Objective: To provide evidence that a pathological process in spermatogonial proliferation and apoptosis may participate in developing hypospermatogenesis of infertile men.
Design: Case-controlled retrospective analysis.
Setting: University-based male infertility clinic.
Patient(s): Thirty-four patients with idiopathic hypospermatogenesis.
Intervention(s): Collecting blood samples for measurement of hormones and performing testicular biopsy for assessment of spermatogenesis.
Main outcome measure(s): The expression of proliferating cell nuclear antigen (PCNA) of spermatogonia and the frequency of apoptosis of spermatogonia demonstrated by the in situ DNA 3'-end-labeling method were investigated to determine the degree of cell degeneration.
Result(s): We could classify 34 infertile patients into four subgroups according to spermatogonial proliferation and differentiation. No significant difference in the expression of PCNA was demonstrated between these four groups and the control group. In all groups, the balance of spermatogonial proliferation (PCNA-positive rate) to apoptosis was significantly lower than that of the control group.
Conclusion(s): It was demonstrated that accelerated apoptosis, rather than proliferative dysfunction in the mitotic phase, may induce the decreased number of spermatogonia in hypospermatogenesis. These findings suggest that disorders of the control and regulation of apoptosis may participate in the pathogenesis of idiopathic hypospermatogenesis.