Dorsal Prostate Lobes Research Articles

A Systematic Study of Biochemical Differences Between the Lobes of the Rat Prostate

The present study constitutes a systematic search for biochemical parameters which could be used to monitor the isolated function of various prostate lobes and accessory sex glands in the rat. Various parameters were measured in the 105 000 × g supernatants of the ventral, lateral and dorsal prostate lobes, and in the coagulating glands and seminal vesicles. These included spermine, citric acid, acid phosphatase, fructose and zinc, as well as the pattern of proteins in both cytosols and secretions, which were determined using one dimensional SDS, polyacrylamide gel electrophoresis. The results suggest that several parameters can be used including: Ventral lobe – spermine or prostatein; Lateral lobe – zinc or a 15 000 dalton protein; Dorsal lobe – spermine or a 60 000 dalton protein; and coagulating gland – fructose.

Zinc Concentration and Content of the Dorsal, Lateral and Medial Prostatic Lobes and of Periurethral Adenomas in Man

The concentration and content of zinc in the prostatic lobes and in periurethral adenomas, when present, were determined in an autopsy series of 45 adult males by atomic absorption spectrophotometry. The zinc distribution within the prostate was found to be related to the anatomically defined lobes, the dorsal lobes having the highest, the medial lobes the lowest and the lateral lobes intermediate zinc concencentrations. The differences in zinc concentration between the lobes were leveled in individuals who died from chronic disease, except in cases with periurethral adenomas. Periurethtral adenomas had higher zinc concentration than prostate proper.

Biochemical and immunohistochemical characterization of prolactin binding in rat ventral, lateral, and dorsal prostate lobes.

A radioligand assay and the soluble peroxidase-antiperoxidase (PAP) technique were used to compare ovine and rat prolactin as ligands for the demonstration of prolactin binding sites in rat ventral, lateral, and dorsal prostate lobes. Biochemical techniques were effective in demonstrating prolactin binding sites in ventral prostate with both ovine and rat prolactin; however, binding sites could not be characterized in lateral or dorsal lobes with either ligand. Using the PAP technique, rat prolactin consistently produced a discrete, dense reaction product over binding sites in the Golgi zone of the ventral prostate; ovine prolactin produced a more dispersed pattern of staining throughout the entire supranuclear region of the cells. In ventral prostate, most epithelial cells were immunoreactive when either ligand was used. However, lateral prostate contained fewer densely immunoreactive cells than did ventral prostate, and rat prolactin was more effective in demonstrating these binding sites than was ovine prolactin. Dorsal prostate epithelium was highly immunoreactive for binding of both ligands; however, there was considerably more staining in this lobe that remained after absorption of the antibody with prolactin. These data suggest that the inability to demonstrate prolactin binding sites in the lateral lobe using radioligand assay may have been due to the fewer numbers of binding sites that were diluted below the sensitivity of the assay when a tissue homogenate preparation was used. Noncompetitive binding in the dorsal lobe, as seen in the radioligand assay, coincided with immunocytochemical findings of relatively high nonabsorbable background staining.

Retinoic acid binding protein in normal and neopolastic rat prostate.

Sucrose density gradient analysis of cytosol from normal and neoplastic rat prostatic tissues exhibited a peak of (3H) retinoic acid binding in the 2S region, corresponding to the cytoplasmic retinoic acid binding protein (cRABP). In the Fisher-Copenhagen F1 rat, cRABP was present in the lateral lobe, but could not be detected in the ventral nor in the dorsal prostatic lobes. Four sublines of the R-3327 rat prostatic tumor contained similar levels of this binding protein. The absence of cRABP in the normal tissue of origin of the R-3327 tumor, the rat dorsal prostate, and reappearance in the neoplastic tissues follows a pattern described in other human and animal tumors. The occurrence of cRABP in the well-differentiated as well as in the anaplastic R-3327 tumors in which markers which reflect a state of differentiation and hormonal regulation, such as androgen receptor, 5 alpha reductase, and secretory acid phosphatase are either markedly reduced or absent, points to cRABP as a marker of malignant transformation.

Metabolism of testosterone in the human prostate and seminal vesicles.

Tissue from the normal, hyperplastic and the cancerous human prostate as well as tissue from the human seminal vesicles are capable of metabolizing testosterone in vitro. By incubating minced tissue with 3H-testosterone for 2 hours at 37 degrees C the following radioactive metabolites were identified: testosterone (17 beta-hydroxyl-4-androsten-3-one), androstenedione (4-androstene-3,17-dione), androstanedione (5alpha-androstane-3,17-dione), 5alpha-dihydrostestosterone (17 beta-hydroxy-5alpha-androstane-3-one, DHT), 3alpha-androstanediol (5alpha-androstane-3alpha,17beta-diol), 3beta-androstanediol (5alpha-androstane-3beta-17beta-diol) and androsterone (3alpha-hydroxy-5alpha-androstane-17-one). When normal human prostatic tissue was incubated with 3H-testosterone approximately 40% of the hormone was metabolized and 30-35% of the metabolites were identified as DHT. There were apparently no differences in testosterone metabolism between the dorsal and lateral prostatic lobes. A much lower conversion of 3H-testosterone was observed in the seminal vesicles (24%). The same metabolites were formed by prostatic carcinoma tissue, although distinctive quantitative differences from the normal prostate were observed. Thus, only 23% of the testosterone was metabolized by cancerous tissue of which 15% was present as DHT. The formation of 17-keto metabolites and androstanediols in the prostatic carcinoma tissue was approximately the same as in the normal prostatic tissue. The most extensive metabolism of testosterone was found by incubation of tissue from benign nodular prostatic hyperplasia. About 65% of the testosterone was metabolized, and 40% of the metabolites were identified as DHT. Hyperplastic prostatic tissue also showed a significantly higher formation of 5alpha-androstanedoils and the other tissues examined. The high formation of DHT and 5alpha-androstanediols in benign nodular prostatic hyperplasia in comparison with normal and cancerous prostatic tissue and seminal vesicle tissue might indicate that these metabolites should be studied more closely as possible aetiological factors for prostatic hyperplasia. The very low metabolism of testosterone in prostatic carcinoma tissue should be examined further in relation to tumour differentiation and clinical effect of endocrine therapy.

Distribution of radioactivity in the different lobes of the rat prostate following administration of testosterone-1,2-3H.

ABSTRACT Testosterone-1,2-3H with a specific activity of 46.5 c/mm was given intramuscularly to 3–4 months old, randomly selected rats, castrated 3 days before the injection. Radioactivity was measured in specimens from the ventral, dorsal and lateral prostatic lobes, and from the coagulating gland. A selective uptake of radioactivity relative to muscle tissue, was found in all parts of the prostate, with the same general pattern of incorporation. When correlated to wet weight, the maximum radioactivity was found in the lateral lobe. Eight hours after the injection the radioactivity in the lateral prostate was about 24 times higher than in muscle. The corresponding ratios for the ventral and dorsal lobes were 20:1 and 11:1, respectively. It is suggested that most of the radioactivity is localized within the cells, with minimal amounts of radioactivity in the secretory fluid.

Plasma Testosterone Levels in Patients with Prostatic Carcinoma Before and after Treatment

No AccessJournal of Urology1 Jun 1968Plasma Testosterone Levels in Patients with Prostatic Carcinoma Before and after Treatment Hugh H. Young, and John R. Kent Hugh H. YoungHugh H. Young Current address: Massachusetts General Hospital, Boston, Massachusetts 02114. More articles by this author , and John R. KentJohn R. Kent More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(17)62795-2AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail © 1968 by The American Urological Association Education and Research, Inc.FiguresReferencesRelatedDetailsCited Byvan der Sluis T, Bui H, Meuleman E, Heijboer A, Hartman J, van Adrichem N, Boevé E, de Ronde W, van Moorselaar R and Vis A (2018) Lower Testosterone Levels With Luteinizing Hormone-Releasing Hormone Agonist Therapy Than With Surgical Castration: New Insights Attained by Mass SpectrometryJournal of Urology, VOL. 187, NO. 5, (1601-1607), Online publication date: 1-May-2012.TELOKEN C, DA ROS C, CARAVER F, WEBER F, CAVALHEIRO A and GRAZIOTTIN T (2018) LOW SERUM TESTOSTERONE LEVELS ARE ASSOCIATED WITH POSITIVE SURGICAL MARGINS IN RADICAL RETROPUBIC PROSTATECTOMY: HYPOGONADISM REPRESENTS BAD PROGNOSIS IN PROSTATE CANCERJournal of Urology, VOL. 174, NO. 6, (2178-2180), Online publication date: 1-Dec-2005.Daniell H (2018) Osteoporosis After Orchiectomy for Prostate CancerJournal of Urology, VOL. 157, NO. 2, (439-444), Online publication date: 1-Feb-1997.Ernst D, Hanson J and Venner P (2018) Analysis of Prognostic Factors in Men with Metastatic Prostate CancerJournal of Urology, VOL. 146, NO. 2 Part 1, (372-376), Online publication date: 1-Aug-1991.Osegbe D and Ogunlewe J (2018) Androgen Concentration in Blacks with Benign and Malignant Prostatic DiseaseJournal of Urology, VOL. 140, NO. 1, (160-164), Online publication date: 1-Jul-1988.Hickey D, Todd B and Soloway M (2018) Pre-Treatment Testosterone Levels: Significance in Androgen Deprivation TherapyJournal of Urology, VOL. 136, NO. 5, (1038-1040), Online publication date: 1-Nov-1986.Maatman T, Gupta M and Montie J (2018) Effectiveness of Castration Versus Intravenous Estrogen Therapy in Producing Rapid Endocrine Control of Metastatic Cancer of the ProstateJournal of Urology, VOL. 133, NO. 4, (620-621), Online publication date: 1-Apr-1985.Worgul T, Santen R, Samojlik E, Veldhuis J, Lipton A, Harvey H, Drago J and Rohner T (2018) Clinical and Biochemical Effect of Aminoglutethimide in the Treatment of Advanced Prostatic CarcinomaJournal of Urology, VOL. 129, NO. 1, (51-55), Online publication date: 1-Jan-1983.Tisell L, Fjelkegărd B and Leissner K (2018) Zinc Concentration and Content of the Dorsal, Lateral and Medial Prostatic Lobes and of Periurethral Adenomas in ManJournal of Urology, VOL. 128, NO. 2, (403-405), Online publication date: 1-Aug-1982.Fukutani K, Isurugi K, Ishida H and Yokoyama M (2018) Effects of Estrogens on the Testosterone Levels of peripheral and Spermatic Vein Blood in Patients With Prostatic CancerJournal of Urology, VOL. 122, NO. 5, (624-627), Online publication date: 1-Nov-1979.Catalqna W and Scott W (2018) Carcinoma of the Prostate: A RevivewJournal of Urology, VOL. 119, NO. 1, (1-8), Online publication date: 1-Jan-1978.Walsh P and Siiteri P (2018) Suppression of Plasma Androgens by Spironolactone in Castrated Men with Carcinoma of the ProstateJournal of Urology, VOL. 114, NO. 2, (254-256), Online publication date: 1-Aug-1975.Kent J, Bischoff A, Arduino L, Mellinger G, Byar D, Hill M and Kozbur X (2018) Estrogen Dosage and Suppression of Testosterone Levels in Patients with Prostatic CarcinomaJournal of Urology, VOL. 109, NO. 5, (858-860), Online publication date: 1-May-1973.Mohamed Hanafy H, Gursel E and Veenema R (2018) A Possible Role of Sertoli Cells in Prostatic Cancer Refractory to Estrogen: A Preliminary ReportJournal of Urology, VOL. 108, NO. 6, (914-917), Online publication date: 1-Dec-1972. Volume 99Issue 6June 1968Page: 788-792 Advertisement Copyright & Permissions© 1968 by The American Urological Association Education and Research, Inc.MetricsAuthor Information Hugh H. Young Current address: Massachusetts General Hospital, Boston, Massachusetts 02114. More articles by this author John R. Kent More articles by this author Expand All Advertisement PDF DownloadLoading ...