Growth Of Benign Prostatic Hyperplasia Research Articles

The phytochemical profiles and growth of Prunus africana in Kenya

Abstract. Nyamai DW, Burugu MW, Ng’ang’a MM, Muchugi AN. 2022. The phytochemical profiles and growth of Prunus africana in Kenya. Asian J Nat Prod Biochem 20: 63-74. African mountain ranges are home to the evergreen tree Prunus africana (Hook.f.) Kalkman. Benign prostate hyperplasia can be treated with the bark or extracts from the bark of this plant. The primary goal of this research was to compare the domesticated stand at Muguga (Kenya) to samples taken from a wild stand in Kobujoi and a remnant on-farm stand in Karuri in terms of their growth characteristics and phytochemical profile. Various solvents, including water, hexane, dichloromethane, and methanol, were used in the compound extraction process. The phytochemical analysis was performed with Liquid Chromatography and Gas Chromatography-mass spectrometry. The GC Chemstation version 11 program was used to examine the data from the GC-MS. The trees in the Muguga tamed stand varied in height from 3 meters to 14 meters, with a corresponding range in circumference at breast height from 0.9 centimeters to 104.5 centimeters. A total of 273 trees were planted in the orchard, and 92 (33%) produced fruit when the data was collected. When comparing the raw organic extract yields of the three groups, there was no statistically significant difference (p>0.05). Myristic acid, linoleic acid, lauric acid, methyl myristate, methyl laurate, and methyl linoleate made up the bulk of the essential oils in the bark samples across all three sources. For men with benign prostatic hyperplasia (BPH), these substances reduce cholesterol in the prostate. It was shown that dichloromethane and hexane extracts of the three populations included Campesterol, ?-sitosterol, lup-20(29)-en- 3-one, palmitic acid, ?-sitostenone, (3.?., 5.?)- stigmast-7-en-3-ol, stigmastan-3,5-diene, and ?-tocopherol. Increased urine output and decreased prostaglandin synthesis in the prostate are effects of (3.?., 5.?)-stigmast-7-en-3-ol, ?-sitosterol, and ?-sitostenone. Cyanidin-o-galactoside, cyanidin-3-o-rutinoside, procyanidin B5, and robinetinidol-(4-?-8) catechin-(6,4-?) robinetinol are thought to have anticancer effects by inhibiting cell proliferation and scavenging free radicals in cancer cells. Evidence suggests that ursolic acid can reduce inflammation, prevent cell damage, and slow the growth of BPH. The essential oils of the Karuri people had noticeably (p<0.05) more myristic and lauric acids than any other population. Myristic acid, linoleic acid, methyl myristate, and ?-tocopherol concentrations all varied significantly (p<0.05) between the Muguga population and the Karuri and Kobujoi populations. The findings show that the phytochemical composition of P. africana is not significantly changed by domestication (p>0.05), allowing for its cultivation in agricultural settings. Strategies for the sustainable collection, management, and conservation of this species through cultivation can be derived from the morphological and phytochemical data, which has crucial significance for these areas.

Экспериментальная оценка влияния изоборнилфенолов на развитие ДГПЖ и редокс-потенциал клеток предстательной железы

Introduction. Benign prostatic hyperplasia (BPH) is a common urological disorder in older men. It is characterized by the development of glandularstromal hyperplasia of the prostate with the formation of new glandular structures and subsequent symptoms from the lower urinary tract. It has now been established that the pathogenesis of this disease is multifactorial and one of the possible mechanisms for the development of BPH is oxidative stress. Purpose. Study of the effect of phenols with a bulky isobornyl substituent (2,6-diisobornyl-4-methylphenol and 4-hydroxymethyl-2,6-diisobornylphenol)on the growth of experimental BPH and the antioxidant balance of prostate cells in comparison with Prostamol Uno. Materials and мethods. Experiments were carried out on 50 male Wistar rats. BPH was caused by daily administration of sulpiride (60 days) to male rats of late reproductive age. After 2 months, the animals were weighed and sacrificed in a CO2 chamber. The mass, mass coefficient, volume of the lateral lobe of the pancreas were determined, morphological analysis was performed. Investigated prooxidant and antioxidant activity. The results were processed by the method of variation statistics using the Mann-Whitney nonparametric U test. Results. The efficacy of the investigated drugs in BPH decreased in the following sequence: sulpiride + substance 4-hydroxymethyl-2,6-diisobornylphenol (HDB) → sulpiride + substance Dibornol (DB) → sulpiride + Prostamol Uno (PU). When comparing the results of evaluating the anti-prooxidant status with the therapeutic effect of the studied drugs, it was found that isobornylphenols, which are highly effective as prostatotropic drugs, did not show a more significant effect, compared to PU, on the redox potential of prostatic tissue cells. Conclusions. Drugs DB, HDB, PU have a normalizing effect on the level of severity of redox reactions in the sulpiride model of BPH.

Complement activation by autoantigen recognition in the growth process of benign prostatic hyperplasia

The pathophysiology of benign prostatic hyperplasia (BPH) remained unclear. Here, we concentrated on the complement activation in the growth of BPH using a rat model. BPH tissues were harvested from rats after rat urogenital sinus implantation. The local expression and deposition levels of C1q, C3, mannose-binding lectin (MBL), factor B (FB), and C5b-9 in the rat and human BPH tissues were analyzed by real-time RT-PCR, western blotting and immunohistochemistry (IHC). Serum IgG levels in the rat BPH model were analyzed by ELISA, and IHC was used to assess tissue localization. Proteins binding serum IgG autoantibody in the BPH rats were isolated by immunoprecipitation. C1q, C3, MBL, FB and C5b-9 were highly localized in rat BPH tissues compared to normal tissues. In contrast, C3, FB and C5b-9, but not C1q and MBL, were abundantly detected in human BPH tissues compared to normal tissues. Diffuse localization of IgG in rat BPH tissues was found. Heat shock protein 90, annexin, α-smooth muscle actin, and β-actin were identified as targets for IgG autoantibodies in the BPH model. Our results strongly suggested the role for complement activation in the growth process of BPH, likely triggered by classical pathway activation with autoantibodies.

Sustained density of neuroendocrine cells with aging precedes development of prostatic hyperplasia in spontaneously hypertensive rats

BackgroundNeuroendocrine (NE) cells may have an impact on the development and initial growth of benign prostatic hyperplasia (BPH) according to previous human studies.MethodsTo explore the relationship of NE cells and BPH development, we compared the density of NE cells and also prostatic weight in spontaneously hypertensive rats (SHR), which develop by aging, and Wistar-Kyoto rats (WKY) as control. The total weights of the epithelium and stroma in the ventral lobes of 8-, 12, 16-, 28- and 56-week-old SHR and WKY were calculated using Image J software. NE cells in the ventral prostatic ducts (VPd) were quantified using immunohistochemical staining for serotonin.ResultsAlthough there was no significant difference in the estimated total weight of the epithelium and stroma in the ventral lobes adjusted by body weight (ES weight) between the two groups at 8, 12 and 16 weeks of age, ES weight was significantly greater in the SHR group than in the WKT group at 28 and 56 weeks. The density of NE cells in the VPd decreased with aging in the WKY group, whereas it was sustained until 16 weeks and then decreased with aging in the SHR group. The difference in the density between the two groups was most marked at 16 weeks of age.ConclusionIn the natural history of BPH, NE cells may play an important role in the initial development of BPH because sustained density of NE cells in the VPd precedes the development of prostatic hyperplasia.

Ethanol Extract of Evodia rutaecarpa Attenuates Cell Growth through Caspase-Dependent Apoptosis in Benign Prostatic Hyperplasia-1 Cells.

The dried fruits of Evodia rutaecarpa Bentham have been used widely as a herbal medicine for the treatment of inflammatory disorders and abdominal pain. Benign prostatic hyperplasia (BPH) is a nonmalignant disease characterized by overgrowth of prostates. Despite the pharmacological efficacy of the fruits of E. rutaecarpa against various diseases, their effects against BPH have not been reported. Here, we investigated the inhibitory activity of a 70% ethanol extract of E. rutaecarpa (EEER) against BPH, and its underlying mechanisms regarding cell growth of BPH using BPH-1 cells. An in vitro 5α-reductase activity assay showed that EEER exhibited inhibitory activity against 5α-reductase. In BPH-1 cells, EEER treatment inhibited cell viability and reduced the expression of the proliferating cell nuclear antigen proliferating cell nuclear antigen (PCNA), cyclin D1, and phosphor-ERK1/2 proteins. Moreover, EEER also induced apoptosis, with chromatin condensation, apoptotic bodies, and internucleosomal DNA fragmentation. Regarding its underlying mechanisms, EEER exacerbated the activation of caspase-8 and caspase-3 in a concentration-dependent manner and eventually caused the cleavage of PARP. Taken together, these data demonstrated that EEER had a potent 5α-reductase inhibitory activity and that EEER treatment in BPH-1 cells inhibited cell viability via caspase-8- and caspase-3-dependent apoptosis. Therefore, EEER may be a potential phytotherapeutic agent for the treatment of BPH.

Distribution of Neuroendocrine Cells in the Transition Zone of the Prostate.

Objectives. To evaluate the distribution of neuroendocrine (NE) cells which may influence the development of benign prostatic hyperplasia (BPH) in the transition zone (TZ). Methods. We reviewed specimens from 80 patients who underwent radical prostatectomy in our institution and evaluated the density of NE cells in the TZ. They were histologically classified into 3 groups: those with no adenomatous nodule in the TZ (group A), those with small nodules with normal epithelium and stroma around them in the TZ (group B), and those with large nodules occupying the TZ (group C). In the patients of group B, intra-adenoma (adenomatous nodules) and extra-adenoma (normal tissue) NE cells in the TZ were separately counted. Results. There were 22, 23, and 35 patients in groups A, B, and C, respectively. The median density of NE cells in the TZ of group B patients, 2.80/mm2, was significantly higher than that of NE cells in group A, 1.43/mm2, and group C, 0.61/mm2 (p < 0.001). In group B, the median density of extra-adenoma NE cells was significantly higher than that of intra-adenoma. Conclusions. Many NE cells exist around small adenoma in the TZ. NE cells may influence the initial growth of BPH in a paracrine fashion. Trial Registration. This study approved by our institutional review board was retrospectively registered (#272-14).

APPLICATION OF TRANSURETHRAL MICROWAVE THERMOTHERAPY FOR PATIENTS WITH ACUTE URINARY RETENTION AND SEVERE COMBINED COMORBIDITY FROM BENIGN PROSTATIC HYPERPLASIA

&lt;strong&gt;Background.&lt;/strong&gt; The incidence of benign prostatic hyperplasia (BPH) has grown by almost 35 % over the last five years with an incidence rate of 4438,2 per 100 000 of the respective population (147 677 total patients) in Ukrainian men beyond working age in 2007 [3].&lt;br /&gt;&lt;strong&gt;Objective.&lt;/strong&gt; The aim of the study was to assess the efficacy of TUMT in men where BPH was complicated by AUR and severe comorbidities.&lt;br /&gt;&lt;strong&gt;Method.&lt;/strong&gt; TUMT was performed using the domestically produced equipment ‘ALMGP-01’ at the frequency of 1300 Hz, rectal temperature of 42.5 °C, and urethral temperature of 44.5 °C. The average session duration is 46-55 minutes.&lt;br /&gt;&lt;strong&gt;Results and Discussion.&lt;/strong&gt; Subjective self-assessment: no effect of the procedure was detected (urination not restored) in 9 patients (11.11 %); poor current status with prior temporary improvement (6-9 months of independent urination with repeated AUR) in 14 patients (17.28 %); satisfactory current status with occasional dysuric episodes (however better than pre-TUMT status) in 40 patients (49.38 %). Eight patients (22.22 %) have assessed their status as ‘good’ and ‘excellent’; one patient noted substantial improvement compared to pre-procedure status. The nine patients with lack of success of restoring physiological urination had the following peculiarities: intra-vesical growth of BPH and prostatic volume over 85 cm3 in majority of these patients.&lt;br /&gt;&lt;strong&gt;Conclusions.&lt;/strong&gt; Taking into consideration the minimally invasive nature, favourable tolerability and absence of adverse effects, TUMT can be considered a method of choice in patients with BPH-triggered AUR and contraindications to major surgical treatments and general anaesthesia. Remote outcomes of TUMT may be evaluated as satisfactory, with good effects in 71.62% patients. However in prostatic volumes exceeding 85 cm&lt;sup&gt;3&lt;/sup&gt; and pronounced intravesical pattern of BPH growth the efficcacy of TUMT is arguable.&lt;br /&gt;&lt;br /&gt;&lt;strong&gt;KEY WORDS:&lt;/strong&gt; benign prostatic hyperplasia, acute urinary retention, transurethral microwave hermotherapy.

Perioperative prediction by MRI of prostate volume six to twelve months after laser-induced thermotherapy of benign prostatic hyperplasia.

The purpose of this study was to predict prostate volume outcome 6-12 months after interstitial, laser-induced thermotherapy (LITT) for benign prostatic hyperplasia (BPH) on the basis of prostate magnetic resonance (MR) images obtained within 48 hours before and after LITT. Twenty patients (age, 64.2 +/- 7.4 years) with symptomatic BPH had LITT of the transitional zone of the prostate. MRI was performed within 48 hours before and after LITT, and 6-12 months after LITT (late follow-up). MRI included axial and sagittal T2-weighted fast spin-echo (FSE) images and contrast-enhanced, axial T1-weighted images. Volumes of different prostatic compartments (total prostate, transitional zone, peripheral zone, LITT lesions) were measured by planimetry. Subtraction of LITT lesion volume less than 48 hours after LITT from total and transitional zone volume before LITT, respectively, predicted respective prostatic volumes at late follow-up. Pearson correlations of predicted and measured total prostate and transitional zone volumes were 0.972 and 0.975, respectively. Total prostate volume at late follow-up was accurately predicted (difference, -0.5 +/- 5.7 cc; P = 0.6981, two-tailed paired t-test). Transitional zone volume was underestimated (difference, -3.1 +/- 4.7 cc; P = 0.0075). Peripheral zone volume was overestimated (difference, 2.6 +/- 3.5 cc; P = 0.0034). Perioperative MRI allows accurate prediction of prostate volume 6-12 months after LITT for BPH. Underestimation of transitional zone volume may be due to ongoing growth of BPH. LITT appears to affect peripheral zone tissue outside the target region. J. Magn. Reson. Imaging 2001;13:64-68.

Androgen receptor CAG repeat length polymorphism in benign prostatic hyperplasia (BPH): correlation with adenoma growth.

The androgen receptor (AR) gene has a polymorphic CAG microsatellite encoding variable-length glutamine repeats in the AR protein. The purpose of this study was to evaluate the association between the growth of benign prostatic hyperplasia (BPH) and the AR gene CAG repeat length. We determined CAG repeat lengths in 176 BPH patients who underwent simple prostatectomy and in 41 control subjects without benign prostatic enlargement (non-BPE group). A statistically significant (P < 0.02) trend for large adenoma size with short CAG repeat length was found among the adenoma quartiles. CAG repeat length in the fourth quartile (large adenoma, 21.5 +/- 2.7) was significantly shorter than in the first quartile (small adenoma, 23.3 +/- 2.1, P < 0.02). It tended to be shorter than in the non-BPE group (23.1 +/- 2.4), but CAG repeat lengths in the entire BPH (22.4 +/- 2.5) and non-BPE groups did not significantly differ. The relative risk of large BPH (the fourth quartile) was 2.75 (95% confidence interval, 1.05-7.24; P < 0.05) on comparing CAG repeats of < or = 22-> or = 23. Shorter CAG alleles may be a genetic factor that promotes the growth of BPH.

Androgen receptor CAG repeat length polymorphism in benign prostatic hyperplasia (BPH): Correlation with adenoma growth

BACKGROUND The androgen receptor (AR) gene has a polymorphic CAG microsatellite encoding variable-length glutamine repeats in the AR protein. The purpose of this study was to evaluate the association between the growth of benign prostatic hyperplasia (BPH) and the AR gene CAG repeat length. METHODS We determined CAG repeat lengths in 176 BPH patients who underwent simple prostatectomy and in 41 control subjects without benign prostatic enlargement (non-BPE group). RESULTS A statistically significant (P < 0.02) trend for large adenoma size with short CAG repeat length was found among the adenoma quartiles. CAG repeat length in the fourth quartile (large adenoma, 21.5 ± 2.7) was significantly shorter than in the first quartile (small adenoma, 23.3 ± 2.1, P < 0.02). It tended to be shorter than in the non-BPE group (23.1 ± 2.4), but CAG repeat lengths in the entire BPH (22.4 ± 2.5) and non-BPE groups did not significantly differ. The relative risk of large BPH (the fourth quartile) was 2.75 (95% confidence interval, 1.05–7.24; P < 0.05) on comparing CAG repeats of ≤22–≥23. CONCLUSIONS Shorter CAG alleles may be a genetic factor that promotes the growth of BPH. Prostate 41:253–257, 1999. © 1999 Wiley-Liss, Inc.

Differential growth factor responses of epithelial cell cultures derived from normal human prostate, benign prostatic hyperplasia, and primary prostate carcinoma.

Because of a lack of information of the optimum nutritional requirements, epithelial cells derived from normal human prostate and prostate tumors have been difficult to propagate in vitro, which hinders research in prostate carcinogenesis. In an effort to establish optimum nutritional conditions and differences in growth characteristics of normal human prostate (NP), benign prostatic hyperplasia (BPH), and prostatic carcinoma (PCA), we have compared the effects of several growth factors on cell proliferation and elucidated growth properties of low passage epithelial cells derived from NP, BPH, and PCA of an African-American patient. Primary and low passage cultures were propagated in serum-free keratinocyte basal medium (KBM) supplemented with insulin (5 micrograms/ml), hydrocortisone (0.5 microgram/ml), epidermal growth factor (EGF, 10 ng/ml), bovine pituitary extract (BPE; 50 micrograms/ml), cholera toxin (10 ng/ml), and antibiotics. Almost all NP, BPH, and PCA cells were positive for cytokeratins and prostate-specific antigen (PSA). The NP, BPH, and PCA cells were essentially diploid and lacked mutations in c-K-ras and c-Ha-ras oncogenes, and p53 tumor suppressor gene. However, they exhibited progressively accelerating growth parameters. The population doubling times of NP, BPH and PCA were 51 hr, 37 hr, and 29 hr, respectively; their saturation densities were 2.9 x 10(4)/cm2, 3.3 x 10(4)/cm2, and 7.2 x 10(4)/cm2, respectively. The NP and BPH cells required all of the growth factors in the medium, as deletion of any one of the above factors strongly inhibited their growth. The PCA cells, however, were independent of EGF and hydrocortisone. PC-3, an established human prostate cancer cell line, was independent of the growth factors tested. Fetal bovine serum (FBS) inhibited the growth of NP, BPH and PCA cells. In contrast, FBS stimulated the growth of the PC-3 cells in a concentration-dependent manner. These results indicate that in the absence of any apparent karyotype alterations and mutations in c-K-ras, c-Ha-ras and p53 genes, epithelial cells derived from NP, BPH, and PCA exhibit significant differences in their growth properties and responses to growth factors. These variations may represent early changes involved in prostate cancer, while gene mutations and cytogenetic alterations occur in advanced and/or metastatic tumors.

Immunohistochemical evidence of the existence and localization of aromatase in human prostatic tissues.

Estrogens may be involved in normal growth of the prostate and the development of benign prostatic hyperplasia (BPH). The location of estrogen production is still unclear, and there has never been a direct evidence for the existence of the aromatase system, which converts androgens to estrogens, in the prostate. Using an avidin-biotin technique with a polyclonal anti-human placental aromatase, we demonstrated the existence of aromatase in normal prostates of young men and BPH tissue from elderly men. The staining is more pronounced in the stroma. However, positive stains were also seen in the glandular epithelium. While evidence of the existence of an enzyme system does not equal demonstration of its activity in a specific tissue site, our findings suggest that local estrogen production in the stroma and/or epithelium of the prostate may play a role in the maintenance of normal growth and development of BPH.

Development of canine benign prostatic hyperplasia with age

The prevalence and growth of benign prostatic hyperplasia (BPH) in beagles as a function of age were studied. The normal prostate gland was 12 +/- 3 gm in beagles 2.1-3.0 years of age; this weight remained unchanged unless BPH developed. Histologic evidence of BPH developed at an early age with a prevalence of 16% of the dogs by the age 2 years. Fifty percent of the dogs had BPH, determined histopathologically by age 4.1-5.0 years. The average weight of the prostate gland remained constant until after age 8 years. With age, the pathologic features of BPH changed from glandular to the complex form, with no increase in prostate weight until after 8 years. Reinitiation of growth occurred and prostate weight increased to greater than 36 gm in eight of 185 beagles older than age 8 years.

Effect of age, castration, and testosterone replacement on the development and restoration of canine benign prostatic hyperplasia

An experiment was designed to test the effect of castration and testosterone replacement on the development of benign prostatic hyperplasia (BPH) in young and on the restoration of BPH in old beagles. Twenty beagles were divided by age into young (1.5-2.5-yr) and old (6.0-8.5-yr) groups. Each of these groups was further divided randomly into two additional groups of age-matched, intact, untreated control and castrate beagles. The latter were then treated with testosterone-filled Silastic implants designed to clamp serum testosterone at concentrations similar to those observed in adult beagles for 7 months beginning 5 months after castration. Histopathologic characterization of each prostate was completed on biopsy material obtained at the beginning and end of the experiment. Prostate weights were determined each month for 12 months via a noninvasive two-dimensional X-ray procedure. Testosterone treatment for 7 months allowed BPH to develop in young and restored BPH in old beagles. These results suggest that testosterone in the adult beagle acts permissively to allow BPH to develop in the prostate of the aging dog. Some other testicular product may be required for the continued growth of BPH in aged beagles.

The Development of Human Benign Prostatic Hyperplasia with Age

In this study we report the prevalence and growth rate of human benign prostatic hyperplasia with age by combining and analyzing data from 10 independent studies containing more than 1,000 prostates. The normal prostate reaches 20 plus or minus 6 gm. in men between 21 and 30 years old, and this weight remains essentially constant with increasing age unless benign prostatic hyperplasia develops. The prevalence of pathological benign prostatic hyperplasia is only 8 per cent at the fourth decade; however, 50 per cent of the male population has pathological benign prostatic hyperplasia when they are 51 to 60 years old. The average weight of a prostate that is recognized at autopsy to contain benign prostatic hyperplasia is 33 plus or minus 16 gm. Only 4 per cent of the prostates in men more than 70 years old reach sizes greater than 100 gm.An analysis of a logistic growth curve of benign prostatic hyperplasia lesions removed at prostatectomy indicates that the growth of benign prostatic hyperplasia is initiated probably before the patient is 30 years old. The early phase of benign prostatic hyperplasia growth (men between 31 and 50 years old) is characterized by a doubling time for the tumor weight of 4.5 years. In the mid phase of benign prostatic hyperplasia growth (men between 51 and 70 years old) the doubling time is 10 years, and increases to more than 100 years in patients beyond 70 years old.

Metabolism and action of steroid hormones on human benign prostatic hyperplasia and prostatic carcinoma grown in organ culture

The metabolism of testosterone was examined in normal human prostate, benign prostatic hyperplasia (BPH) and prostatic carcinoma in organ culture. Dihydrotestosterone was the principal metabolite in the normal and hyperplastic prostate and in most of the carcinomas, although over half of the carcinomas produced less DHT than the benign tissue. There was no correlation between their degree of differentiation and their metabolic pattern but carcinomas from the oldest patients formed significantly greater amounts of 17-keto-metabolites. The effect of testosterone, its active metabolites and oestradiol-17β on the growth and differentiation of BPH and prostatic carcinoma in organ culture were correlated with changes in DNA and RNA synthesis, studied by autoradiographic methods. In the absence of hormones, explants of BPH grew well but showed signs of squamous transformation. Treatment with androgens prevented the metaplasia and preserved the secretory activity of the epithelium, while oestradiol caused cellular necrosis. In the BPH, DNA synthesis was depressed by oestradiol and unaffected by the androgens, except for 3α-androstanediol which increased it. RNA synthesis was increased by the androgens and reduced by oestradiol. In the carcinoma, the androgens as well as oestradiol depressed DNA synthesis while RNA synthesis was increased by the androgens but not affected by oestradiol. In both BPH and carcinoma, the stromal cells and the epithelium responded similarly to hormonal treatment.

The effect of steroid hormones on the growth pattern and RNA synthesis in human benign prostatic hyperplasia in organ culture.

The effect of testosterone, dihydrotestosterone, 3 beta-androstanediol and oestradiol-17 beta on the morphology and RNA synthesis in human benign prostatic hyperplasia (BPH) in organ culture has been investigated. In hormone treated and untreated explants alike, the epithelium multiplied to form several layers. This effect was most marked after exposure to dihydrotestosterone. In explants grown in non-supplemented medium the epithelium showed some squamous changes; testosterone or dihydrotestosterone preserved the secretory character of the epithelium while oestradiol-17 beta caused cellular degeneration. The incorporation of 3H-uridine into RNA was studied by autoradiography. In the epithelium, testosterone or dihydrotestosterone raised the uptake significantly over that measured in the control explants, oestradiol-17 beta reduced it while 3 beta-androstanediol produced similar values to those found in the control explants. The incorporation of 3H-uridine in the smooth muscle cells was increased by testosterone and decreased by oestradiol-17 beta. A comparison with normal rat prostatic epithelium in organ culture showed that in the absence of androgens the incorporation of 3H-uridine was lower than in BPH and the effect of testosterone correspondingly greater. The results suggest that although the growth of human BPH in organ culture appears to be androgen dependent, it still remains hormone sensitive and can be influenced by steroid hormones in a similar manner to that in rat prostatic gland. They further show that the smooth muscle of the stroma is also hormone sensitive, a point which should be considered in the hormonal management of benign prostatic hyperplasia.