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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of a number of prostaglandins on the metabolism of fructose by epididymal and ejaculated ram spermatozoa were investigated using conventional Warburg techniques. Spermatozoa from the two sources were collected concurrently during electrical stimulation; the epididymal spermatozoa were harvested via a cannula inserted chronically into one vas deferens and thus were free from exposure to the seminal prostaglandins. In general, the metabolism of fructose by the spermatozoa was little affected by a wide range of prostaglandins at a concentration of 20 micrograms/ml. Of the PGs present in semen, PGE2, PGE3 and PGF2alpha had no significant effects whereas PGE1 and PGF1alpha significantly increased lactate accumulation and the latter increased oxygen uptake, in both cases without significantly changing fructose utilization, fructose oxidized or CO2 production. Both 15-methyl-substituted PGE2 and PGF2alpha and their corresponding methyl esters failed to change fructose metabolism and it is unlikely therefore that the lack of response to PGE2 and PGF2alpha was due to their being metabolized by the spermatozoa during the incubation. Of a number of breakdown products tested, PGA1 and to a lesser extent PGA2 appeared to inhibit the Krebs tricarbocyclic acid cycle and 15-keto 13,14-dihydro-PGF2alpha appeared to stimulate it. In general, epididymal spermatozoa responded to the PGs in the same way as ejaculated spermatozoa. Thus we did not confirm a suggestion in the literature that spermatozoa have lowered sensitivity to PGs in vitro once they have been in contact with the PGs in seminal plasma.
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PMID:Effect of various prostaglandins on the metabolism of fructose by epididymal and ejaculated ram spermatozoa in vitro. 73 77

Parenchymal tissue-uptake (TU) and permeability-surface area (PS) product of [3H]prostaglandins (PG) D2, E2 and F2 alpha [1.85 MBq, 0.5 mg/kg (270 nmol)] were examined in 98 regions of the brain and in 19 other tissues of urethane-anesthetized male rats (180-200 g) 15 sec after i.v. administration with [14C]dextran [0.185 MBq, 0.6 mg/kg (2 nmol)] used as a blood spacer. Slight and insignificant change in blood volume was observed in most of the tissues and brain regions between vehicle- and PG-administered groups. TU for the three PG was markedly high in kidney and lung (2388-3952 ng/g), exceeding the blood concentration (2021-2320 ng/ml), but low (less than 10% of the blood concentration) in epididymis, epididymal fat, testis (59-163 ng/g), brain and spinal cord (33-67 ng/g). TU in brain were detected about 0.1% of the administered PG. Based on a two-compartment model, the PS product for the three PG ranged from 0.75 to 4.16 microliters/g/sec in the latter tissues. The value of brain was 1.22 +/- 0.18 microliters/g/sec for PGD2, 1.69 +/- 0.05 for PGE2 and 1.33 +/- 0.13 for PGF2 alpha, indicating that PGE2 enters the brain more readily than PGD2 and PGF2 alpha. In various brain structures, the ranges of the PS product were large and completely overlapped among the three PG (PGD2, 0.14-1.56 microliters/g/sec; PGE2, 0.05-1.78; PGF2 alpha, 0.05-1.82). The highest PS product for the three PG was found in olfactory bulb and cerebellum (0.96-1.82 microliters/g/sec) and the lowest was in septum (0.05-0.53). However, the level of the PS product was different among the PG in each brain region as follows: PGD2 greater than PGE2, PGF2 alpha in septum and anterior part of pyriform cortex; PGE2 greater than PGD2, PGF2 alpha in olfactory bulb, frontal cortex, basal forebrain, middle part of pyriform cortex, thalamus, hippocampus and lateral neocortex; and PGF2 alpha greater than PGD2, PGE2 in posterior part of pyriform cortex, hypothalamus, amygdala and entorhinal and retrosplenial cortices. Low correlation coefficients (0.708, 0.522 and 0.562 for PGD2, PGE2 and PGF2 alpha, respectively) between the PS product and cerebrovascular volume in various regions revealed heterogeneous cerebrovascular permeabilities of PG.
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PMID:Permeability of brain structures and other peripheral tissues to prostaglandins D2, E2 and F2 alpha in rats. 152 17

PGE2 is a potent antilipolytic agent produced by adipose tissue, but its role as a physiological regulator of triglyceride lipolysis is controversial because inhibitors of prostaglandin synthesis have not enhanced hormone-stimulated lipolysis in adipose tissue consistently. Adipose tissue also produces PGI2, but this eicosanoid has not had a demonstrated effect on lipolysis under physiological conditions previously. We investigated both PGE2 and PGI2 production and their effects on lipolysis in rat adipose tissue. We found that 1) EPI-stimulated PGE2 production (like PGI2 production) requires the cooperation of adipocytes and endothelial cells, 2) adipose tissue produces PGE2 and PGI2 at comparable rates, 3) indomethacin inhibits EPI-induced PGE2 and PGI2 production and has no effect on EPI-stimulated lipolysis when added to a mixture of adipocytes and endothelial cells or to intact epididymal fat pads, 4) PGI2 is a potent lipolytic agent when added to isolated adipocytes in the absence of endothelial cells under physiological conditions, 5) the magnitudes and the ED50s of the antilipolytic effect of PGE2 and the lipolytic effect of PGI2 in isolated adipocytes in the absence of endothelial cells are comparable, 6) PGI2 antagonizes the antilipolytic effect of PGE2 in isolated adipocytes in the absence of endothelial cells in a dosage-related manner, and 7) the antilipolytic effect of added PGE2 in isolated adipocytes is greater in the absence of endothelial cells than in their presence, suggesting that endogenous eicosanoid production reduces the effectiveness of added PGE2. These studies demonstrate that catecholamine-induced lipolysis is under the coordinate control of PGE2, a potent antilipolytic agent, and PGI2, a potent lipolytic agent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Coordinate control of lipolysis by prostaglandin E2 and prostacyclin in rat adipose tissue. 162 67

Viprostol, a novel prostaglandin E2 congener, was assessed for in vitro antilipolytic activity in the spontaneously obese rat. In isolated epididymal adipocytes, viprostol exhibited a dose-dependent inhibition of catecholamine-stimulated lipolysis at concentrations ranging from 10 microM to 1 mM, but was ineffective at lower concentrations. Additionally, viprostol exhibited approximately 50% of the antilipolytic activity of naturally-occurring PGE1 and PGE2 at similar concentrations, but was as potent as PGF2 alpha. At 10 microM, viprostol inhibited maximum catecholamine-stimulated lipolysis by approximately 35% of the total, hormone-stimulated glycerol release. The results of these experiments indicate that viprostol exhibits antilipolytic activity in vitro, but is less potent than the naturally-occurring PGE's to which it is most closely related structurally.
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PMID:Antilipolytic activity of viprostol, a transdermally active antihypertensive PGE2 analog. 243 24

Prostaglandins (PGE2, PGF2 alpha) in the excurrent ducts of the male reproductive tract appear to be both modulators of ductal contractility for transport of spermatozoa and factors involved in the regulation of sperm maturation. To identify the tissue sites for the production of prostaglandins (PGs) in the excurrent ductal system, we have employed an immunohistochemical technique to localize prostaglandin H (PGH) synthase in the epididymis and vas deferens of the mouse. A mouse monoclonal antibody to PGH synthase was used and was shown to be specific for the mouse enzyme by Western blot analysis. In sexually mature mice, PGH synthase was primarily localized to the epithelium of the epididymis and vas deferens. Within the epididymal epithelium, immunoactivity appeared in all cell types of the initial segment, in a subpopulation of cells with predominantly apically oriented nuclei in the caput and corpus, and in low levels in the cauda. PGH synthase reactivity was the most intense in the epithelial cells of the vas deferens. PGH synthase was not detected in smooth muscle cells, spermatozoa, or luminal fluid. This study suggests that the epithelium of the excurrent ductal system of the mouse is the major site for PG production. The regionalization of PGH synthase to cells in the epididymis thought to be involved in the absorption of luminal fluid suggests that PGs may play a role in fluid and ion transport.
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PMID:Immunohistochemical localization of prostaglandin H synthase in the epididymis and vas deferens of the mouse. 251 36

Both NaCl and NaF promoted PGE2 binding to epididymal adipocyte membranes by apparent increase in the binding affinity. In order to distinguish between the effect of fluoride and the 'salt effect' of sodium on PGE2 binding, the effects of Mg2+ and guanyl nucleotides on PGE2 binding in the presence of NaCl or NaF were compared. Mg2+ decreased PGE2 binding; high NaF concentration abolished this inhibition, while increased NaCl concentrations did not affect the Mg2+ inhibition. In the presence of Mg2+ the effects of NaCl and NaF were additive. The enhancement of PGE2 binding by fluoride, unlike sodium, was dependent on the presence of Mg2+. Incubation of the membranes with GDP beta S, Gpp(NH)p, GTP or GTP gamma S increased PGE2 binding. Gradual increase in NaF concentrations in the presence of guanyl nucleotides resulted in stimulation of PGE2 binding at low NaF concentrations and inhibition of PGE2 binding at high NaF concentrations. No changes in the stimulatory action of NaCl on PGE2 binding were observed in the simultaneous presence of NaCl and guanyl nucleotides. A biphasic effect on PGE2 binding was observed with a wide concentration range of guanyl nucleotides. Treatment of the isolated membranes with cholera or pertussis toxins stimulated the adenylyl cyclase activity of the membranes, but failed to influence PGE2 binding. The implications of these findings are discussed.
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PMID:Biphasic effect of sodium fluoride and guanyl nucleotides on binding to prostaglandin E2 receptors in rat epididymal adipocyte membranes. 256 48

The effects of a minor tranquilizer, zopiclone, on endocrine system in male rats were assessed to clarify the mechanisms whereby large doses of zopiclone may induce testicular damage. 1) Zopiclone had no significant effect on plasma and tissue levels of hormones of the hypophyseo-gonadal or -thyroid system in rats given 10, 100 and 250 mg/kg/day orally for 28 days. 2) Rats given zopiclone in doses of 10 and 100 mg/kg/day orally for 14 days had lowered serum levels of PGE2 and PGF2 alpha but the testicular PGF2 alpha concentration remained unchanged. Therefore, oral administration of high doses of zopiclone to rats has no evident influence on endocrine system related to male reproduction. And these findings support our previous paper that repeated dose of zopiclone cause no significant change in plasma or epididymal TS levels, nor to any change in lipid peroxidation in testicular tissues.
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PMID:Effects of repeated dosing of zopiclone on endocrine system in male rats. 274 Jun 18

The masculinizing effects of prostaglandins (PGS) PGE2 and PGF2 alpha on mouse fetal genital tract differentiation were studied both in vivo and in vitro. Prenatal exposure to PGE2 and PGF2 alpha on days 11-17 of gestation (the critical period of the differentiation) increased the anogenital distance of the female fetuses in a dose-dependent manner. PGE2 also increased the anogenital distance of male fetuses in the presence of an inhibitor of testosterone synthesis, namely estradiol (2 mg/kg.day), and in the androgen-insensitive Tfmy males. Internally, PGE2 induced the epididymal duct in the females, estrogen-exposed males, and Tfmy males. However, no other changes were noticed in the internal genital tract of these fetuses. To avoid the problems associated with the placental transfer of any external agent, we also studied the effect of PGE2 in an in vitro system. Female genital ducts on day 13 of gestation were cultured in the presence and absence of different concentrations of PGE2 for a total of 6 days. PGE2 at doses 0.2 and 1 microgram/ml induced and stimulated the Wolffian and epididymal ducts. Thus, PGs appear to have a masculinizing role in androgen-induced sexual differentiation.
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PMID:Prostaglandins masculinize the mouse genital tract. 292 22

Tumor necrosis factor (TNF, cachectin) is a macrophage product that has been suggested to signal the loss of body weight, the decrease in adipose tissue and muscle mass, and anorexia during infections or chronic illness. To test this possibility, young growing rats were injected subcutaneously or intraperitoneally with human or murine recombinant TNF. After 3-4 h, these animals developed a 1-2 degrees fever which lasted approximately 4 h. With repeated daily TNF injections for 5 d, the animals developed fevers similarly each day. In contrast, rats injected with endotoxin show a single febrile episode and then are tolerant to subsequent daily injections of endotoxin (but do not develop tolerance to TNF or interleukin-1). On the first day of TNF treatment, the rats did not grow, but on subsequent days, despite their fevers, they grew at similar rates as controls. Although the TNF-treated rats consumed slightly less food than control animals, the ratio of growth per amount of food intake was identical in the two groups. When rats are administered endotoxin, they develop a fever, and their muscles show increased protein degradation and prostaglandin (PG)E2 production. However, when fevers were induced with TNF, there was no change in muscle proteolysis or PGE2 production, and in adipose tissue no increase in basal or catecholamine-induced lipolysis. Also TNF addition in vitro did not enhance lipolysis in epididymal fat pads or proteolysis in soleus muscles. Thus, TNF treatment can induce fever without producing a catabolic state similar to that induced by endotoxin.
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PMID:Tumor necrosis factor can induce fever in rats without activating protein breakdown in muscle or lipolysis in adipose tissue. 316 48

Using an isolated rat epididymal adipocyte system we have studied the development of tolerance to and cross-tolerance between nicotinic acid, 5-methylpyrazole-3-carboxylic acid and pyridyl-3-tetrazole. Preincubating isolated adipocytes with any one of these compounds results in a reduction of the antilipolytic activity of that compound when the cells are exposed to a subsequent challenge dose. Furthermore, preincubation with nicotinic acid, 5-methylpyrazole-3-carboxylic acid or pyridyl-3-tetrazole results in a reduction of the antilipolytic response to challenge with either of the other two compounds. Preincubation of isolated adipocytes with nicotinic acid does not affect the subsequent antilipolytic activity of the PGE2 analogue, sulprostone. Preincubation with sulprostone does not lead to the development of tolerance to its own antilipolytic actions. The results obtained from these studies suggest that nicotinic acid, 5-methylpyrazole-3-carboxylic acid and pyridyl-3-tetrazole exert their antilipolytic activity via a common biochemical pathway which is distinct from that mediating the antilipolytic activity of prostaglandins. These findings also indicate that the development of tolerance occurs prior to the involvement of adenylate cyclase in lipolysis.
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PMID:The development of tolerance to antilipolytic agents by isolated rat adipocytes. 396 29


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