Soluble forms of Fas and Fas ligand concentrations in the seminal plasma of infertile men with varicocele.
OBJECTIVE
The Fas system in the testis has been identified as a key physiological regulator of apoptosis, an ongoing physiological process that limits the size of the germ cell population so it can be supported. Recently it was reported that the soluble form of Fas blocks Fas dependent apoptosis. In the present study we measured soluble Fas (sFas) concentrations in seminal plasma of oligozoospermic men with and without varicocele, and in normal men, looking for an association between seminal sFas and sFas ligand with spermatogenesis.


METHODS
A total of 27 oligozoospermic men with varicocele, 59 oligozoospermic men without varicocele and 34 normal volunteers were included in this study. Patients were evaluated clinically according to the protocol of the World Health Organization. sFas and sFas ligand were measured using a commercially available double antibody enzyme linked immunoassay. Follicle-stimulating hormone, luteinizing hormone, testosterone and estradiol concentrations were determined by chemiluminescence assays.


RESULTS
Seminal concentrations of sFas in oligozoospermic men with varicocele (3.6 +/- 2.4 ng/ml) were significantly lower than those in oligozoospermic men without varicocele (4.9 +/- 2.7 ng/ml, p = 0.0321) and normal men (5.1 +/- 2.4 ng/ml, p = 0.0201). The seminal sFas concentration significantly correlated with sperm concentration (r = 0.517, p = 0.0058). After varicocelectomy the increase in sperm concentration significantly correlated with an increase in sFas in seminal plasma (r = 0.555, p = 0.0026). The serum concentration of luteinizing hormone, follicle-stimulating hormone, testosterone or estradiol did not correlate significantly with the seminal sFas concentration. The sFas ligand concentration in seminal plasma was less than the limit of detection.


CONCLUSIONS
The sFas concentration in seminal plasma shows a strong association with spermatogenesis. Subnormal levels of sFas may be responsible for increased apoptosis induced by the Fas system, resulting in impaired spermatogenesis in patients with varicocele.
Fujisawa
Masato
M
Department of Urology, Kawasaki Medical School, Kurashiki, Japan. masato@med.kawasaki-m.ac.jp
Ishikawa
Tomomoto
T
D000328:Adult; D017209:Apoptosis; D004797:Enzyme-Linked Immunosorbent Assay; D004958:Estradiol / Q000097:blood; D053222:Fas Ligand Protein; D005640:Follicle Stimulating Hormone / Q000097:blood; D006801:Humans; D007248:Infertility, Male / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology; D008163:Luminescent Measurements; D007986:Luteinizing Hormone / Q000097:blood; D008297:Male; D008562:Membrane Glycoproteins / Q000032:analysis*; D009845:Oligospermia / Q000378:metabolism / Q000503:physiopathology; D012661:Semen / Q000737:chemistry*; D013076:Sperm Count; D013091:Spermatogenesis; D013739:Testosterone / Q000097:blood; D014646:Varicocele / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D019014:fas Receptor / Q000032:analysis*
C505661:FASLG protein, human; D053222:Fas Ligand Protein; D008562:Membrane Glycoproteins; D019014:fas Receptor; D013739:Testosterone; D004958:Estradiol; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone