In the male genital tract, reactive oxygen species (ROS) are generated by spermatozoa and leukocytes including neutrophils and macrophages. ROS are involved in the regulation of sperm functions such as capacitation and the acrosome reaction. Infections lead to an excessive ROS production, resulting in an 'oxidative burst' from neutrophils/macrophages as a first-line defence mechanism. This is modulated by several cytokines and the pro-oxidant mechanisms of bacteria and viruses. At the site of an infection, the degree of activation of leukocytes, i.e. the amount of ROS produced, and the available antioxidative systems determine whether spermatozoa are damaged or not. During an infection, an imbalance of pro- and antioxidants favouring the former results in oxidative stress which impairs the sperm functions mentioned, as well as motility and fertilization. ROS produced during infections of the testis and epididymis are especially harmful to spermatozoa due to the longer contact time and the lack of antioxidant protection. In the final ejaculate, only very high numbers of ROS-producing leukocytes are detrimental to sperm functions. An infectious injury involving ROS in the prostate gland, seminal vesicles or epididymis could impair sperm functions indirectly. Pro- and antioxidative properties of therapeutics are currently receiving more attention as part of anti-infectious therapies. At present, there are many unresolved questions concerning the exact role of ROS during infections of the male genital tract because of the difficulty of specifically assessing the site of generation and the short-lived effects of ROS. New techniques may enable specific studies to fill this gap in the near future.

Peroxidative damage induced by reactive oxygen species (ROS) has been proposed as one of the major causes of defective sperm function. The ROS detected in semen reflect an imbalance between ROS generation and degradation. The objective of the present study was to investigate the relationship between the oxidative and anti-oxidative potential in semen of infertile patients and healthy donors. Specimens were obtained from 28 patients and 18 healthy donors (controls). A conventional spermiogram, measurement of luminol-chemiluminescence (CL) in washed semen, and high performance liquid chromatography determination of ascorbic acid and urate concentrations in seminal plasma were performed. Oligozoospermic patients exhibited higher CL signals than controls (P < 0.001). Normozoospermic patients showed lower ascorbic acid (mean +/- SE: 491 +/- 46 microM, P < 0.04) and urate concentrations (320 +/- 22 microM, P < 0.009) than controls (612 +/- 35 and 426 +/- 26 microM respectively). Seminal plasma ascorbic acid was negatively correlated with the CL signals (P < 0.0006) and positively correlated with the percentage of spermatozoa with normal morphology (P < 0.006). This is the first report of a correlation between the anti-oxidant ascorbic acid in seminal plasma and ROS generation in human semen. Furthermore, the reduced ascorbic acid/urate concentrations found in semen of normozoospermic patients might be indicative of a reduced anti-oxidative protection.

IgA-chlamydial antibodies in seminal plasma appeared to be specific against C. trachomatis and were associated with an inflammatory response in the male genital tract.

Luminol-dependent chemiluminescence (CL) can be used to determine the production of reactive oxygen species (ROS) by cells. Enhanced formation of ROS in human semen was reported to be of pathological significance for a disturbed sperm function. To investigate incidence of elevated CL-signals in semen samples and their correlation to conventional semen parameters, CL-signals in the semen of both 49 consecutive infertile men and 20 controls were measured. Semen was analysed according to WHO-criteria including bovine mucuspenetration-and water-test. A CL-signal of 1.5 x lo5 counts min-'/2 x lo6 spermatozoa was considered to be the upper normal limit. The CL in infertile men's semen was elevated with statistically significant differences in oligozoospermia patients/controls (P< 0.000 1) and normozoospermia patients/controls (P< 0.05). In the group with elevated CL-signals, a higher percentage of spermatozoa with a pathologic morphology was detected (P=O.O5). In the groups with pathologic results of eosin-and water-tests, the CL-counts were elevated (P< 0.006; P< 0.03). The spermatozoa motility in the group with elevated CL-counts was significantly reduced after 4 h (P

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