Oxidative Stress and Chronic Bacterial Prostatitis

Bacteria responsible for prostate infection may originate from the urinary tract or can be sexually transmitted [28, 29] . The OS observed during chronic bacterial prostatitis is the result of elevated ROS production and/or reduced total antioxidant capacity [20, 30]. Indeed, infecting microorganisms trigger an inflammatory defense reaction in the prostate with a resulting OS due to ROS overproduction

[18, 25, 31, 32]. Current or past C. trachomatis infection has also been linked with an increased oxidative damage to spermatozoa [33].

Some bacteria (Gram-negative enteropathogens, U. urealyticum, C. trachomatis) may contribute to ROS overproduction by themselves, through products of their membrane (LPS from Gram negative or C. trachomatis) and/or through toxic metabolites (H2O2 and NH3 produced by U. urealyticum) [32, 34, 35]. Only few studies have focused their attention on the correlation between the type of germ, OS, and sperm quality. In vitro incubation of spermatozoa from normozoospermic healthy men with various strains of bacteria resulted in a significant increase of malondialdehyde (MDA), an end-product of OS, after exposure to Bacteroides ure-olyticus, Staphylococcus hemolyticus, or E. coli [34].

Shahed and Shoskes [36] showed that sperm OS in symptomatic patients with chronic bacterial prostatitis related to both ROS overproduction (especially with positive cultures) and reduced antioxidant capacity in men with category III prosta-titis. Furthermore, the observed increased levels of OS markers and their decrease after treatment with antimicrobials (category II) or with the antioxidant dietary supplement (category III) suggested that Gram-positive bacteria in the EPS of some men with chronic pelvic pain syndrome may represent true pathogens on the basis of the clinical response to antibiotics. Zhou et al. [37] showed a significant increase of OS markers (plasma nitric oxide and erythrocyte MDA) in patients with chronic bacterial prostatitis compared to healthy normal volunteers, whereas plasma vitamin C, vitamin E, and P-carotene as well as erythrocyte superoxide dismutase, cata-lase, and glutathione peroxidase activities were significantly lower in patients with chronic bacterial prostatitis. Furthermore, OS and oxidative damage were closely related to the course of chronic bacterial prostatitis.

Although the demonstration of an increased OS is clear in these studies, the causal role of the infectious agents is limited by the number of studies on a specific strain of microorganisms and by the methodological approach which requires conventional peroxidase staining for the detection of seminal leukocytes which results in the identification of polymorphonuclear leukocytes and macrophages only.

Other studies about inflammatory prostatitis (category IIIA, NIH classification) cannot be included, since it represents another category of prostatitis, according to the NIH classification, improperly used to evaluate the involvement of leukocytes and/or proinflammatory cytokines (IL-1, IL-6, IL-8, TNF-a) during the infective process in the onset of the OS [18, 25, 34, 38].

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