Phosphatidylserine translocation in human spermatozoa from impaired spermatogenesis.
The aim of the present study was to evaluate phosphatidylserine translocation in specific patient groups and compare the rates of apoptosis between ejaculated and testicular spermatozoa. Fifty-six patients undergoing infertility treatments were included in the present study. Semen samples (n = 37) were obtained from cases with normozoospermia (n = 9) and abnormal semen parameters (n = 28). Testicular biopsy was performed in 19 patients, eight with obstructive and six with non-obstructive (hypospermatogenesis) azoospermia, and in five patients without azoospermia (anejaculation and oligozoospermia). Phosphatidylserine externalization was assessed using annexin-V binding and fluorescence microscopy, and propidium iodide exclusion tests were used to distinguish live from dead cells. In semen, oligoasthenoteratozoospermia showed significantly increased rates of sperm apoptosis (60.3 +/- 12.9) than normozoospermia (47.5 +/- 10.2). In testis, hypospermatogenesis (63.3 +/- 10.3) and obstructive azoospermia (63.6 +/- 15.1) showed significantly increased rates of sperm apoptosis than non-azoospermic patients (49.6 +/- 25.5). Comparisons between semen and testis showed that oligozoospermia had significantly higher rates of sperm apoptosis in semen (57.9 +/- 11.9) than in testis (29.4 +/- 1.1). The results suggest the presence of a post-testicular apoptotic induction factor and the potential beneficial use of testicular spermatozoa in clinical treatments.
Almeida
C
C
Department of Genetics, Faculty of Medicine, University of Porto, 4200-319 Porto, Portugal. carola@med.up.pt
Sousa
M
M
Barros
A
A
D017304:Annexin A5; D017209:Apoptosis; D006801:Humans; D007248:Infertility, Male / Q000503:physiopathology; D008297:Male; D009845:Oligospermia / Q000503:physiopathology; D010718:Phosphatidylserines / Q000378:metabolism*; D013094:Spermatozoa / Q000378:metabolism* / Q000473:pathology
D017304:Annexin A5; D010718:Phosphatidylserines