The effect of in-vitro treatment by polyvinylpyrrolidone (PVP) on the ultrastructure of human spermatozoa has been tested previously with the statistical analysis of B. Baccetti et al. (1995, J. Androl., 16, 356-371). PVP had a primary detrimental action on the plasma membrane, as well as on acrosomal and mitochondrial membranes. Furthermore, membrane damage induces deterioration of the chromatin, axonemal tubules, fibrous sheath, and accessory fibres.

The effects of follicle stimulating hormone (FSH) treatment on the quality of human spermatozoa were assessed by examining the ultrastructure and the function of infertile human spermatozoa using a previously-defined formula. Using the spermatozoa as an andrological monitor shows that the therapeutic effect of FSH depends on the type of sperm defect. The response to FSH is, in many cases, positive and can be evaluated by examining the state of the ejaculated spermatozoa. From an initial group of 81 patients, 15 were placebo-treated controls, and 19 were non-responders (mainly with microbially infected semen). Out of 47 responders, after therapy nine achieved improved sperm quality which approached the natural fertility threshold. These responders all had spermatozoa affected by immaturity or apoptosis (n = 27). The 20 microbially-infected responders also had immature spermatozoa and never achieved the quality level of natural fertility. Thus, a natural fertility level was only achieved by nine responders out of 27 (three with immature spermatozoa, and six with apoptotic spermatozoa). Using our method of sperm analysis, these patients' spermatozoa were clearly categorized before treatment as either immature or apoptotic. In consequence, the success of the therapy was predictable. The response of individual organelles to therapy was examined. Certain qualities of the acrosome, the chromatin, the mitochondria, and the axoneme appear to be sensitive to FSH. Most of the previous conflicting results reported in the literature may be due to a lack of relevant discrimination between the different defects present in the spermatozoa of the patients, without assessing the likelihood of their response.

No abstract