A D Hancock1, D M de Kretser. 1. Department of Anatomy, Monash University, Melbourne, Victoria, Australia.
Abstract
OBJECTIVE: To determine with the use of transmission electron microscopy (TEM) the proportion of patients with the semen pattern of severe asthenospermia (less than 20% motility) that have an abnormality of sperm axonemal structure as the basis for this disorder. DESIGN: Transverse sections of sperm tail axonemes were quantitatively analyzed, and the mean frequency per axoneme of the doublet microtubules, central pair, outer dynein arms, inner dynein arms, and radial spokes were determined. SETTING: Patients were being investigated for male infertility at the Reproductive Medicine Clinic at Monash Medical Centre (Melbourne). Semen samples were processed for and analyzed by TEM in the university laboratory. PATIENTS: Ten asthenospermic patients in whom repeated semen analysis demonstrated a percentage of sperm motility less than 20% were selected. MAIN OUTCOME MEASURE(S): The main measure was the quantitative analysis of sperm axonemes. The hypothesis that a reduction of axonemal components causes lowered motility derived from the results. RESULTS: Individual asthenospermic patients demonstrated significant reductions in at least three axonemal structures when compared with the normal mean. Statistical analysis of the grouped data showed that all axonemal components were significantly lower than the normal mean. CONCLUSIONS: The consistent reduction of axonemal components strongly suggests that axonemal deficiencies are the cause of lowered motility in asthenospermic patients.
OBJECTIVE: To determine with the use of transmission electron microscopy (TEM) the proportion of patients with the semen pattern of severe asthenospermia (less than 20% motility) that have an abnormality of sperm axonemal structure as the basis for this disorder. DESIGN: Transverse sections of sperm tail axonemes were quantitatively analyzed, and the mean frequency per axoneme of the doublet microtubules, central pair, outer dynein arms, inner dynein arms, and radial spokes were determined. SETTING:Patients were being investigated for male infertility at the Reproductive Medicine Clinic at Monash Medical Centre (Melbourne). Semen samples were processed for and analyzed by TEM in the university laboratory. PATIENTS: Ten asthenospermic patients in whom repeated semen analysis demonstrated a percentage of sperm motility less than 20% were selected. MAIN OUTCOME MEASURE(S): The main measure was the quantitative analysis of sperm axonemes. The hypothesis that a reduction of axonemal components causes lowered motility derived from the results. RESULTS: Individual asthenospermic patients demonstrated significant reductions in at least three axonemal structures when compared with the normal mean. Statistical analysis of the grouped data showed that all axonemal components were significantly lower than the normal mean. CONCLUSIONS: The consistent reduction of axonemal components strongly suggests that axonemal deficiencies are the cause of lowered motility in asthenospermic patients.