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)

Adult male rats were dosed orally on d 0 with 0 or 2000 mg/kg of boric acid and killed on posttreatment d 2, 14, 28, and 57, or dosed with 0, 250, 500, 1000, or 2000 mg/kg of boric acid and killed on posttreatment d 14. At d 14, atypical structures that appeared to be enlarged irregular cytoplasmic lobes of Step 19 spermatids were observed in Stage VIII seminiferous tubules of rats dosed with 1000 and 2000 mg/kg. Abnormal retention of Step 19 spermatids and residual bodies was also observed in Stage IX-XIII tubules of these rats. The retained spermatids and residual bodies were seen in both the luminal and basal regions of the epithelium. A substantial increase in the testicular sperm head count occurred in animals dosed with 2000 mg/kg. Abnormal caput epididymal sperm morphology and reduced caput epididymal sperm reserves were observed at 1000 mg/kg and higher. Serum LH, FSH, TSH, and prolactin values were not affected at any dosage. At d 28, rats dosed with 2000 mg/kg exhibited continued retention of Step 19 spermatids into Stage X, abnormal caput and cauda sperm morphology, and decreased percentages of motile cauda spermatozoa with reduced straight-line swimming velocities. By d 57 substantial recovery was apparent; some retention of Step 19 spermatids into Stage X tubules was still present in two out of six rats but the sperm parameters were comparable to controls. The study indicated that acute oral exposure to boric acid adversely affected spermiation and sperm quality in the adult male rat. At the dosages used the effects appeared reversible. The no-effect level was 500 mg/kg.
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PMID:Effect of acute exposure to boric acid on the male reproductive system of the rat. 221 25

Developmental changes in pituitary content and secretory patterns of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL), testicular size and steroidogenic function, testicular LH- and FSH-binding activity, and growth of the accessory sex organs were examined for 24 Dorset X Leicester X Suffolk rams (born in March) every 30 days from 30 to 150 days of age, and again at 200 days. Pituitary LH and FSH contents increased between 30 and 60 days of age and remained constant until 150 days, when contents were somewhat greater than on either 120 or 200 days. LH-pulse amplitude and frequency, and mean FSH concentration, were highest at 60 and (or) 90 days of age. Testicular growth increased dramatically between 90 and 150 days of age in association with increases in the number of LH- (100-fold) and FSH- (33-fold) binding sites in the testis and a small increase in blood testosterone concentration (1 ng/ml). During the same period, pituitary content and blood concentration of PRL increased to maximal values, epididymal, vesicular gland and bulbourethral gland weights increased 6-fold, and body weight doubled. Between 150 and 200 days of age, testosterone concentration increased considerably (8 ng/ml), as did LH-pulse frequency and the amount of LH- and FSH- binding in the testis; the reproductive organs continued to grow at a rate faster than that of the body as a whole. Testicular development of ram lambs was accompanied by increases in the secretion of all three pituitary hormones with gonadotropic properties, and in the number of LH and FSH receptors.
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PMID:Pubertal changes in the secretion of gonadotropic hormones, testicular gonadotropic receptors and testicular function in the ram. 250 35

The effects of hypophysectomy and gonadotropin replacement on transepithelial movement of 3H-androgen in the rat epididymis were examined by in vivo microperifusion of 3H-testosterone followed by in vivo micropuncture to obtain peritubular and intraluminal fluid. In the caput epididymidis of normal rats, intraluminal 3H-androgen concentrations were approximately 300% of those in the interstitial space. In contrast, proluminal movement of 3H-androgen into rat caput epididymal tubules was significantly decreased 10 days after hypophysectomy. 3H-Testosterone movement across the caput epididymal epithelium was completely returned to normal by supplementation with 24 micrograms/day follicle-stimulating hormone (FSH) or 24 micrograms/day luteinizing hormone (LH). However, neither 0.12 micrograms/day FSH nor 250 micrograms/day prolactin returned proluminal androgen movement to normal. It is speculated that epididymal uptake of peritubular testosterone is mediated by androgen-binding protein, which is known to be secreted by Sertoli cells after stimulation by FSH or testosterone.
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PMID:Proluminal movement of 3H-androgen across the epididymal epithelium in the rat after hypophysectomy and gonadotropin supplementation. 251 35

The goal of this study was to discriminate between two hypotheses regarding how the circadian rhythm of pineal melatonin (MEL) production transmits photoperiodic information: (1) A circadian rhythm of sensitivity to MEL regulates the hormone's effect; (2) the duration of the MEL signal, rather than its circadian timing, is the critical parameter of the MEL rhythm. The experiment examined the response of pinealectomized (PINX) male Siberian hamsters to 10-hr (short-day-type) versus 6-hr (long-day-type) duration MEL infusions (10 ng/infusion) in cycles with period lengths (T) of 18, 24, 36, and 48 hr. After cannula implantation, animals were moved from LD 16:8 to LD 10:14 (lights-on from 0500 to 1500 hr, EST), where the timed infusions began. Additional T 24 cycles included as controls employed 18-hr MEL, 18-hr saline (SAL), and 10-hr SAL infusions: Body weight and food intake were measured weekly. After 6 weeks, animals were killed; blood samples were taken for radioimmunoassay (RIA) of serum follicle-stimulating hormone (FSH) and prolactin (PRL); and terminal body, epididymal white adipose tissue (EPIWAT), and paired testis weights were recorded. Six-hour MEL infusions failed to induce short-day-type effects, regardless of the period (T) of the infusion cycle. In contrast, compared to SAL and 6-hr MEL infusions, 10-hr MEL resulted in decreases in body, EPIWAT, and testis weights in T 24, but not in T 36 or T 48. In T 18, testis, body, and EPIWAT mass were decreased, but not to the same extent as in T 24. Similarly, daily 18-hr MEL infusions (T24) were less effective as a short-day stimulus than were 10-hr MEL infusions. The effectiveness of 10-hr, but not 6-hr, MEL infusions in T 18 and T 24 is consistent with the duration hypothesis and argues against the circadian hypothesis. Neither hypothesis could have predicted that all infusion cycles of T greater than or equal to 36 hr, regardless of the infusion durations, would fail to elicit short-day-type responses. This outcome suggests a need for relatively frequent (T less than 36 hr) MEL stimulation in addition to the requirement for adequate duration of each MEL infusion.
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PMID:Effect of melatonin infusion duration and frequency on gonad, lipid, and body mass in pinealectomized male Siberian hamsters. 251 5

Hypoprolactinemia inhibited epididymal energy metabolism and steroidogenesis and retarded growth of epididymal structure. Hyperprolactinemia promoted the above parameters. Bromocriptine had no direct effect on epididymis, while prolactin directly influenced the tissue metabolism. The epididymal maturation seems to be dependent on the circulating levels of prolactin.
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PMID:Maturation events of epididymis in albino rats during puberal transition under hypo and hyperprolactinemia. 262 Sep 30

Serum corticosterone excess was induced by the administration of corticosterone acetate to adrenal intact rats. Different lipid classes were studied in unwashed and washed (epididymal sperm and fluid free) caput and cauda epididymides. The unwashed caput epididymidis registered a significant decrease in total lipid, cholesterol and phospholipid while total glyceride glycerol and its fractions were not altered after corticosterone treatment. Among phospholipid fractions phosphatidyl inositol, choline and ethanolamine showed a significant decrease. Unlike the unwashed caput epididymidis, the washed caput region recorded a marked increase in total lipid, glyceride glycerol and its fractions. However, total lipid in the washed cauda region significantly increased and the increase was mainly due to triacyl glycerol. Though the phospholipid fractions phosphatidyl choline and ethanolamine showed an increase, the total phospholipid was not altered significantly. Serum testosterone and prolactin registered a significant decrease while gonadotropins were unaltered. On the withdrawal of corticosterone treatment, all the lipid classes turned to normalcy along with serum testosterone and prolactin. It is concluded that corticosterone excess favours lipid accumulation in the sperm free epididymal tissue and its influence on epididymis is region specific and reversible.
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PMID:Effect of corticosterone on epididymal lipids in pubertal rat. 263 80

The aim of the performed studies has been to find out wether or not the ultrastructural alterations of the epithelial cells in the rat's epididymal caput occur in hyperprolactinemia induced by metoclopramide and to see if the observed changes are of reversible character. It has been revealed that prolactin concentration was twice as high as in control animals due to peritoneal administration of metoclopramide in a dose of 2.2 mg/kg body mass, given for 14 days. The ultrastructural alterations in the principal cells of epididymal caput affected cellular organelles being involved in proteins synthesis, glycosylation, secretion as well as energetic processes. They were manifested by decreased amount of rough endoplasmic reticulum, widening of its cisternae combined with degranulation, distension of Golgi apparatus cisternae, elevated number of vesicles in apical part of the cells, and changes in mitochondria. The termination of metoclopramide administration made prolactin concentration exhibit values being almost similar to those determined in control rats, whereas the ultrastructural changes in the principal cells were found to be reversible.
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PMID:Ultrastructure of epithelial cells in rat's epididymal caput in experimental hyperprolactinemia induced by metoclopramide. 263 74

This report juxtaposes findings from weanling rats with precise lesions in the ventromedial (VMNL rats) to data of weanling rats with lesions in the dorsomedial (DMNL) hypothalamic nuclei. Despite the proximity of the two nuclei their destruction produces opposite effects in most cases but similar responses in other parameters. Absolute and relative food intake are normal in VMNL rats yet they become obese in the face of normal body weight gains. DMNL rats show both reduced absolute food intake and body weight but normal relative food intake and body composition. Both VMNL and DMNL cause reduced linear growth and running wheel activity. DMNL rats defend their lower body weight set point against various challenges and maintain normal body composition. Organ growth in both absolute and relative terms is reduced in VMNL rats. In DMNL rats relative organ growth is normal. Pancreatic growth, protein/pancreas and content and concentrations of several pancreatic enzymes are normal in DMNL but reduced in VMNL rats. Mean 24-hour plasma growth hormone (GH) and corticosterone (B) levels are reduced and insulin levels are greatly elevated in VMNL rats; prolactin (PRL) levels are normal. In DMNL rats, GH, B, insulin and somatomedin activity are normal but PRL is elevated. Circadian rhythms of GH, insulin and triiodothyronine are normal in DMNL rats but B levels are disrupted, as they are in VMNL rats. Glucose incorporation and oxidation in adipose tissue of VMNL rats are enhanced in VMNL rats but normal in DMNL rats. Gluconeogenesis in VMNL rats is enhanced as early as 4 hours post-operatively; in DMNL rats it is normal at this time and several weeks thereafter. Basal lipolysis in epididymal fat pads is elevated in both VMNL and DMNL rats but epinephrine-stimulated lipolysis is elevated in VMNL and decreased in DMNL rats. Both VMNL and DMNL rats show normal basal and epinephrine-stimulated lipolysis in interscapular brown adipose tissue. Several hepatic enzymes are normal in DMNL and depressed in VMNL rats. The above data suggest that the DMN and its circuitry are part of an "organismic" set point system with a "true" body weight and no fat set point, as seems to be the case in the VMNL rat.
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PMID:Ventromedial and dorsomedial hypothalamic syndromes in the weanling rat: is the "center" concept really outmoded? 286 69

In the present study rats were dosed from weaning, through puberty and gestation, to Day 15 of lactation with methoxychlor at 25, 50, 100, or 200 mg/kg/day. Morphological landmarks of puberty were measured, including the ages at vaginal opening, first estrus, and first estrous cycle in females and at preputial separation in males. In the female, estrous cyclicity, fertility, litter size, number of implantation sites, organ weights, and ovarian and uterine histology were also measured. The viability of the offspring (F1) and their fertility were evaluated using a continuous breeding protocol. Males were necropsied after breeding, the reproductive organs were weighed, and the cauda epididymal sperm counts were determined. One testis was used for histopathology, while the other was used to quantify interstitial fluid (IF) content, IF testosterone concentration, and testicular sperm production. Testosterone and androgen-binding protein were measured in the caput epididymis, and sperm motility and morphology were evaluated from a caudal sample. The serum and pituitary were saved for hormonal determinations. Methoxychlor accelerated the age at vaginal opening and first estrus, and the vaginal smears were cornified. Growth was retarded at 100 and 200 mg/kg/day and fertility was reduced when the females were bred with untreated or similarly treated males. In the highest-dose group, the mated females went from constant estrus into pseudopregnancy following mating, but they had no implants. In males, methoxychlor treatment markedly reduced growth, seminal vesicle weight, cauda epididymal weight, caudal sperm content, and pituitary weight. Puberty was delayed in the two highest-dosage groups. Testicular sperm measures were much less affected than caudal measures. Testis weight and histology were slightly affected, and testicular sperm production, sperm morphology, and motility were unaffected. Endocrine function of the testes and pituitary was altered by methoxychlor administration. Leydig cell testosterone production, in response to human chorionic gonadotropin challenge, was reduced and pituitary levels of prolactin, thyroid-stimulating hormone (TSH), and follicle-stimulating hormone (FSH) were altered. In contrast, serum levels of prolactin, FSH, and luteinizing hormone were unaffected. Serum TSH was reduced by 50% of control at 100 and 200 mg/kg/day, while pituitary levels were increased. Gonadotropin-releasing hormone concentration in the mediobasal hypothalamus was also elevated. In spite of the many reproductive alterations, the fertility of treated males was not reduced when they were mated with untreated females.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:A dose-response analysis of methoxychlor-induced alterations of reproductive development and function in the rat. 292 22

Effect of insulin on glucagon binding to rat epididymal adipocytes was studied in vitro. [125I]iodoglucagon binding to isolated adipocytes was increased by preincubation of the cells with insulin. Maximal increase was observed with 7 X 10(-10) M insulin. In Scatchard analysis, [125I]iodoglucagon competition data generated one binding site with a single affinity for glucagon binding in the cells pretreated with buffer alone. Pretreatment of the cells with insulin increased the affinity without changes in the number of binding sites. [125I]iodoglucagon binding to isolated adipocytes was not affected by pretreatment of the cells with luteinizing hormone, follicle-stimulating hormone, growth hormone, or with prolactin. These results suggest that insulin stimulates glucagon binding to adipocytes.
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PMID:Effect of insulin on glucagon binding to isolated rat epididymal adipocytes. 302 93


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