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)

To study the antifertility effect of an extract (alcoholic) of the leaf-stalk of Piper betle Linn., one set of experiments with two different doses in Swiss male albino mice were evaluated. Initially, 500 mg of the leaf-stalk extractive for 30 days and then 1000 mg for next 30 days/animal/day/kg body weight were administered orally. The extract reduced fertility to 0% within 60 days. Suppression of cauda epididymal sperm count and motility (p <0.05) was observed. Biochemical parameters did not show any marked alterations in testosterone content in serum nor 17beta-hydroxysteroid dehydrogenase (17beta-HSD) activity in testes although fructose content in seminal vesicles was reduced as are the weights of reproductive organs. The cholesterol content in testes increased, although not appreciably. After cessation of drug (plant extract) treatment, the altered parameters recovered. Results suggest that the contraceptive effect of the extract of leaf-stalk of Piper betle Linn. is mainly on the maturation process of spermatozoa in epididymides without influencing hystemic hormonal profiles. Withdrawal of the extract restored all altered parameters including organ weights and fertility after 60 days.
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PMID:The reversible antifertility effect of Piper betle Linn. on Swiss albino male mice. 1117 98

Swimming exercise for 1, 2 and 3 hr for 5 days/week for consecutive 4 weeks, results in a significant reduction in testicular, epididymal, prostetic, seminal vesicle somatic indices; epididymal sperm count, sperm motility; preleptotine spermatocytes, mid pachytene spermatocytes and stage 7 spermatids; plasma levels of testosterone, luteinizing hormone; testicular delta5, 3beta-hydroxysteroid dehydrogenase, 17beta-hydroxysteroid dehydrogenase; testicular superoxide dismutase, catalase, glutathione peroxidase, glutathione-s-transferase and glutathione along with significant elevation in malondialdehyde in male albino rats. However, no significant change was noted in final body weight, spermatogonia-A and plasma level of follicle stimulating hormone. The results that oxidative stress develops with the increasing of exercise intensity, which may interfere in male reproductive activities.
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PMID:Effect of different intensities of swimming exercise on testicular oxidative stress and reproductive dysfunction in mature male albino Wistar rats. 1557 34

The primary source of 17beta-estradiol (E2) in the male is the testis, which expresses the enzyme complex aromatase that is involved in E2 biosynthesis. However, recent evidences suggest that the epididymis is also capable of E2 biosynthesis. Our results demonstrate the presence of cytochrome P450 aromatase (P450(AROM)) and 17beta-hydroxysteroid dehydrogenase I messenger ribonucleic acid (mRNA) in the caput and cauda regions of rat epididymis. The androgenic substrates testosterone and androstenedione could be utilized by the rat epididymal aromatase for E2 biosynthesis as assessed by radioimmunoassay. P450(AROM) expression is transcriptionally regulated in a tissue-specific manner by various factors including androgens and luteinizing hormone (LH). Androgens could positively modulate epididymal P450(AROM) mRNA levels as assessed by castration studies, treatment with flutamide or in vitro incubation of tissue minces with 5 alpha-dihydrotestosterone (DHT). Several extra-gonadal tissues including the epididymis are known to express LH receptors (LHR). Our study revealed a higher level of LHR mRNA expression in the cauda region compared to the caput. Caudal membrane extracts could bind human chorionic gonadotropin (hCG), which resulted in the production of cAMP. Interestingly, hCG could also regulate P450(AROM) mRNA expression in vitro and enhance E2 biosynthesis. Together our results highlight the presence of a functional aromatase in the epididymis that is subject to regulation by LH and androgens.
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PMID:Expression of functional aromatase in the epididymis: role of androgens and LH in modulation of expression and activity. 1656 75

Fluoride contamination of drinking water can disrupt male gametogenesis and steroidogenesis and induce testicular oxidative stress. Treatment of rats with sodium fluoride at the dose of 20 mg/kg/day for 28 days resulted in significant diminution of testicular Delta5,3beta-hydroxysteroid dehydrogenase (HSD) and 17beta-hydroxysteroid dehydrogenase (HSD) activities and low plasma levels of testosterone, follicular stimulating hormone (FSH) and leutinizing hormone (LH). Spermatogenesis inhibited after sodium fluoride treatment has been assessed here by the quantification of different generation of germ cells like spermatogonia A (ASg), preleptotene spermatocyte (PLSc), midpachytene spermatocyte (MPSc) and step 7 spermatid (7Sd) at stage VII of seminiferous epithelial cycle. Furthermore, fluoride treatment was associated with low activities of testicular, prostatic and epididymal catalase (CAT), superoxide dismutase (SOD) and peroxidase along with elevation of malondialdehyde (MDA) and conjugated dienes (CD) in those tissues. Co-administration of calcium and Vitamin-E with fluoride resulted in a significant recovery from testicular disorders and oxidative stress in the testis and male accessory sex organs. The results of this study demonstrate that fluoride exposure, at the dose available in drinking water in contaminated areas, led to inhibition of testicular gametogenesis and steroidogenesis in association with oxidative stress in the testis and male accessory sex organs, which are protected significantly by dietary agents like Vitamin-E and calcium.
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PMID:Management of fluoride induced testicular disorders by calcium and vitamin-E co-administration in the albino rat. 1676

The present study was designed to assess potential reproductive toxicity caused by fentin and fenbutatin in the mice. Adult male mice received i.p. injections of fentin hydroxide and fenbutatin oxide at a dose of 0, 10 or 25 microg/kg body weight on 1st, 3rd and 5th day of experimentation. Mice were sacrificed on day 25 and analyzed for spermatogenesis and steroidogenesis. A significant decrease in epididymal sperm count, sperm motility, sperm viability and sperm function (HOS coiling) were observed in experimental mice when compared with controls. The decrease in sperm quantity and quality was significant in the 25 microg/kg group than that in the control group. The activity levels of testicular steroidogenic enzymes, 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and 17beta-hydroxysteroid dehydrogenase (17beta-HSD) were significantly decreased in treated mice indicating decreased steroidogenesis after organotin compounds administration. The levels of serum testosterone decreased with an increase in follicle stimulating hormone and luteinizing hormone in experimental mice when compared to control mice. The results suggest that fentin and fenbutatin cause impairment of spermatogenesis through the inhibition of testosterone production.
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PMID:Reduction of spermatogenesis and steroidogenesis in mice after fentin and fenbutatin administration. 1680 47

Overweight male rats received oral oleoyl-estrone (OE) for 10 days, and were compared with controls. The expression of 17beta-hydroxysteroid dehydrogenase (17betaHSDH) isoenzymes, and other proteins related to sex hormone metabolism, were analyzed in testicle, liver, adrenals and two white adipose sites: subcutaneous inguinal and epididymal pads using a semiquantitative RT-PCR method. Androstenedione, testosterone, estrone and estradiol levels were measured by HPLC-MS/MS. Isoenzyme expressions were grouped according to their main physiological function (oxidative or reductive) and preferred substrate (androgen or estrogen). As expected, testicle was the main site for synthesis of testosterone and estradiol, and the liver the main organ oxidizing them to androstenedione and estrone. Overall oxidative capacity was 6.5-fold higher than the reductive, and estradiol synthesis and oxidation potential were higher than for testosterone. OE decreased serum androgens, and increased estrone, but not estradiol. This was due to decreased testicle ability to produce testosterone, because of smaller size and decreased 17betaHSDH3 expression, but also to lower availability of precursors. High estrone availability (from OE hydrolysis) does not translate into higher estradiol because of decreased testicle reductive 17betaHSDH expression and decreased aromatase. In consequence, we can assume that OE effects on androgens, and the hypothalamic-pituitary-gonadal axis are limited to testicles.
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PMID:Influence of oleoyl-estrone treatment on circulating testosterone. Role of 17beta-hydroxysteroid dehydrogenase isoenzymes. 1943 21