Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Progesterone, epitestosterone (4-androstene-17 alpha-ol-3-one, EpiT) and 4- androstene-3-one-17 beta-carboxylic acid (COOH), three known in vitro inhibitors of 5 alpha reductase, were injected daily for 30 days to male rats to study their effect on some parameters of epididymal function. Progesterone at the dose of 750 and 2000 micrograms/day decreased fertility by 59% and 50% respectively. EpiT at a dose of 1500 micrograms/day decreased fertility by 74%. These treatments did not change the sperm counts in the cauda epididymis. Treatment with COOH did not decrease fertility. Progesterone at 750 and 2000 micrograms/day and EpiT at 750 micrograms/day decreased the weight of the epididymis, prostate and seminal vesicles. None of the compounds tested produced variations in body weight or in the weight of liver and testis. The 5 alpha reductase activity of epididymis, testis and liver was diminished by progesterone treatment, while EpiT decreased only that of testis and liver.
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PMID:Effect of in vivo administration of 5 alpha reductase inhibitors on epididymal function. 26 19

Male (1--60 days old) and female (1--30 days old) hamsters were decapitated and serum levels of LH, FSH, PRL, progesterone, androgens (males), and estradiol (females) were measured by RIA. Males and females had similar levels of LH until 15 days of age and of FSH until 12 days of age, at which times gonadotropin levels increased significantly in females. Peak levels for females occurred on days 19--21 for LH and on days -2--24 for FSH, later than the times reported for female rats. Adjusting female gonadotropin peaks for gestation length places these peaks for hamsters and rats at the same time in postmating age. In female hamsters, large variations occur in LH between 16--25 days of age, as reported for female rats. Males reached peak serum levels of LH and FSH on day 40, just before the first motile epididymal sperm. Serum PRL levels were identical in male and female hamsters until at least day 30. PRL levels sharply increased in both sexes after day 18 and remained elevated until at least day 30. In males, serum androgens were low until 30 days of age, in contrast to high levels reported for infantile rats. Androgens rose sharply in male hamsters after day 30 to peak levels on day 50. Progesterone in males also remained low until after day 30. Serum estradiol in females did not attain the extremely high elevations seen in rats. Some fluctuations occurred between 10--30 days of age, which presumably represent maturational changes in the ovary. Serum progesterone in females followed a pattern of development similar to estradiol.
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PMID:The development of gonadotropin and steroid hormone patterns in male and female hamsters from birth to puberty. 47 8

Single dose administration of Prolactin(P), Progesterone (PP) and a combination of both (PPP) affected the epididymal lipids considerably. Caput and Cauda showed differential responses. PP and PPP showed significant alterations in Caput epididymis. However, Prolactin was effective in Cauda epididymis. The importance of these changes in relation to physiological functions of epididymis is discussed.
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PMID:Hormonal influence on epididymal lipids. 48 93

Sixty-day-old rats were divided into four groups and treated for 30 days with either medroxyprogesterone acetate (Provera), gonadotropins (bovine LH and ovine FSH), Provera plus gonadotropins, or saline. The progestin treatment resulted in a lowering of plasma levels of testosterone, androstenedione, and LH, as well as in a reduction of epididymal sperm counts and accessory sex organ weights. The progestin-treated groups showed markedly lower levels of testicular 17 beta-hydroxysteroid dehydrogenase activity (35% of controls) and delta 5,3 beta-hydroxysteroid dehydrogenase activity (70% of controls). Rats treated with only gonadotropins exhibited reduced 17 beta-hydroxysteroid dehydrogenase but increased delta 5,3 beta-hydroxysteroid dehydrogenase activities. It was concluded from these results that progestins may affect testicular steroidogenesis and spermatogenesis not only by reducing LH secretion but also by a direct effect on the testis, as LH suppression could not account for the inhibition of 17 beta-hydroxysteroid dehydrogenase activity. Long term progestin treatment did not alter the steroidogenic response of the testis to acute administration of LH, although the testosterone to androstenedione ratio in plasma was decreased.
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PMID:A direct effect of medroxyprogesterone acetate on 17 beta-hydroxysteroid dehydrogenase in adult rat testis. 74 49

The combination of a progestin and androgen has received attention as a possible male contraceptive. The progestin is thought to reduce gonadotropin release and suppress spermatogenesis, while the sex accessory organs and male characteristics are maintained by the simultaneous administration of testosterone. In the present study, the histology and ultrastructure of parts of the male reproductive tract of rats treated with medroxyprogesterone (Provera, Upjohn) (1 mg/100 g body weight/day) alone and combined with testosterone (15, 30, or 100 mug/100 g/day) were studied following treatment for up to 16 weeks. The testes and epididymides of rats administered Provera alone or Provera and testosterone weighed less than those of control rats. The weights of the accessory glands of rats treated with Provera were greatly reduced; it was possible to maintain them at approximately control levels by simultaneously administering sufficient testosterone (100 mug/100 g body weight/day). The fertility of some of the animals was tested by caging them with female rats, and none of the treated rats tested in this way was fertile. Similar microscopic alterations were present in the testes of animals administered Provera alone or Provera and different levels of testosterone. Spermatogonia, spermatocytes, and early spermatids were abundant in treated rats and did not show ultrastructural changes. However, many degenerating or necrotic spermatids of the cap phase (approximately stages 6-7) and later were present. Late spermatids of the acrosome and maturation phases were rare. Some necrotic spermatids were surrounded by Sertoli cells, and parts of spermatids lay within lysosome-lyke structures in the cytoplasm of Sertoli cells. Many large lipid droplets were also present in Sertoli cells of treated rats. Leydig cells were smaller in treated animals than in control rats. The results suggest that germ cells can develop up to cap phase spermatids but then undergo degeneration. These alterations in spermatogenesis may be responsible in large part for the antifertility effect of the progestin and androgen combination. Some rats were permitted to recover following the end of treatment. The microscopic appearance of the testis returned to normal within three to six weeks, although epididymal alterations persisted in some animals six weeks after the end of treatment. By 9 to 12 weeks after the end of treatment the reproductive organs had a normal microscopic appearance in all the rats studied.
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PMID:The influence of progestin and androgen on the fine structure of the male reproductive tract of the rat. I. General effects and observations on the testis. 84 78

Young adult male rats were administered medroxyprogesterone (Provera, Upjohn) alone and in combination with testosterone,as has been done to inhibit male fertility. The histology and the fine structure of several segments of the epididymis, the ventral prostate, and the seminal vesicle were studied at intervals after treatment for up to 16 weeks. The epididymides of treated animals weighed less than those of control rats. Microscopic alterations in the epididymis were similar in rats treated with Provera alone and in those animals that received Provera and testosterone, but the changes varied with the segment of the epididymis. In the middle segment in the caput epididymidis, the normally abundant luminal sperm were absent but the epithelium retained its normal ultrastructural features. In the terminal segment in the cauda epididymidis, different changes were observed in the proximal and distal portions. In the proximal cauda epididymidis, the lumen was small, irregular in outline, and virtually devoid of sperm. The light cells of the epididymal epithelium in the proximal cauda contained extremely large numbers of dense bodies resembling lysosomes, which occupied most of the supranuclear and basal cytoplasm. In contrast, in the distal part of the cauda epididymidis, the epithelium had a normal appearance but the lumen was filled with debris, sperm, and spherical masses of cytoplasm that were apparently derived from germ cells. It is suggested that the clearing of the lumen of the proximal cauda epididymidis may reflect the greater activity of light cells of the epididymal epithelium in that region. Although alterations in spermatogenesis may be most important in the antifertility effect of progestin and androgen, these alterations in epididymal sperm and epithelium may also play a role. The weights of the prostate and seminal vesicles of rats treated with Provera (1 mg/100 g/day) were greatly reduced compared to those of control rats. Although there was considerable variation, in many specimens treated with Provera alone the epithelium of the prostate showed a change from a columnar to a cuboidal or squamous shape, and there was a reduction in the size and abundance of organelles involved in the formation of secretions. The microscopic structure of the seminal vesicle of rats treated with Provera was less severely affected than the prostate. Although the seminal vesicle epithelium of Provera-treated rats was generally not as tall as in control animals, the cells possessed parallel cisternae of rough endoplasmic reticulum, secretory vacuoles, and an active-appearing Golgi apparatus, suggesting that they continued to be able to form secretions in the presence of Provera. The weights of the sex accessory glands were maintained at control levels by the administration of testosterone, 100 mug/100 g/day, along with the Provera. A normal fine structure was present in the epithelium of both the prostate and seminal vesicle of rats administered this amount of testosterone in addition to Provera...
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PMID:The influence of progestin and androgen on the fine structure of the male reproductive tract of the rat. II. Epididymis and sex accessory glands. 84 79

The original study conducted 22 years earlier at the Chicago Lying-in Hospital attempted to determine the value of diethylstilbestrol (DES) in maintaining pregnancy. The number completing the course of therapy was 840 in the DES group; there were 860 in a control group. Increasing doses were given beginning during the 7th week of pregnancy. The present study was to determine the level of risk of cancer and other anomalies in the female and male offspring of mothers who participated in the study. So far, 84 DES-exposed females, 43 female controls, 43 DES-exposed males, and 37 male controls have been examined. No cases of cancer have been found. The average age was 22 years. For female patients the medical history, a general physical examination, a gynecological examination, a colposcopic study, and laboratory tests were made. Laboratory tests consisted of cervical, endocervical, and 4 vaginal wall Pap smears, urine cytology, and follicle stimulating hormone and luteinizing hormone determinations. Biopsies were performed when indicated. Progesterone and total estrogens were determined only in patients with irregular menstrual cycles. In male patients, a general physical examination, urologic studies, and laboratory work-up were done. Medical records of all the newborn infants were surveyed and pediatric records examined. No cases of congenital malformations were recorded. Minor differences in menstrual histories and in ability to conceive were noted. The differences appeared mainly at vaginal examinations. Circumferential ridges in the vagina and cervix were seen in 39% of the exposed females but in none of the controls. Erythroplakia of the cervix was seen in 67% of the exposed and in 53% of the controls. Colposcopic findings in the vagina revealed vaginal epithelial changes in 78% of the DES-exposed females and 2% of female controls. Iodine negative areas in the vagina were noted in 78% of the exposed females compared with 2% of the unexposed females. Iodine negative areas on the cervix were seen in 74% of the exposed and 58% of the unexposed. All dysplastic lesions were confirmed by histology. The cytology was negative in all. In the males abnormal findings were noted mainly in the DES-exposed group. An undersized penis was noted in 2, small testes in 2, varicocele in 1, and epididymal cysts in 4. Urine cy tology and prostatic fluid cytology did not reveal unusual findings. A more detailed analysis of findings will follow when material is larger and older.
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PMID:Follow-up study of male and female offspring of DES-treated mothers a preliminary report. 117 Dec 34

The in vivo and in vitro metabolism of 3H-testosterone by rat epididymis and the changes in epididymal weight have been studied after castration and treatment with anti-androgens. The utilization of 3H-testosterone was greatly reduced after castration as was the formation of 5alpha-reduced 17 beta-hydroxy metabolites. The formation of the 17 -keto metabolites was unaffected. Castration had no effect on the ratio between water and ether soluble radioactivity. Administration of testosterone propionate, necessary for giving normal stimulated prostate weight (150 mug/day), restored the metabolism of testosterone to approximately normal values. Estradiol benzoate and progesterone inhibited metabolism of testosterone in vitro and greatly reduced the formation of DHT (17 beta-hydroxy-5alpha-androstan-3-one) and 3 alpha-diol(5 alpha-androstane-3 alpha-17 beta-diol) by experiments both in vivo and in vitro. No effect of cyproterone acetate could be demonstrated on either the in vitro or in vivo metabolism of testosterone. Castration for 14 days reduced the epididymal weight to about 30% of that found in intact animals. Administration of testosterone propionate restored the epididymal weight to about 80% of normal. Estradiol benzoate and cyproterone acetate given to intact rats led to a decrease in the epididymal weight. Progesterone had no such effect. In 14 days castrated rats receiving testosterone propionate all three anti-androgens reduced the weight of the epididymis. In conclusion, our results show that the metabolic conversion of testosterone in epididymis to DHT and 3 alpha-diol is dramatically dependent on the hormonal status of the animal; castration or treatment with anti-androgens causes a reduced formation of the "active" androgens whilst testosterone replacement treatment restores the metabolism of testosterone to normal.
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PMID:Androgen metabolism by rat epididymis. 3. Effect of castration and anti-androgens. 126 92

An inhibitory effect of fatty acid oxidation on glucose uptake and oxidation has been demonstrated in heart and skeletal muscle under certain experimental conditions. This reciprocal relationship has been termed the glucose-fatty acid cycle. The purpose of the present study was to determine under in vivo conditions whether this interaction was operational in various nonmuscle tissues, and whether infection altered the activity of this cycle. Oral administration of alpha-methylpalmoxirate (MPA; 75 mg/kg), a known inhibitor of long-chain fatty acid oxidation, suppressed hepatic glucose production by 54% and increased whole body glucose disappearance by 15% in nonseptic rats. In contrast, MPA produced a larger reduction of glucose output in septic rats, but did not enhance glucose disposal. In vivo glucose uptake (Rg) by individual tissues was determined using the tracer 2-deoxyglucose technique. In nonseptic animals, MPA increased Rg in "working" muscles (heart and diaphragm; 12-fold and two-fold respectively), but not in "resting" skeletal muscles. MPA increased the Rg of heart and diaphragm to the same level in septic animals. Inhibition of fatty acid oxidation in nonseptic rats also enhanced Rg in liver (174%), spleen (158%), lung (153%), ileum (52%), skin (28%), kidney (115%), and epididymal fat (135%). In septic rats, MPA only increased Rg in the ileum (23%) and kidney (50%). This increased glucose uptake was independent of increases in plasma glucose and insulin concentrations. The infusion of heparin and intralipid, which increased circulating levels of fatty acids, failed to produce consistent changes in either the whole body glucose turnover or glucose uptake by individual tissues. We conclude that under basal in vivo conditions the inhibition of fatty acid oxidation suppresses glucose production and increases peripheral glucose disposal in nonseptic animals. These data support the presence of the glucose-fatty acid cycle in nonmuscle tissues and emphasizes its importance in whole body glucose homeostasis in situations where fatty acid oxidation is impaired. Infection increases glucose uptake by nonmuscle tissues which, for the most part, cannot be further enhanced by the inhibition of lipid oxidation.
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PMID:Regulation of glucose metabolism by free fatty acid availability in septic and nonseptic rats. 142 26

The oestrogen mestranol (0, 0.01, 0.1 mg/kg body weight per day) and the progestins medroxyprogesterone-acetate and norethisterone (0, 2, 20 mg/kg body weight per day each) in sesame oil were intubated intragastrically daily during gestational days 14.5 through 19.5 to pregnant rats. Males were studied as 20.5-day-old foetuses and 4-month-old adults for serum testosterone and LH concentrations, in vitro testosterone synthesis, anogenital distance (foetuses only) and testes, seminal vesicle and ventral prostate weights. Administration of 0.1 mg mestranol decreased by 35 to 70% basal and LH-stimulated testosterone synthesis by both foetal and adult testes in vitro (P less than 0.01). Foetal body weights (P less than 0.05), but not anogenital distances, were significantly decreased. Testosterone content in adult sera was reduced significantly (P less than 0.05) to less than 50% of control. Testes, ventral prostate, seminal vesicle and epididymal weights were unaffected by treatment. Medroxyprogesterone acetate or norethisterone administration did not alter testes endocrine function in foetal or adult offspring. In a small number of rats, pregnant for 10.5, 14.5 or 18.5 days, [3H]ethinyloestradiol was intubated and foetal and placental tissue examined for appearance and content of radioactivity. Radioactivity was detected in 10.5, 14.5 and 18.5 days old placentas, and 14.5 and 18.5 days old foetal liver, gonads and external genitalia. With [3H]medroxyprogesterone acetate, radioactivity was localized in 14.5 day placenta and foetal tissues. Thin-layer chromatographic analysis showed most of the activity to migrate as authentic ethinyloestradiol or medroxyprogesterone acetate. These results demonstrate inhibition of testicular testosterone synthesis by mestranol, presumably by being transferred across the placenta and acting in the foetus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of prenatal administration of mestranol and two progestins on testosterone synthesis and reproductive tract development in male rats. 295 83


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