OBJECTIVE: To study the effects of alcohol administration on benign prostate hyperplasia(BPH) and the reproductive toxicity during development of benign prostate hyperplasia. METHODS: Seventy adult male Kunming mice were randomly divided into seven groups:control (group CON), negative control (group NC, injected subcutaneously with soybean oil, 25 mg/(kg·d), intragastric administration of distilled water, 7.5 ml/(kg·d)), alcohol for 7 and 21 days (group AL7 and AL21, intragastric administration with wine of 50% alcohol, 7.5 ml/(kg·d)), testosterone propionate for 7 and 21 days (group TP7 and TP21, injected subcutaneously with testosterone propionate, 25 mg/(kg·d)), testosterone propionate+alcohol for 7 days (group TP+AL7, injected subcutaneously with testosterone propionate, 25 mg/(kg·d), and intragastric administration with wine of 50% alcohol, 7.5 ml/(kg·d)),10 mice in each groups. Twenty-four hours after the last administration, mice were sacrificed. The indexes of prostate and testis and the parameters of sperm were determined in mice. The levels of free radicals, antioxidation and histopathological changes in testis and prostate were determined. RESULTS: Compared with the control, TP7d group, AL7 and AL21d groups, the prostate coefficient of TP + AL7d group was increased significantly and the quantity and quality of sperm were decreased significantly (<0.05), the content of MDA in prostate and testis was increased significantly, meanwhile the activities of SOD and GPx were decreased significantly (< 0.05). Compared with TP21d group, the prostate coefficient of TP + AL7d group had no significant difference (>0.05). CONCLUSIONS The typical BPH state could be induced after 7-day treatment of testosterone propionate and alcohol. The testicular and sperm were damaged which enhanced the oxidative stress in reproductive system. The results indicated that alcohol could significantly promote the prostate hyperplasia induced by testosterone propionate in mice.
Animals ; Male ; Mice ; Plant Extracts ; Prostatic Hyperplasia ; Testosterone Propionate

OBJECTIVETo establish a prostatic hyperplasia model with Beagle canines.

METHODSTwenty-four two-year-old male Beagle canines were divided into treatment and control groups at random and were administrated testosterone propionate (TP) through intramuscular injection two months after castration. Three treatment groups were given 0.8, 2.5 and 7.5 mg/kg TP respectively, and the control was given the same volume of vehicle. Two months later, half of the animals were killed and the serum and prostate were prepared. After the wet weight and volume of prostate were measured, the dihydrotestosterone (DHT) level of serum and prostate were detected with DHT radioimmunoassay (RIA) kit, and paraffine section from canine prostate was stained by the HE methods. Pictures were taken by digital camera under microscope, and all the pictures were analyzed by computer for epithelial cell height and acinar luminal area of prostate with micro image analysis software. The canine prostate volume was measured with ultrasonic diagnosis instrument before castration, at two months after castration and at two months after being given TP.

RESULTSThe ultrasonic results showed that the prostate volumes of all the canines were smaller at two months after castration than before castration (P < 0.05), and after having been administrated TP for two months, and the prostate volumes of all treatment groups were larger than those of the control group (P < 0.01). The wet weight of the prostate of the treatment group was higher than that of the control group (P < 0.05), and both had dose-dependent relationship. The DHT level of serum and prostate of the canines became higher with the increase of TP dose. The results of micro image analysis showed that the acinar luminal area of prostate was enlarged, and the epithelial cell height increased with larger dose of TP.

CONCLUSIONSIt is practicable to establish prostatic hyperplasia model in Beagle canines after two months of TP administration.

Animals ; Dihydrotestosterone ; blood ; Disease Models, Animal ; Dogs ; Male ; Orchiectomy ; Prostatic Hyperplasia ; etiology ; Testosterone Propionate ; pharmacology

Normal diet, high protein high fat diet and high carbohydrate diet were prepared and given to young male white rats to study the effects of the diets on the prostatic concentration of citric acid. Also, the effects of exogenous testosterone propionate, castration and exogenous testosterone propionate and on sexual activity were studied. The first experiment was a 60 day observation. In the controls and among the animals administered testosterone propionate, the prostate-body weight ratio was higher in the high protein, high fat diet group than in the groups fed high carbohydrate and normal diets. The prostatic citrate, however, was higher in the high carbohydrate diet group. By administration of testosterone propionate, citric acid concentration of the prostate was higher in the high protein, high fat diet group and sexual activity in this group caused a more marked increase in the prostatic citrate concentration. The second experiment was continued for 203 days. The high protein, high fat diet caused an increase in the prostate-body weight ratio and a relatively higher but insignificant concentration of prostatic citrate. Sexual activity did not cause an increase in the prostatic citrate concentration. Concentration of the prostatic citrate can not be taken as an index of androgenic activity.
Animals ; Castration ; Citric Acid* ; Diet ; Diet, High-Fat ; Humans ; Male ; Prostate ; Rats ; Sexual Behavior ; Testosterone Propionate

PURPOSE: Androgen plays an important role during penile development and is essential for a normal libido in the male, but its role in the regulation of the androgen receptor and maintenance of erectile response has been controversial. We investigated the effect of androgen on apoptosis, proliferation of the penile erectile tissue and androgen receptor after castration and temporary androgen replacement. MATERIALS AND METHODS: Male adult Sprague Dawley rats were divided into three groups; sham-operation, castration, and androgen replacement after castration. Androgens (testosterone, DHT) were administrated for 7 days at week 1, 2, 3, and 4 after castration. The weight of whole body and corpus cavernosum and serum testosterone concentration were measured. Androgen receptor expression, percentage of proliferating cells incorporating Ki-67(proliferative index) and percentage of apoptotic cells assessed by morphological analysis(apoptotic index, TUNEL) were analyzed in the penile erectile tissue. RESULTS: Castration induced a significant decrease in serum testosterone concentration from day 1 and a progressive decrease in the corpus cavernosal weight from day 14. Androgen receptor expression decreased after androgen depletion and was restored with androgen replacement. The proliferative and apoptotic index varied as follows after castration and androgen replacement: a significant increase was noted for apoptotic index with a decrease in the proliferative index and androgen receptor expression after castration. Replacement of testosterone propionate and DHT after castration decreased the apoptotic index with an increase in the proliferative index and the expression rate of androgen receptor. CONCLUSIONS: The penile erectile tissue of the adult rat was affected by the androgen milieu via the androgen receptor as seen by either cellular apoptosis or proliferation. Therefore, androgens such as testosterone and DHT play a direct role in the erectile function of the rat at the level of the penile erectile tissue.
Adult* ; Androgens ; Animals ; Apoptosis* ; Castration ; Humans ; Libido ; Male ; Rats* ; Rats, Sprague-Dawley ; Receptors, Androgen* ; Testosterone ; Testosterone Propionate

Androgenic and estrogenic hormones were administered to adult male white rats with intact gonads and adult male white castrate rats to study their effects on citric acid concentration of the prostate gland. In this study 30 male rats, 14 to 16 weeks of age, weighing approximately 250 to 300 gm., were divided into 5 groups of six rats: Group 1: Control Group 2: Administration of testosterone propionate 0.5 mg., 7 doses Group 3: Administration of estradiol 0.2 mg., 7 doses Group 4: Castration and administration of testosterone propionate 0.5 mg., 7 doses Group 5: Castration and administration of both testosterone propionate 0.5 mg. and estradiol 0.2 mg., 7 doses each. One day after the final injection with sex hormones, the animals were sacrificed and the prostatic citrate was determined using the Kim-Tesar modification of the Taylor's method. Estrogen administration to the male rats with intact gonads caused an increase in the prostatic citrate concentration. Testosterone propionate administration after castration returned the citrate concentration to normal, but estradiol administration along with testosterone propionate after castration caused a rise in the prostatic concentration of citric acid. Hypophysectomized white rats purchased from the Hormone Assay Laboratory were castrated and were administered androgen and estrogen to study their effects on the prostatic concentration of citric acid, 36 rats were divided into 6 groups of six rats: Group 1: Control (no hypophysectomy) Group 2: Hypophysectomy and castration Group 3: Hypophysectomy, castration and administration of testosterone propionate 0.5 mg., 7 doses Group 4: Hypophysectomy, castration and administration of both testosterone propionate 0.5 mg, and estradiol 0.5 mg., 7 doses each Group 5: Hypophysectomy castration and administration of both testosterone propionate 0.5 mg. and estradiol 0.25 mg., 7 doses each Group 6: Hypophysectomy, castration and administration of both testosterone propionate 0.5 mg. and estradiol 0.125 mg., 7 doses each. Hypophysectomy and castration caused a marked increase in the prostatic concentration of citric acid. When testosterone propionate was administered to hypophysectomized castrate, the ciric acid value returned to normal. Administration of estradiol along with testosterone propionate to hypophysectomized castrate caused changes in the prostatic citrate concentration according to the dosage of estradiol administered, the more the dosage, the more the concentration of the prostatic citrate. Concentration of the prostatic citrate can not be taken as an index of androgenic activity.
Adult ; Animals ; Castration ; Citric Acid* ; Estradiol ; Estrogens ; Gonadal Steroid Hormones* ; Gonads ; Humans ; Hypophysectomy ; Male* ; Prostate ; Rats* ; Testosterone Propionate

PURPOSE: This study examined the changes in intracavernous pressure, expression of nitric oxide synthase(NOS), and content of penile smooth muscle in castrated rats and testosterone-supplied castrated rats. MATERIALS AND METHODS: Sprague Dawley rats were used for this study and divided into control, castrated, and testosterone-supplied castrated groups. Castration was performed by bilateral orchietomy under general anesthesia, and testosterone propionate 3 mg/kg was injected subcutaneously daily for a week beginning 4 weeks after orchiectomy. Intracavernous pressure was measured by stimulating the cavernous nerve at 10 volts, 2.4 mA. Expression of NOS was measured by immunohistochemical staining for NADPH diaphorase, and content of penile smooth muscle was measured by H&E staining of the corpus cavernosum. The stained area-to-tissue ratio was calculated by computer scanning for each case. RESULTS: Compared with the control group(3.45+/-0.25 ng/ml), the serum testosterone level of the castrated group (0.78+/-0.34 ng/ml) was lower. Serum testosterone level was restored in the testosterone-supplied castrated group. Compared with the(67.2+/-14.3 cmH2O) was decreased (p <0.05). There was no significant difference between the testosterone-supplied group(94.7+/-11.4 cmH2O) and control group, so intracavernosal pressure was restored by testosterone treatment. Immunohistochemical staining for NOS showed that NADPH diaphorase was stained as brown nerve fiber. Compared with the control group(37.5+/-2.8%), the NOS activity of the castrated group(7.5+/-2.1%) was significantly decreased(p <0.05). NOS activity was slightly increased in the testosterone-supplied group(47.5+/-2.4%) compared with the control group, but the difference was not statistically significant. Thus, testosterone treatment restored NOS activity after castration. By H&E staining, the content of penile smooth muscle was 76.5+/-2.8% in the control group, but significantly lower in the castrated group(46.2+/-3.4% p <0.05). Smooth muscle content was slightly decreased in the testosterone-supplied group(63.8+/-4.7%) compared with control group, but the difference was not statistically significant. Thus, smooth muscle content was restored by testosterone treatment after castration. CONCLUSIONS: Decline of factors involved in erectile function can be restored by testosterone replacement after castration.
Anesthesia, General ; Animals ; Castration ; Male ; Muscle, Smooth ; NADPH Dehydrogenase ; Nerve Fibers ; Nitric Oxide ; Orchiectomy ; Penile Erection* ; Rats* ; Rats, Sprague-Dawley ; Testosterone Propionate ; Testosterone*

PURPOSE: Benign prostatic hyperplasia (BPH) is one of the common diseases in elderly men. Recently, the old-aged population has increased, with the interest in the clinical importance of BPH ever growing. Catechin, an extract of green tea, has the effect of the 5-alpha reductase inhibitor. Typically, BPH has been shown to be influenced by 5-alpha reductase. Therefore, the relationship between BPH and catechin was evaluated. MATERIALS AND METHODS: An experimental prostatic hyperplasia was induced in male Wistar rats by the administration of testosterone propionate, 3mg/kg sc, for 4 weeks. The Wistar rats were divided into four experimental groups: the control, BPH-induced, oral finasteride ingestion and oral catechin ingestion groups. After 4 weeks, the prostates were removed, and analyzed for their prostatic weight and histological examination. RESULTS: The prostate weights were measured in each group, and found to be 330.0+/-40.7, 970.0+/-1.1, 358.0+/-39.9 and 415.0+/-45.3mg in the control, BPH-induced, oral finasteride ingestion and oral catechin ingestion groups, respectively. The oral finasteride and catechin ingestion groups showed statistically significant decreases in their prostatic weights compared with the BPH-induced group (p<0.05), but with no significant difference between the oral finasteride and catechin ingestion groups (p>0.05). Histologically injected testosterone lead to prostatic hyperplasia in rats, but oral catechin ingestion decreased this change. CONCLUSIONS: These results suggest that catechin may be effective in BPH, and the consumption of green tea may be effective in preventing BPH.
Aged ; Animals ; Catechin* ; Cholestenone 5 alpha-Reductase ; Eating* ; Finasteride ; Humans ; Male ; Models, Animal* ; Oxidoreductases ; Prostate ; Prostatic Hyperplasia* ; Rats* ; Rats, Wistar ; Tea ; Testosterone ; Testosterone Propionate ; Weights and Measures

Testosterone therapy in high doses produces male infertility. There are reports that atrophy of the interstitial cells and decrease in testicular size occur in the rat after treatment with testosterone, and the azoospermia which resulted from testosterone therapy could be reversed by simultaneous treatment with HCG. This study was evaluated for 45 days to clarify microscopic changes in the testis. A total of 60 male mice, 30 BALB/C strain, aged 3-4 weeks and with an average body weight of l2 g and 30 BALB/C strain, aged 3 months and with an average body weight of 20 g, were divided into 2 groups; for one group treatment with testosterone propionate only and another group fur treatment with testosterone propionate and HCG. The results of histological structure were as follows: 1. Mature group, treated with testosterone propionate (0.25mg/g B.W.) daily, reduced Leydig cell numbers and showed germinal epithelium atrophy, and inhibited spermatogenesis. 2. Mature group, treated with testosterone propionate (0.25mg/g B.W.) daily and HCG (2.5 I.U./g B.W.) every 3 days, showed normal variation of interstitial cell, germinal epithelium and spermatogenesis. 3. Immature group, treated with testosterone propionate (0.25mg/g B.W.) daily, increased in numbers of Leydig cells slightly and showed tortuous tubules and spermatogenesis. 4. Immature group, treated with testosterone propionate (0.2.mg/g B.W.) daily and HCG (2.5 I.U./g B.W.) every 3 days, showed normal variation of interstitial cell, germinal epithelium and spermatogenesis.
Animals ; Atrophy ; Azoospermia ; Body Weight ; Cell Count ; Epithelium ; Humans ; Infertility, Male ; Leydig Cells ; Male ; Mice* ; Rats ; Spermatogenesis ; Testis* ; Testosterone Propionate ; Testosterone*

PURPOSE: Anthocyanin is known as a water soluble natural pigment and potent antioxidant. We extracted anthocyanin mediating antioxidant reaction from black soybeans, administered the extract to rats induced prostatic hyperplasia, and evaluate the effect of anthocyanin. MATERIALS AND METHODS: Twenty four male rats were divided into 4 experimental groups: the control, BPH-induced, BPHinduced, and oral anthocyanin (40 mg/kg, 80 mg/kg)-administered groups. For exclusion of intrinsic testosterone influence, a bilateral orchiectomy was done on all except the control group. An experimental prostate hyperplasia was induced by the subcutaneous administration of 3 mg/kg testosterone propionate for 4 weeks to all except the control group. Anthocyanin administration was done in the last 4 weeks in the anthocyanin-administered groups. After 8 weeks, the prostates were removed and analyzed for their prostatic weight and histological examination. Then TUNEL staining was done on each group's specimens, and they were analyzed for their apoptotic body counts. RESULTS: The mean prostate weight was found to be 674.17+/-28.24 mg, 1,098.33+/-131.31 mg, 323.00+/-22.41 mg, and 324.00+/-26.80 mg in the control, BPH-induced, and oral anthocyanin-administered (40 mg/kg, 80 mg/kg) groups, respectively. The BPH-induced group showed statistically significant increases in their prostate weights compared with the control group (p<0.05) and the anthocyanin administered groups showed statistically significant decreases compared to the control and BPH-induced groups (p<0.05). Histologically injected testosterone led to prostatic hyperplasia, but anthocyanin-administered groups experienced this change to a lesser extent. Apoptotic body counts in 5x400/HPF were found to be 3.67+/-0.86, 1+/-0.94, 15.67+/-2.36, and 28.33+/-1.71 in each group. The anthocyanin-administered groups showed statistically significant increases in apoptotic body counts compared with the control and BPH induced groups (p<0.05). CONCLUSIONS: In a prostatic hyperplasia-induced rat model, administration of anthocyanin showed the reduction of prostate weight and the increase of apoptosis. We thought that such results were caused by antioxidant reactions of anthocyanin, and administration of the anthocyanin may be effective in benign prostatic hyperplasia, which is the representative geriatric disease of the urological system.
Animals ; Anthocyanins ; Apoptosis ; Humans ; Hyperplasia ; In Situ Nick-End Labeling ; Male ; Negotiating ; Orchiectomy ; Prostate ; Prostatic Hyperplasia ; Rats ; Soybeans ; Testosterone ; Testosterone Propionate ; Weights and Measures

BACKGROUND AND OBJECTIVE: Previous reports suggest that some cases of sensorineural hearing loss (SNHL) may be the results of abnormal immune reaction. However, specific diagnostic tests and treatment have not been established. This study was performed to evaluate the effect of testosterone in the treatment of immune-mediated SNHL. MATERIALS AND METHODS: Immune-mediated SNHL was induced in female Wistar rats by sensitizing with bovine inner ear antigen 3 times weekly. Two fifty microgram of testosterone propionate was injected subcutaneously 3 times a week from one week before and after the first sensitization. Auditory brainstem response (ABR) and collection of blood were performed prior to each antigen challenge at 1, 2, 3, 4, 6, 8 weeks following sensitization. Collected sera were analyzed using the western blot immunoassay against bovine inner ear antigen preparation. RESULTS: Testosterone-treated animals showed better hearing than the controls, but they also showed incidence of hearing loss over 20 dB (25.0% vs. 53.3%). None of testosterone-treated animals showed hearing loss over 30dR, whereas 40% of control animal revealed hearing loss over 30dB. Five of 9 animals (55.5%) with hearing loss over 20 dB showed a band at 68kD MW, while only one of 14 testosterone-treated animals displayed a band at 68kD MW. CONCLUSION: These results suggest that testosterone may be effective in prevention, and early recovery from immune-mediated SNHL can be used as one of the treatment modalities for immune-mediated hearing loss in the future.
Animals ; Blotting, Western ; Diagnostic Tests, Routine ; Ear, Inner ; Evoked Potentials, Auditory, Brain Stem ; Female ; Hearing Loss* ; Hearing Loss, Sensorineural ; Hearing* ; Humans ; Immunoassay ; Incidence ; Rats, Wistar ; Testosterone Propionate ; Testosterone*