Decrease of Prostaglandin E 2 and 5–Bromo–2′–deoxyuridine Labeling but Not Prostate Tumor Development by Indomethacin Treatment of Rats Given 3,2′–Dimethyl‐4‐aminobiphenyl and Testosterone Propionate

The modifying effects of indomethacin (IM) on rat prostate carcinogenesis induced by 3,2′–dimethyl–4–aminobiphenyl (DMAB) were investigated. F344 rats were given 50 mg/kg body weight of DMAB at 2–week intervals for 20 weeks and then received IM at a dose of 20 ppm in the drinking water for 37 weeks....

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Bibliographic Details
Published in:Cancer science 1997-04, Vol.88 (4)
Main Authors: Kawabe, Mayumi, Masa‐Aki Shibata, Sano, Masashi, Takesada, Yasuko, Tamano, Seiko, Ito, Nobuyuki, Shirai, Tomoyuki
Format: Article
Language:English
Subjects:
Body weight
Carcinogenesis
Carcinoma
Drinking water
Indomethacin
Propionic acid
Prostaglandin E
Prostaglandin E2
Prostate
Seminal vesicle
Testosterone
Testosterone propionate
Vesicles
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Summary:The modifying effects of indomethacin (IM) on rat prostate carcinogenesis induced by 3,2′–dimethyl–4–aminobiphenyl (DMAB) were investigated. F344 rats were given 50 mg/kg body weight of DMAB at 2–week intervals for 20 weeks and then received IM at a dose of 20 ppm in the drinking water for 37 weeks. Separate groups additionally received testosterone propionate (TP) in Silastic tubes throughout the experiment. DMAB alone induced carcinomas in situ in the ventral lobe and in combination with TP caused invasive carcinomas of the dorso–lateral and anterior lobes and seminal vesicles. No clear suppression by IM of development of in situ carcinomas or in vasive carcinomas was observed. In a short–term satellite experiment, it was revealed that prostaglandin E2 (PGE2) levels in the dorso–lateral prostate and seminal vesicles, but not the ventral prostate, were significantly reduced by IM and that TP itself also suppressed PGE2 levels. The 5–bromo–2′–deoxyuridine labeling index in the ventral prostate was significantly decreased by IM administration. These results indicate that while IM can efficiently suppress tissue PGE2 levels, it does not inhibit tumor development in the prostate or seminal vesicles of rats in the present model.
ISSN:1347-9032
1349-7006