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Finasteride-induced prostatic involution by apoptosis in dogs with benign prostatic hypertrophy

Kaitkanoke SirinarumitrDepartment of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Minnesota, St. Paul, MN 55108.
Present address is Department of Obstetrics, Gynaecology and Animal Reproduction, Faculty of Veterinary Medicine, Kasetsart University, Bangkok 10903, Thailand.

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Theerapol SirinarumitrDepartment of Pathology, Faculty of Veterinary Medicine, Kasetsart University, Bangkok 10903, Thailand.

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Shirley D. JohnstonDepartment of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Minnesota, St. Paul, MN 55108.
Present address is College of Veterinary Medicine, Western University of Health Sciences, Pomona, CA 91766-1854.

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Dipak K. SarkarDepartment of Clinical Sciences, College of Veterinary Medicine, Washington State University, Pullman, WA 99164.
Present address is Endocrinology Program, Cook College, Rutgers, The State University of New Jersey, New Brunswick, NJ 08901-8525.

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Margaret V. Root KustritzDepartment of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Minnesota, St. Paul, MN 55108.

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Abstract

Objective—To determine the effect of finasteride on programmed cell death (apoptosis) of prostatic cells during prostatic involution in dogs with benign prostatic hypertrophy (BPH).

Animals—9 dogs with BPH.

Procedure—Dogs were randomly assigned to treatment or control groups. Treatment dogs (n = 5) were administered finasteride (0.1 to 0.5 mg/kg, PO, q 24 h) for 16 weeks, whereas the 4 control dogs were administered an inert compound. Prostatic cells from the prostatic fluid portion of the ejaculate of treatment and control dogs were obtained before and 1, 2, 3, 4, 8, and 16 weeks after initiation of treatment. Cells were concentrated by use of centrifugation. Prostatic cells were examined for indications of apoptosis by use of a terminal deoxyribonucleotidyl transferase- mediated deoxyuracil triphosphate nick-end labeling technique. After receiving the inert compound for 16 weeks, the 4 control dogs were administered finasteride for 16 weeks, and evaluations were repeated.

Results—Percentage of apoptotic prostatic cells in ejaculated prostatic fluid of treatment dogs increased significantly (from 9% before treatment to 33, 31, 26, and 27% after 1, 2, 3, and 8 weeks of treatment, respectively). There was no significant change in percentage of apoptotic prostatic cells in the ejaculated prostatic fluid of control dogs.

Conclusions and Clinical Relevance—Finasterideinduced prostatic involution appears to be via apoptosis in dogs with BPH. Finasteride treatment of dogs with BPH causes prostatic involution by apoptosis rather than necrosis. (Am J Vet Res 2002;63:495–498)

Abstract

Objective—To determine the effect of finasteride on programmed cell death (apoptosis) of prostatic cells during prostatic involution in dogs with benign prostatic hypertrophy (BPH).

Animals—9 dogs with BPH.

Procedure—Dogs were randomly assigned to treatment or control groups. Treatment dogs (n = 5) were administered finasteride (0.1 to 0.5 mg/kg, PO, q 24 h) for 16 weeks, whereas the 4 control dogs were administered an inert compound. Prostatic cells from the prostatic fluid portion of the ejaculate of treatment and control dogs were obtained before and 1, 2, 3, 4, 8, and 16 weeks after initiation of treatment. Cells were concentrated by use of centrifugation. Prostatic cells were examined for indications of apoptosis by use of a terminal deoxyribonucleotidyl transferase- mediated deoxyuracil triphosphate nick-end labeling technique. After receiving the inert compound for 16 weeks, the 4 control dogs were administered finasteride for 16 weeks, and evaluations were repeated.

Results—Percentage of apoptotic prostatic cells in ejaculated prostatic fluid of treatment dogs increased significantly (from 9% before treatment to 33, 31, 26, and 27% after 1, 2, 3, and 8 weeks of treatment, respectively). There was no significant change in percentage of apoptotic prostatic cells in the ejaculated prostatic fluid of control dogs.

Conclusions and Clinical Relevance—Finasterideinduced prostatic involution appears to be via apoptosis in dogs with BPH. Finasteride treatment of dogs with BPH causes prostatic involution by apoptosis rather than necrosis. (Am J Vet Res 2002;63:495–498)