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Human & Experimental Toxicology
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Inhibitory effect of all-trans retinoic acid on androgen-induced growth of mouse seminal vesicles in vivo and its mechanism

Hideki Sato

Department of Urology, Ehime University, School of Medicine, Ehime, Japan

Nozomu Tanji

Department of Urology, Ehime University, School of Medicine, Shitsukawa, Shigenobu, Onsengun, Ehime 791-0295, Japan tanji{at}m.ehime-u.ac.jp

Motomu Tsuji

Division of Pathology, Department of Laboratory Medicine, Osaka Medical College Hospital, Takatsuki, Osaka, Japan

Nobuyuki Terada

Department of Pathology, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan

Kenshi Yamasaki

Department of Dermatology, Ehime University, School of Medicine, Ehime, Japan

Jianbo Wang

Department of Urology, Ehime University, School of Medicine, Ehime, Japan

Kenshi Sakayama

Department of Orthopaedic Surgery, Ehime University, School of Medicine, Ehime, Japan

Masayoshi Yokoyama

Department of Urology, Ehime University, School of Medicine, Ehime, Japan

We examined the effect of all-trans retinoic acid (ATRA) on the androgen-induced growth of mouse seminal vesicles (SVs) in vivo and its mechanisms. Testosterone propionate (TP) alone or with ATRA was injected daily into adult castrated BALB/c mice. Injections of ATRA significantly inhibited the TP-induced growth of SVs in terms of wet weight and DNA synthesis by a pair of SVs evaluated by [3H]thymidine uptake. The bromodeoxyuridine labelling index showed that ATRA inhibited the proliferation of both epithelial and stromal cells. Immunoreactivity for retinoic acid receptor-a was found in the basal epithelial cells. Injections of ATRA affected neither 5a-reductase activity nor the expression of mRNAs for TGF-b1, 2 and 3 and TGF-b receptor 1 and 2 in the SVs. However, androgen receptor (AR) binding assays and Western blotting revealed a decrease in AR without a change in ligand-binding affinity. The present study showed that retinoid inhibited the androgen-induced growth of mouse SVs in vivo, and suggests that a decrease in AR is one of its mechanisms.

Key Words: androgen receptor • in vivo • RAR-a • retinoic acid • seminal vesicle

Human & Experimental Toxicology, Vol. 24, No. 9, 467-474 (2005)
DOI: 10.1191/0960327105ht555oa
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