in oxidative stress and alterations in intracellular glutathione levels and the activity of other detoxification enzymes required for the maintenance of the cellular prooxidant-antioxidant balance such as gamma-glutamyl transpeptidase) [15], enzymatic factors, dietary factors [21–23], inflammatory genes [17, 24] and Gleason score grading system (Fig. 1) which is used to evaluate the prognosis of PCa [12]. Reactive nitrogen species (RNS) and ROS are byproducts of normal cellular metabolism which impact on cell signaling. Increase in the levels of ROS and RNS induces oxidative stress, causing the cells to activate a variety of mechanisms that allow them to cope with these changes [25]. It is known that OS contributes to the initiation and progression of PCa by regulating molecules such as DNA, transcription factors, and cell cycle regulators [12]. Other studies have shown that antioxidants and other molecules that protect cells against OS play a role in the prevention of PCa. The potential chemoprotective role of ROS regulators in the fight against PCa has been reported [26]. Chronic increases in ROS over time are known to induce somatic mutations and neoplastic transformation [27]. As shown in Fig. 2, several predisposing factors have been postulated to contribute to PCa initiation, promotion and progression. Age, race and family history play predominant roles however environmental factors such as chronic prostatitis, diet, medication and exposure radiation are associated with PCa. Cellular dysfunction including aberrant signaling, genotoxicity, gene mutation, DNA damage, cell cycle arrest, apoptosis and mitochondrial mutation also affect the PCa carcinogenesis and metastasis.Fig. 1

View Article: PubMed Central - PubMed

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.

No MeSH data available.


Related in: MedlinePlus