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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.

A case control study was carried out to determine the value of sperm chromatin condensation in the assessment of male fertility. A total of 165 semen samples from 90 patients (cases) and 75 healthy donors (control) were examined for chromatin condensation (aniline blue staining), as well as conventional sperm parameters, notably sperm morphology, sperm count, and progressive motility. Whereas only 55 +/- 12.0% of the samples from the infertile patients were unstained by aniline blue (chromatin condensed), 78 +/- 19.0% of the samples in the control group did not take up the stain (chromatin condensed). A significant difference (p < .001) was observed between the two groups. Similarly, the difference between the mean percentage of morphologically normal spermatozoa for the infertile patients (12.1 +/- 1.2%) and the control (23.9 +/- 1.9%) was very significant (p < .001). In addition, only 50 out of the 90 patients (55.5%) had a normal sperm count, whereas all the 75 (100%) were normal in the control group. By comparing between the two groups a significant difference (p < .001) was also observed. Furthermore, a significant difference (p < .001) was also found between the cases and the control with regard to the percentage of spermatozoa illustrating linear progressive motility (40 +/- 9.7% vs. 70 +/- 12.3%). However, no correlation was found between sperm chromatin condensation and morphology, count, and motility. This study suggests that chromatin condensation constitutes a valuable parameter in the assessment of male fertility, completely independent of conventional sperm parameters. Consequently, the inclusion of chromatin condensation to routine laboratory investigations of semen prior to assisted reproduction is strongly recommended.

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