ИСТИНА

Background. Male infertility is commonly associated with reduced sperm motility - asthenozoospermia (Asz) which may be caused by different factors. So-called monomorphic forms of Asz (primary ciliary dyskinesia, PCD; dysplasia of the fibrous sheath, DFS) are considered to be genetically determined. In multifactorial Asz, defects in mitochondria and chromatin can be of crucial importance. Main Questions. The aim of the study was to evaluate the prevalence of genetic forms in severe Asz and to investigate correlation between sperm motility and sperm mitochondria or chromatin defects. Experimental Design. We examined semen of 4031 patients with fertility problems. The quantitative transmission electron microscopy (TEM) was performed for 287 samples (sperm concentration ≥10 million/ml): group I (n=85) - patients with progressive sperm motility (PR) ≤5%, group II (n=101) - PR 6%-31%, group III (n=101) - PR≥32%. The transmembrane potential of mitochondria (TMP) was assessed using a fluorescent probe Mito Tracker Red FM (Invitrogen). Results. Decreased PR was detected in 3428 (85%) samples. Asz without other forms of pathozoospermia was revealed in 1791 (44.4%) semen samples. In 1046 cases (25.7%) Asz was combined with teratozoospermia, in 591 (14.7%) – with oligoteratozoospermia. Severe Asz (PR ≤5%) was detected in 85 (2.1%) samples. PCD resulted from lack of inner and outer dynein arms was revealed in 4 patients from group I (3 with total Asz, 1 – with total sperm motility 4%). DFS was revealed in 20 patients from this group (11 with total Asz, and 9 with total motility 1-4%). The percentage of spermatozoa with a regular mitochondrial helix determined by TEM differed statistically in the groups (p<0.05). Motility was significantly higher in samples with higher percentage of regular mitochondrial helix. Percentage of swollen mitochondria in group I was significantly higher than in the other groups (p<0.05). Progressive motility had weak negative correlation with immature chromatin (IC) in group II (r=-0.35) and with mitochondrial helix disorganization (MHD) in group III (r=-0.35) (p<0.05). The length of the mitochondrial helix did not differ between groups. Strong positive correlation was revealed between progressive motility and TMP (r=0.98). Conclusions. Genetically determined forms of Ast were found in 24 infertile men (0.6%). In patients with severe form of Asz genetically determined forms were in 28%. Sperm motility weakly correlated with ultrastructural pathology (IC, MHD) and strongly correlated with TMP.