Sperm mitochondrial dysfunction and oxidative stress as possible reasons for isolated asthenozoospermia.

Reduced sperm motility, defined as asthenozoospermia, is a frequent cause of male infertility, and is mainly connected with the dysfunction of sperm mitochondria. The aim of this study was to identify the proteins, and thereby the metabolic pathways, responsible for asthenozoospermia, using 2-DE and MALDI-TOF MS, and correlate the results obtained with those of two mitochondrial tests: JC-1 and MitoSox Red. The JC-1 test was performed to test sperm mitochondrial activity, and the MitoSox Red test was performed to check whether the observed sperm poor motility is associated with mitochondrial reactive oxygen species (ROS) production. To identify proteins strictly connected with reduced sperm motility, men with isolated asthenozoospermia (n = 4 versus 10 normozoospermic controls) alone were included in the study. The proteomic analyses resulted in the identification of 25 sperm proteins that are differentially expressed in asthenozoospermic individuals. Most of the identified proteins were downregulated and were involved in energy production; however, we have also identified structural sperm proteins and proteins secreted by the epididymis. The latter, together with the results from MitoSox Red assay, may provide insights into the pathophysiological basis of asthenozoospermia.

Severe antioxidase deficiency in human semen samples with pathological spermiogram parameters.

Spermatozoa of 103 ejaculates from infertile patients and fertile healthy individuals were separated from seminal plasma and purified on Percoll gradient to determine the activities of superoxide dismutase (SOD) and catalase (CAT) in seminal plasma as well as in spermatozoal supernatants after hypotonic disintegration of the sperm plasma membrane. Out of collected specimens, a subgroup of ejaculates from 40 individuals was examined whose female partners had developed malignant processes in the cervix uteri (oncological subgroup). All sperm samples were classified into normal and pathological semen samples according to WHO criteria. While no significant differences of SOD levels were detected in seminal plasma of patients with primary infertility, a catalase deficiency seemed to be associated with combined sperm pathology-oligoasthenoteratozoospermia (OAT). Liberated concentrations of both SOD and catalase were diminished by 10-70% in the oncological subgroup compared to normozoospermia. In four OAT samples obtained from infertile males of the oncological subgroup, total depletion from both antioxidases was observed. A lack of sufficient antioxidase protection in cases of severe sperm pathology (OAT) may also lead to cervical dysplasia.

Oxidative stress and male infertility.

We have studied the activity of substances (superoxide dismutase [SOD], catalase [Cat], malonaldehyde, xanthine oxidase [XO], nitric oxide [NOx]) participating in oxidative stress. Seminal plasma samples of 147 ejaculates obtained from normal and from infertile males were examined. Activities of SOD, Cat, and XO were measured chemiluminometrically while malonaldehydes and NOx were measured by spectrophotometer in seminal plasma samples. Ejaculates were previously characterized according to World Health Organization andrological criteria (sperm number, motility, and morphology). Procedures were performed in a university laboratory. Statistically significant changes (in comparison to normozoospermic samples) were noted in activities of SOD, XO, and malonaldehyde levels. The SOD activity exceeded values obtained for normozoospermic samples only in oligozoospermia. Otherwise low SOD levels in analyzed infertile subgroups inversely related to elevated malonaldehydes. Because diminished activity of SOD in seminal plasma was associated with increased levels of malonaldehydes and XO, we could postulate some significance of these monitored substances in evaluation of the cause of male infertility.