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Background: Inflammatory prostatitis patients are characterized by oxidative stress (OxS) at local and systemic levels. Less is known about the occurrence of OxS in the case of other frequent male genital tract disorders., Methods: The study included 196 men: controls (n = 28), asymptomatic inflammatory (NIH category IV) prostatitis patients (n = 21), non-inflammatory (NIH category IIIb) chronic prostatitis/chronic pelvic pain syndrome (CP/CPPS) patients (n = 48), inflammatory (NIH category IIIa) CP/CPPS patients (n = 44), benign prostate hyperplasia (BPH) patients (n = 33), and patients with BPH and NIH IV category prostatitis (n = 22). In all subjects, 8-isoprostanes (8-EPI) in urine were determined by competitive enzyme-linked immunoassay., Results: The levels of 8-EPI were substantially higher in all diseased groups-inflammatory CP/CPPS (P < 0.001), non-inflammatory CP/CPPS (P = 0.03), asymptomatic inflammatory prostatitis (AIP; P = 0.02), BPH (P = 0.007), and BPH + AIP (P = 0.014) in comparison with controls. Importantly, our study showed that OxS is also present in the case of NIH IIIb category prostatitis when the patients have just chronic pelvic pain but no inflammation in prostate-specific materials, as well as in the patients with just lower urinary tract symptoms without pain or overt inflammation., Conclusions: This study revealed that several male genital tract disorders-BPH and different forms of prostatitis (NIH categories IIIa, IIIb, and IV)-are tightly interconnected via OxS-mediated pathways. Acknowledging OxS as an important pathogenesis mechanism of these diseases helps to open up new horizons for their treatment., (Copyright © 2011 Wiley Periodicals, Inc.)

Prostatitis is a disease that seriously affects the quality of patients' life. In the majority of cases, chronic prostatitis (chronic pelvic pain syndrome--CPPS) has an unclear pathogenesis. Anti-inflammatory and anti-infectious treatments have remained controversial. According to the latest research, prostatitis has been associated with oxidative stress (OxS) and/or OxS-related genetic polymorphisms. We have observed that prostatitis patients have systemic OxS in case of inflammation and pain. We propose a new explanation for the role of OxS in the pathogenesis of prostatitis and describe the putative OxS-related pathways in detail. The neural vicious circle starts by activation of primary sensory afferents. Glutamate mediates the signal to the neurons in the dorsal horn of the spinal cord, and facilitates calcium influx into their mitochondria. The latter causes an increased production of superoxide radicals. If the superoxide production is not effectively controlled by mitochondrial superoxide dismutase (Mn-SOD), then superoxide leads to OxS and lipid peroxidation. Consequent release of electrophilic lipid peroxidation products (LPP) from dorsal horn of the spinal cord causes pain by activating the primary sensory afferents, again. Additional LPP-mediated causes of pain include glutathione depletion and neuron sensitisation by isoprostanes. Excretion of LPP into urine may exert positive feedback as well. Currently, different information exists about chronic prostatitis (inflammation, pain, oxidative stress, neural sensitisation, lower urinary tract symptoms). The clear links between these data are actually absent. We propose that vicious circle based on LPP, especially isoprostanes, is the linking mechanism., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

The aim of this study was to contribute to the knowledge concerning pathogenesis of inflammatory chronic prostatitis by revealing possible shifts in the balance of markers of oxidative stress and anti-oxidative activity in case of leucocytospermic prostatitis. We also attempted to identify possible relations between seminal micro-organisms and oxidative stress parameters. A many-sided complex of local (spermatozoa, seminal plasma) and general (blood, urine) markers in 21 prostatitis patients and nine controls was compared. In both spermatozoa and seminal plasma, the content of diene conjugates was significantly higher in prostatitis patients compared with healthy controls. At the same time total anti-oxidative status in spermatozoa and total anti-oxidative activity in seminal plasma were lower in prostatitis patients than in controls. In urine, the level of 8-isoprostanes was significantly higher in prostatitis patients than in healthy controls, correlating well with 8-hydroxy-2'-deoxyguanosine. The latter correlated with cellular Fe and Ni contents as well, confirming that these metals with varying valency may cause DNA damage. Reduced glutathione showed higher levels in blood of controls than in prostatitis patients. Coryneform bacteria appeared to be associated with prostatitis-related oxidative stress. In conclusion, leucocytospermic prostatitis patients are characterised by oxidative stress at all levels: systemic (general), seminal plasma and cellular.