Introduction

Hyperplasia and metaplasia of prostate are common only in the dogs. Enlargement of the prostate is relatively common in old dogs, and the dog is only animal species that spontaneously develops prostatic hyperplasia with age. Removal of androgen by castration of affected dogs causes of atrophic changes in glandular cells of prostate gland. Normal and abnormal prostate growth contributes to the pathogenesis of two common prostatic diseases: benign prostate hyperplasia (BPH) and prostate cancer. Androgen is the most potent mitogen to the prostate, playing a central role in normal and abnormal prostate growth. Maintenance of the structural and functional integrity of the normal prostate requires a constant supply of androgen. The main source of androgen is the testis. Androgen ablation by castration results in a rapid regression of the prostate via massive apoptosis of glandular epithelial cells. The purpose of this study is to test whether removal of androgen by castration of affected dogs causes apoptotic changes in glandular cells of prostate gland.

Material and Methods

Totally ten dogs, 5 of them were surgically performed castrate, and the rest were as control group. Seven days later the prostatic tissues were obtained from castrated adult dogs and the tissues were immediately fixed in 10% phosphate-buffered formalin and processed to paraffin. The paraffin block was consecutively cut at 3 μm for hematoxylin and eosin and TUNEL detection technique.

Results

Light microscopic studies revealed for treatment group: condensation and fragmentation of chromatin and chromatin crescent in prostatic cells and TUNEL staining of prostatic tissue reveled markedly apoptotic cells. In contrary, in the control group, there were no significant changes of apoptosis, due to castration.

Conclusion

This study demonstrated that castration in canine model could induce prostate gland cells apoptosis. This study suggests that testosterone stimulates vascular growth in the prostate gland indirectly by increasing epithelial VEGF synthesis and that this is a necessary component in testosterone-stimulated prostate growth. Castration reduces VEGF mRNA expression in benign prostate tissue and generally in those prostate tumors where castration also induces tumor cell apoptosis. This suggests that a therapy-induced down-regulation of VEGF could be important for tumor cell death. Castration induces the expression of caspase-1 transcripts in the epithelia of ventral prostate and seminal vesicle. These observations suggest a possible role of caspase-1 in apoptosis in male accessory sex organs.

References

1.  Kyprianou N, Isaacs JT 1988 Activation of programmed cell death in the rat ventral prostate after castration. Endocrinology 122:552-562

2.  English HF, Kyprianou N, Isaacs JT 1989 Relationship between DNA fragmentation and apoptosis in the programmed cell death in the rat ventral prostate following castration. Prostate 15:233-251

3.  Banerjee PP, Banerjee S, Tilly KI, Tilly JL, Brown TR, Zirkin BR 1995 Lobe-specific apoptotic cell death in rat prostate after androgen ablation by castration. Endocrinology 136:4368-4376