Metabolism of Testosterone-4-<sup>14</sup>C by the Canine Prostate and Urinary Bladder<i>in Vivo</i>

Morfin, Robert; Aliapoulios, Menelaos A.; Chamberlain, Joseph P.; Ofner, P.

doi:10.1210/endo-87-2-394

Cited by 30 publications

(7 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This finding is in agreement with our previous results of comparative zn uiuo testosterone-4-'4C metabolism in the canine prostate and urinary bladder. 27 The biopsy containing only fibromuscular stroma produced barely detectable Sa-dihydrotestosterone but significant amounts of androstenedione. The varying stromal contents in the biopsies of BPH glands and well differentiated prostate carcinomas therefore dilute the amounts of 5a-reduced 17P-hydroxysteroid radiometabolites and thereby contribute to the variations found in the data from individual specimens.…”

Section: Discussionmentioning

confidence: 99%

Correlative study of the morphology and C19‐steroid metabolism of benign and cancerous human prostatic tissue

Morfin

Leav

Charles³

et al. 1977

Cancer

View full text Add to dashboard Cite

Perineal punch biopsy specimens of human prostate with benign hyperplasia (BPH), well- and poorly-differentiated adenocarcinoma and transitional-cell carcinoma were incubated with testosterone-1,2-3H and 5alpha-dihydrotestosterone-1,2-3H. Incubations were carried out using a single tissue-radiosubstrate ratio and time point. Resulting radiosteroid patterns were related to histologic and ultrastructural features of these tissues. Well differentiated neoplasms had ultrastructural characteristics closely resembling hyperplastic epithelia. Both in BPH and in well differentiated carcinomas the C19-steroids were mainly metabolized by the 17beta-hydroxysteroid pathway. In contrast, cells in poorly-differentiated adenocarcinoma and transitional-cell carcinoma lacked the cytoplasmic organelles responsible for secretion; formation of 5alpha-reduced 17beta-hydroxysteroids was decreased in these carcinomas, while conversion to 17-oxosteroid radiometabolites remained unchanged or was greatly increased. These results indicate that loss of prostatic differentiation is attended by a trend from reductive toward oxidative radiotestosterone metabolism. Even in NAPDH-supplemented preparations of the majority of poorly-differentiated tumors, there was diminished transformation to 5alpha-dihydrotestosterone, the key intracellular hormone in the expression of androgenic activity in the prostate. These findings may explain why poorly-differentiated prostatic neoplasms are frequently unresponsive to anti-androgenic therapy.

show abstract

Section: Discussionmentioning

confidence: 99%

Correlative study of the morphology and C19‐steroid metabolism of benign and cancerous human prostatic tissue

Morfin

Leav

Charles³

et al. 1977

Cancer

View full text Add to dashboard Cite

show abstract

“…Testosterone metabolic profiles of the cultured W H cells. In direct contrast to prostatic epithelial cells, which metabolize testosterone primarily through a 5a-reductase pathway (Bruchovsky and Wilson, 1968), canine urinary bladder rnetabolizes testosterone principally through an oxidative pathway (Morfin et al, 1970). To explore further the possible use of this biochemical divergent pathway of testosterone metabolism by the bladder and prostate cells as a cell-specific marker, we compared the testosterone metabolic profiles in human bladder WH epithelial cells, human bladder fibroblasts (a negative control), and a cultured rat prostatic epithelial cell line, NbE-1 (a positive control) (Chung et al, 1989;Chang and Chung, 1989).…”

Section: Characterization Of Wh and Rugm Cellsmentioning

confidence: 99%

A fetal rat urogenital sinus mesenchymal cell line (rUGM): Accelerated growth and conferral of androgen‐induced growth responsiveness upon a human bladder cancer epithelial cell line IN VIVO

Zhau

Hong

Chung

1994

Intl Journal of Cancer

View full text Add to dashboard Cite

A cell-cell interaction model was developed to examine the intercellular communication between mesenchymal and epithelial cells in vivo, and to define the role of androgen and paracrine growth factors in promoting growth and differentiation of the target epithelial cells. Using this model system, we have demonstrated that, in the presence of androgenic steroids, a fetal urogenital sinus mesenchymal cell line exhibited androgen-induced growth responses which resulted in an induction of growth of a non-androgen target epithelial cell line derived from human urinary bladder. Our results show that: (1) a rat fetal urogenital sinus mesenchyme-derived cell line (rUGM) accelerated growth and conferred androgen-induced growth responsiveness upon a non-androgen target cell line, WH, derived from a human bladder transitional-cell carcinoma (TCC); this induction of epithelial tumor growth in vivo occurred in a fibroblast-specific manner; (2) live fetal rUGM cells are required to promote WH tumor growth in vivo, which suggests that continuous production of factors that may serve as mediators for paracrine/autocrine pathways are responsible for androgen stimulation of WH tumor growth in vivo; and (3) although WH tumor growth, mediated by the presence of rUGM cells, was markedly accelerated by the presence of androgen in vivo, androgen and rUGM cells failed to promote the expression of a human prostate-specific antigen (PSA) by WH tumors in vivo. Our results emphasize the importance of organ-specific fibroblasts that promote tumor growth and mediate androgen-induced growth responses; the accelerated growth of the bladder epithelium was not accompanied by the expression of PSA, a known differentiated gene product produced by human prostatic epithelial cells. This report also discusses the potential significance of mesenchymal-epithelial cellular interaction which mediates androgen action and may play an important role by influencing human prostate tumor growth, progression and differentiation.

show abstract

“…In contrast to the prostatic secretion, canine of testosterone catabolism by canine salivary salivation appears to be unaffected by an-gland tissue differs from that produced by drogenic and estrogenic steroids (Huggins the canine prostate (Morfin et al 1970, & Sommer 1953. The prostate gland is a Leav et al 1974).…”

mentioning

confidence: 99%

In vitro metabolism of testosterone‐4‐¹⁴C by canine salivary glands

Mosadoml

Ofner

1976

J Oral Pathology Medicine

View full text Add to dashboard Cite

Abstract. Testosterone‐4‐14C (2430 pmol, 0.48 μM) was incubated aerobically in 67 mM phosphate buffer pH 7.4 with homogenates and minces of salivary glands from male dogs. Extracted radiosteroids were resolved by thin‐layer chromatography on silica gel, removed and quantitated. Substantially higher NAD+‐dependent 17 β‐hydroxy‐C19‐steroid oxidoreductase activity was found in submaxillary gland homogenates than in similar parotid‐gland preparations. Preliminary evidence is presented that the enzyme activity per unit wet weight of the minced submaxillary gland is decreased in the 2‐week male castrate, in the absence of any recognizable histologic changes in the gland. Testosterone metabolism by canine salivary glands is thus oxidative, contrasting with the reductive 17 β‐hydroxysteroid pathway characteristic of androgen‐dependent organs such as the prostate, and is more extensive than in this accessory sex tissue. Our findings suggest that the canine salivary glands are not target organs for circulating male hormone.

show abstract

Metabolism of Testosterone-4-¹⁴C by the Canine Prostate and Urinary Bladderin Vivo

Cited by 30 publications

References 0 publications

Correlative study of the morphology and C19‐steroid metabolism of benign and cancerous human prostatic tissue

Correlative study of the morphology and C19‐steroid metabolism of benign and cancerous human prostatic tissue

A fetal rat urogenital sinus mesenchymal cell line (rUGM): Accelerated growth and conferral of androgen‐induced growth responsiveness upon a human bladder cancer epithelial cell line IN VIVO

In vitro metabolism of testosterone‐4‐¹⁴C by canine salivary glands

Contact Info

Product

Resources

About

Metabolism of Testosterone-4-14C by the Canine Prostate and Urinary Bladderin Vivo

Cited by 30 publications

References 0 publications

Correlative study of the morphology and C19‐steroid metabolism of benign and cancerous human prostatic tissue

Correlative study of the morphology and C19‐steroid metabolism of benign and cancerous human prostatic tissue

A fetal rat urogenital sinus mesenchymal cell line (rUGM): Accelerated growth and conferral of androgen‐induced growth responsiveness upon a human bladder cancer epithelial cell line IN VIVO

In vitro metabolism of testosterone‐4‐14C by canine salivary glands

Contact Info

Product

Resources

About

Metabolism of Testosterone-4-¹⁴C by the Canine Prostate and Urinary Bladderin Vivo

In vitro metabolism of testosterone‐4‐¹⁴C by canine salivary glands