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 transgenic mice overexpressing human insulin-like growth factor-binding protein-1 in the liver present reproductive abnormalities in both sexes. In the present work, we have investigated the mechanisms responsible for limiting breeding capacity in these transgenic male mice. Homozygous adult transgenic male mice (3-6 months old) exhibited irregular copulatory behavior and a reduction of the number of pregnancies per female as well as of litter size per pregnancy. Genital tract weight, more specifically epididymal and seminal vesicle weights, were reduced by 45% in homozygous transgenic vs. nontransgenic mice. Homozygous transgenic mice exhibited a 30% reduction of the length of seminiferous tubules (P = 0.007), a 30% decrease in daily sperm production per testis (P = 0.019), and a 50% decrease in the number of spermatozoa in testis (P = 0.037), associated with morphological abnormalities of the sperm heads leading to an approximately 50% reduction of fertilized two-cell eggs (P = 0.002) and of implanted embryos on d 5.5 after mating (P = 0.004). The round spermatids also appeared altered in their morphology. In addition, Leydig cells in homozygous transgenic mice exhibited an altered appearance, with a 1.8-fold increase in lipid droplets in their cytoplasm (P < 0.001). Moreover, the concentration of 3beta-hydroxysteroid dehydrogenase was 66% lower in testis from transgenics compared with those from normal mice (P = 0.01), leading to a tendency toward lower plasma testosterone levels (P = 0.1). Interestingly, LH concentrations were increased by 40% in transgenic pituitary extracts (P = 0.02), and basal LH secretion by pituitary explants in vitro was increased by 60% in homozygous transgenic vs. normal mice (P = 0.04), suggesting an alteration of LH pulsatile secretion in vivo. In conclusion, these data suggest that the breeding impairment of human insulin-like growth factor-binding protein-1 transgenic males is due at least in part to an alteration of the process of spermatogenesis, leading to a diminution of sperm production and of its quality. Minor impairment of steroidogenesis may also contribute to the reduced reproductive capacity of these animals. Our observations are consistent with the idea that normal spermatogenesis and perhaps also steroidogenesis are dependent on the actions of sufficient concentrations of unbound IGF-I.
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PMID:Reproductive abnormalities in human insulin-like growth factor-binding protein-1 transgenic male mice. 1472 51

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

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

The present study investigates the testicular and adrenocortical activities under different doses and durations of chromium (Cr) exposure and their interactions. Mature male Sprague Dawley rats were injected daily with three different doses (0.2, 0.4, and 0.6 mg/kg bw) of Cr salt (K(2)Cr(2)O(7)) intraperitonealy for 13 and 26 days, respectively. The medium (0.4 mg/kg bw/day) and higher dose (0.6 mg/kg bw/day) of Cr significantly (p<0.05) decrease accessory sex organs weight, testicular Delta(5)3beta-hydroxysteroid dehydrogenase (HSD) and 17beta-HSD activities, epididymal sperm count, effective spermatid degeneration, serum testosterone, LH level, testicular catalase and superoxide dismutase (SOD) activities while testicular lipid peroxidation, serum FSH, corticosterone level, adrenal weight and adrenal Delta(5)3beta-HSD activity increased significantly than that of control and lower dose (0.2 mg/kg bw/day) Cr exposed animals. Testicular histoarchitechture shows deterioration after critical dose (0.4 mg/kg bw/day) and duration (26 days) of Cr exposure. Cr induced alterations on testicular and adrenocortical activities are dose and duration dependent. Adrecortical hyperactivity accompanied by testicular oxidative stress might have a crucial role for Cr induced male reproductive impairment.
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PMID:Chromium induced testicular impairment in relation to adrenocortical activities in adult albino rats. 1782 70

To investigate the ameliorative potential of sodium selenite and zinc sulfate on intensive-swimming-induced testicular disorders, 48 Wistar male rats (age, 4 months; mass, 146.2 +/- 3.6 g) were randomly divided into 4 groups: the unexercised-control group (n = 12); the exercised group (n = 12); the control supplemented group (n = 12); and the exercised supplemented group (n = 12). For 10 weeks, the exercised rats underwent a protocol that consisted of 4 h.d-1 swimming, for 6 d.week-1; the control rats did not exercise. For 10 weeks, both the supplemented groups received an oral daily dose of a combination of sodium selenite and zinc sulfate (6 and 3 mg.kg body mass-1, respectively). After 10 weeks, a significant reduction (p < 0.05) was seen in rats in the exercised group, compared with rats in both control groups, in paired testicular masses; in epididymal sperm count; in testicular Delta5, 3beta-hydroxysteroid dehydrogenase (HSD) and 17beta-HSD; in plasma levels of testosterone, luteinizing hormone, follicle-stimulating hormone, and prolactin; in the numbers of preleptotine spermatocytes, midpachytene spermatocytes, and stage 7 spermatids of the stage VII seminiferous epithelium cycle; and in fertility performance. As well, a significant increase (p < 0.05) was seen in the exercised group, compared with both control groups, in plasma corticosterone levels and in testicular content of malondialdehyde and catalase activity. At the same time, there was a significant reduction (p < 0.05) in the exercised group, compared with both control groups, in plasma concentrations of zinc and selenium; in the testicular content of glutathione (GSH), the glutathione and glutathione disulphide (GSSG) ratio, ascorbic acid, and alpha-tocopherol; and in testicular activities of superoxide dismutase, glutathione-peroxidase, and glutathione-S-transferase in the testes. No significant changes were seen in the number of spermatogonia-A from the stage VII seminiferous epithelium cycle or the testicular content of GSSG among the groups. Sodium selenite and zinc sulfate supplementation significantly protected against exercise-induced testicular gamatogenic and spermatogenic disorders, prevented testicular oxidative stress, and increased antioxidant status. It can be concluded that intensive-swimming-induced oxidative stress causes dysfunctions in the male reproductive system, which can be protected by the coadministration of sodium selenite and zinc sulfate.
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PMID:Protective effect of sodium selenite and zinc sulfate on intensive swimming-induced testicular gamatogenic and steroidogenic disorders in mature male rats. 1892 65

In the adult rat, the superior spermatic nerve (SSN) and inferior spermatic nerve (ISN) are involved in regulating testosterone secretion and spermatogenesis, in addition to endocrine control mechanisms. However, there are currently few data on how the testis nerve supply regulates testicular development and related mechanisms. The present study was thus designed to investigate the regulating effects of testis nerve supply to testicular maturation, spermatogenesis and the involved mechanisms from prepuberty to adulthood in rats. We transected the SSNs and ISNs of rats on postnatal day (PD) 30 and then analyzed changes in testicular morphology and cauda epididymal sperm content, cell proliferation and apoptosis and primary spermatocyte meiosis on PD60 and PD90. The results demonstrated that testicular denervation significantly reduced testis mass, cauda epididymal sperm counts and serum testosterone concentrations. Proliferating cell nuclear antigen (PCNA) and cleaved caspase-3 immunohistochemistry staining proved that the denervation had no influence on the proliferation of spermatogonia and primary spermatocytes, but obviously promoted the apoptosis of round spermatids and Leydig cells. It is novel that denervation reduced the meiotic activation of zygotene and pachytene spermatocytes through the expression of synaptonemal complex protein 3 (SCP3)-a marker of meiosis. In addition, RT-PCR showed that testis denervation significantly decreased testis 3beta-hydroxysteroid dehydrogenase 1 (3beta-HSD1) and luteinizing hormone receptor (LHR) mRNA levels, but had no obvious influence on testis follicle stimulating hormone receptor (FSHR) mRNA expression. These results suggest that the testicular nerve supply plays an important role in supporting seminiferous tubule development and spermatogenesis from prepuberty to adulthood.
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PMID:Testicular denervation in prepuberty rat inhibits seminiferous tubule development and spermatogenesis. 2042 80


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