Atrophy and apoptosis in ventral prostate of rats induced by 5 alpha-reductase inhibitor, epristeride

AIM: To study molecular mechanism of epristeride in the treatment of benign prostatic hyperplasia and discuss the possibility of using prostate acid p hosphatase (ACP) as a marker of the atrophy of prostatic gland in vivo. MET HOD: Morphological changes in cells were observed by light microscope. TdT- mediated dUTP-biotin nick end labeling (TUNEL) technique and agarose gel el ectrophoresis were performed to detect the nucleosomal DNA fragmentation. T he activity of pACP was also assayed. RESULTS: Apoptosis occurred in both c astration- and epristeride- treatment group. Both the degree and extent of apoptosis are much larger in the group of castration than that of epristeri de-treated group. Both epristeride and castration decreased the prostate we t weight and DNA content but increased the prostate DNA concentration. Maxi mal or near maximal decreases were seen by d 10 in both groups. The activit y of ACP was decreased by both castration and epristeride treatment. Change s in the ACP activity during treatment were coincide with other changes suc h as the prostate wet weight and DNA content. CONCLUSION: Apoptosis induced by epristeride was one of mechanisms in the treatment of benign prostatic hyperplasia and the activity of ACP could be used as a marker of prostate a trophy.