Immunohistochemistry of the Canine Prostate.

Murakoshi, Masanori; Ikeda, Rie; Tagawa, Masashi

doi:10.1267/ahc.34.147

Cited by 3 publications

(2 citation statements)

References 31 publications

(31 reference statements)

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“…Examples of this phenomenon are provided by synthetic analogs of gonadotropin-releasing hormone such as goserelin, which produces a decrease in prostatic weight in a number of species, including humans. 47 Treatment of rats and dogs with bicalutamide (Casodex s ), another non-steroidal antiandrogen used in the treatment of prostate cancer, also produced prostatic atrophy in preclinical studies. 44 Leuprolide another synthetic analog of gonadotropin-releasing hormone also produces castration-like changes in laboratory animals.…”

Section: Drug-induced Atrophymentioning

confidence: 99%

Male Genital Tract

Greaves

2012

Histopathology of Preclinical Toxicity Studies

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Section: Drug-induced Atrophymentioning

confidence: 99%

Male Genital Tract

Greaves

2012

Histopathology of Preclinical Toxicity Studies

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“…The results of this study indicated that CMA binds to the rat prostatic AR and that oral administration caused regression of the hyperplastic prostatic weight. Therefore, CMA is considered to be a steroidal antiandrogen receptor antagonist [14,16,17].…”

Section: Effect Of Antiandrogenmentioning

confidence: 99%

Glutathione-Peroxidase (GSH-PO) and Androgen Action in Prostate: An Immunohistochemical Study

Murakoshi

Osamura

2003

Acta Histochem. Cytochem

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The effect of testosterone and estradiol on the prostate of castrated rats (rat prostatic hyperplasia model after combined treatment with testosterone and estradiol) were investigated by histopathologically and immunohistochemical procedures. The castrated rats were treated for 6 weeks with 1) testosterone 1 mg/animal and 2) testosterone 1 mg/ animal plus 17beta-estradiol (estradiol) 10 mg/animal. Histopathologically, glandular hyperplasia of the ventral prostate and glandular hyperplasia with fibromuscular stromal proliferation in the dorsolateral prostate, was clearly observed. Immunohistochemical localization of glutathione peroxidase (GSH-PO) which effectively reduces the lipid peroxides, was predominantly observed in the glandular epithelial cells of the ventral prostate. The intensity of GSH-PO staining in the glandular epithelial cells was remarkably decreased after castration, and that it was clearly recovered by testosterone or testosterone plus estradiol treatment to the castrated rats. In contrast, GSH-PO was clearly observed in the glandular epithelial cells of the dorsolateral prostate following testosterone alone or testosterone plus estradiol. Androgen receptor (AR) is mainly localized in nuclei. In the dorsolateral prostate, AR was also detected in the nuclei of the proliferated stromal fibromuscular cells. Furthermore, immunodetectable AR rapidly declined after androgen withdrawal and returned to intact levels of staining intensity after androgen replacement. These findings strongly suggest that expressions of GSH-PO and AR in the prostate are testosterone-dependent. It is concluded that immunohistochemical analysis, using GSH-PO and AR, may be a useful method for prediction of the effects of androgen action on the rat prostate.

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Male Genital Tract

Greaves¹

2007

Histopathology of Preclinical Toxicity Studies

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Immunohistochemistry of the Canine Prostate.

Cited by 3 publications

References 31 publications

Male Genital Tract

Male Genital Tract

Glutathione-Peroxidase (GSH-PO) and Androgen Action in Prostate: An Immunohistochemical Study

Male Genital Tract

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