The apoptotic mechanisms underlying spermatogenesis in testis are poorly understood. In the present study, the rates of testicular spermatozoa with active
caspase-3 were quantified in testicular samples with normal and impaired spermatogenesis. Testicular spermatozoa were collected from 18 men after testicular biopsy during assisted reproductive treatments: five presented
oligozoospermia, four congenital bilateral absence of the vas deferens (CBAVD), five secondary obstructive
azoospermia (
sOAZ) and four
hypospermatogenesis. Ejaculated samples were derived from six normozoospermic patients. Testicular spermatozoa were analysed using a fluorescence microscope and differences among groups were calculated using regression logistic models. Total rates of spermatozoa with active
caspase-3 were significantly higher in
sOAZ (78.6±13.9), followed by
hypospermatogenesis (70.8±5.8), CBAVD (55.9±25.5),
oligozoospermia (31.7±31.0) and normozoospermia (20.4±15.5). Distinct patterns of active
caspase-3 were observed in testicular spermatozoa compartments: midpiece, equatorial region, acrosomal vesicle region, nucleus and cytoplasm.
Hypospermatogenesis showed active
caspase-3 mainly in the midpiece. In CBAVD,
sOAZ and
oligozoospermia, active
caspase-3 was mainly in the nucleus, although no differences were found between
oligozoospermia and
hypospermatogenesis. In
sOAZ, active
caspase-3 in the spermatozoa nucleus was 1.89-fold higher than in CBAVD. Results suggest that tubular obstruction may induce nuclear lesions and that disrupted spermatozoa production observed in cases of
hypospermatogenesis might be associated with mitochondrial lesions.