Title page for ETD etd-06062008-170416

Type of Document Dissertation
Author Kukucka, Mark A
URN etd-06062008-170416
Title Mechanisms by which hypoxia augments Leydig cell viability and differentiated cell function in vitro
Degree PhD
Department Veterinary Medical Sciences
Advisory Committee
Advisor Name Title
Misra, Hara P. Committee Chair
Caceci, Thomas Committee Member
Gwazdauskas, Francis C. Committee Member
Keith, James C. Jr Committee Member
Pfeiffer, Carl J. Committee Member
  • oxytocin
  • antioxidant
  • free radical toxicology
  • Leydig cells
Date of Defense 1993-04-18
Availability restricted
The 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.

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