Mechanisms by which hypoxia augments Leydig cell viability and differentiated cell function in vitro

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dc.contributor.authorKukucka, Mark A.en
dc.contributor.committeechairMisra, Hara P.en
dc.contributor.committeememberCaceci, Thomasen
dc.contributor.committeememberGwazdauskas, Francis C.en
dc.contributor.committeememberPfeiffer, Carl J.en
dc.contributor.committeememberKeith, James C. Jr.en
dc.contributor.departmentVeterinary Medical Sciencesen
dc.date.accessioned2014-03-14T21:14:12Zen
dc.date.adate2008-06-06en
dc.date.available2014-03-14T21:14:12Zen
dc.date.issued1993-04-18en
dc.date.rdate2008-06-06en
dc.date.sdate2008-06-06en
dc.description.abstractThe 1980's heralded the discovery and identification of extra-pituitary sources of the neurohypophysial hormone oxytocin in non-neural tissues of several animal species. The presence, location and biosynthesis of significant amounts of oxytocin in the ovarian corpus luteum was followed by the immunocytochemical demonstration of an oxytocin-like peptide in the testicular interstitial cells. Leydig cells, which comprise up to 80% of the testicular intertubular cell population, are known to synthesize testosterone in situ. Indirect evidence indicated that an oxytocin-like peptide was also present in Leydig cells. The question arose whether this peptide was synthesized de novo by Leydig cells or was taken up and stored by the cells following biosynthesis at some other intra- and/or extra-gonadal source(s). Since luteinizing hormone (LH) and ascorbate are known to augment the production of oxytocin in ovarian granulosa cells, varying concentrations of these two stimulants were used to monitor the biosynthesis of oxytocin from isolated Leydig cells in culture.en
dc.description.degreePh. D.en
dc.format.extentxix, 171 leavesen
dc.format.mediumBTDen
dc.format.mimetypeapplication/pdfen
dc.identifier.otheretd-06062008-170416en
dc.identifier.sourceurlhttp://scholar.lib.vt.edu/theses/available/etd-06062008-170416/en
dc.identifier.urihttp://hdl.handle.net/10919/38407en
dc.language.isoenen
dc.publisherVirginia Techen
dc.relation.haspartLD5655.V856_1993.K858.pdfen
dc.relation.isformatofOCLC# 28529198en
dc.rightsIn Copyrighten
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en
dc.subjectantioxidanten
dc.subjectfree radical toxicologyen
dc.subject.lccLD5655.V856 1993.K858en
dc.subject.lcshCell differentiationen
dc.subject.lcshCellular control mechanismsen
dc.subject.lcshLeydig cellsen
dc.subject.lcshOxytocin -- Researchen
dc.titleMechanisms by which hypoxia augments Leydig cell viability and differentiated cell function in vitroen
dc.typeDissertationen
dc.type.dcmitypeTexten
thesis.degree.disciplineVeterinary Medical Sciencesen
thesis.degree.grantorVirginia Polytechnic Institute and State Universityen
thesis.degree.leveldoctoralen
thesis.degree.namePh. D.en

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