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)

The present study was undertaken to evaluate the endocrinologic and spermatogenic effects of carbon disulfide (CS2) exposure in the rat. Adult, male rats were exposed to either 600 ppm CS2 or filtered air for 6 hr/day for 5 days/week for 10 weeks. One week prior to exposure and then at Weeks 1, 4, 7, and 10, males were placed with ovariectomized, hormonally primed females, and copulatory behaviors were scored. Fifteen minutes postcopulation, the female was killed and the ejaculate was recovered from the excised uterine tract along with the semen plug. Sperm counts, sperm motility, and morphology were determined. A blood sample was obtained for analyses of testosterone, follicle-stimulating (FSH), and luteinizing hormone (LH). At the end of the 10th week, five animals in each group were challenged with either human chorionic gonadotropin (HCG, 50 IU/animal, iv) or gonadotropin-releasing hormone (GnRH, 100 ng/animal, iv), and the testosterone or gonadotropin responses were monitored over time. Animals were subsequently killed with one epididymis and testis processed for histology and a sperm count determined from the other epididymis. Analysis revealed that CS2 exposure produced significant alterations in copulatory behavior and a decrease in ejaculated sperm counts by the fourth and seventh weeks of exposure, respectively. No endocrinologic alterations were observed. Moreover, caudal epididymal sperm counts were not depressed and the testes appeared histologically normal. These data suggest that CS2 does not exert a direct effect on the testes, but rather may interfere with the processes regulating sperm transport and ejaculation.
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PMID:An evaluation of the copulatory, endocrinologic, and spermatotoxic effects of carbon disulfide in the rat. 642 68

Two experimental protocols were employed to determine the effects of carbon disulfide (CS2) on the reproductive system of the male rat. In the first experiment, adult Long Evans hooded rats were exposed to 0, 350 or 600 ppm CS2 vapor for 10 weeks (5 h/day, 5 days/week). CS2 exposure caused no change in reproductive organ weights nor in plasma gonadotropin levels. However, animals exposed to 600 ppm CS2 had slightly lower epididymal sperm counts and significantly reduced plasma testosterone levels. In order to determine if monitoring hormone levels and sperm status in the same male over time might increase the sensitivity of detecting a toxic reaction, the second protocol was employed. Male rats were exposed to 0 or 600 ppm CS2. After 0, 1, 4, 7 and 10 weeks of exposure, males were observed for mating behavior, and ejaculated sperm count and plasma hormone levels were determined. Animals exposed to 600 ppm CS2 had significantly shorter times to mount and to ejaculate and decreased ejaculated sperm counts. Plasma gonadotropin levels were similar in both groups while plasma testosterone levels were marginally depressed in CS2-exposed animals in the early weeks. These data indicate that CS2 is a toxin of the male reproductive system resulting in abnormal coital behavior and decreased sperm counts. The second experimental protocol proves to be a sensitive method for assessing adverse effects in the male reproductive system.
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PMID:The effects of carbon disulfide on the reproductive system of the male rat. 642 1

A molecular screen for a mouse homologue of a Drosophila carbohydrate binding protein, called Gliolectin, yielded a cDNA encoding mST3GalV/GM3 synthase (CMP-NeuAc: lactosylceramide alpha2, 3-sialyltransferase). By in situ hybridization and immunohistochemistry, mST3GalV exhibits differential expression in neural and non-neural tissues. Although expressed by all neurons in the central nervous system, neuronal populations that contribute their axons to myelinated efferent projections, such as cerebellar Purkinje cells and spinal motorneurons, demonstrate the highest ST3GalV expression. When stained with anti-mST3GalV antiserum (designated CS2), subpopulations of neurons display an elaborate Golgi apparatus, frequently extending into one or more dendritic processes. The extended spatial distribution of the neuronal Golgi apparatus, particularly in spinal motorneurons, allowed the confocal immunohistochemical colocalization of mST3GalV with markers for medial/trans-Golgi but not the cis-Golgi or trans-Golgi network, consistent with previous observations suggesting that ganglioside glycosyltransferases are enriched in late Golgi compartments. Among non-neural tissues, liver and testes demonstrate cell-type specific CS2 staining. In liver, endothelial cells lining a ring of sinusoids, concentric with the central vein, express mST3GalV. Kupffer cells are also stained with CS2 antiserum but hepatocyte expression is undetectable. In the seminiferous tubules of the testes, ST3GalV is found in somatic (Leydig, Sertoli) and early germline cells (spermatogonia and primary spermatocytes); the epididymal epithelium exhibits intense ST3GalV expression. Since GM3 is a precursor for the synthesis of a- and b-series gangliosides, the range of mST3GalV/GM3 synthase expression among various cell populations indicates that certain cell types possess greater reliance on ganglioside function than others.
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PMID:Molecular identification, tissue distribution and subcellular localization of mST3GalV/GM3 synthase. 1076 24