Effects of hypoxia on testosterone release in rat Leydig cells.

  • Hwang G
  • Chen S
  • Chen T
 et al. 
  • 13


    Mendeley users who have this article in their library.
  • N/A


    Citations of this article.


The aim of this study was to explore the effect and action mechanisms of intermittent hypoxia on the production of testosterone both in vivo and in vitro. Male rats were housed in a hypoxic chamber (12% O(2) + 88% N(2), 1.5 l/ml) 8 h/day for 4 days. Normoxic rats were used as control. In an in vivo experiment, hypoxic and normoxic rats were euthanized and the blood samples collected. In the in vitro experiment, the enzymatically dispersed rat Leydig cells were prepared and challenged with forskolin (an adenylyl cyclase activator, 10(-4) M), 8-Br-cAMP (a membrane-permeable analog of cAMP, 10(-4) M), hCG (0.05 IU), the precursors of the biosynthesis testosterone, including 25-OH-C (10(-5) M), pregnenolone (10(-7) M), progesterone (10(-7) M), 17-OH-progesterone (10(-7) M), and androstendione (10(-7)-10(-5) M), nifedipine (L-type Ca(2+) channel blocker, 10(-6)-10(-4) M), nimodipine (L-type Ca(2+) channel blocker, 10(-5) M), tetrandrine (L-type Ca(2+) channel blocker, 10(-5) M), and NAADP (calcium-signaling messenger causing release of calcium from intracellular stores, 10(-6)-10(-4) M). The concentrations of testosterone in plasma and medium were measured by radioimmunoassay. The level of plasma testosterone in hypoxic rats was higher than that in normoxic rats. Enhanced testosterone production was observed in rat Leydig cells treated with hCG, 8-Br-cAMP, or forskolin in both normoxic and hypoxic conditions. Intermittent hypoxia resulted in a further increase of testosterone production in response to the testosterone precursors. The activity of 17β-hydroxysteroid dehydrogenase was stimulated by the treatment of intermittent hypoxia in vitro. The intermittent hypoxia-induced higher production of testosterone was accompanied with the influx of calcium via L-type calcium channel and the increase of intracellular calcium via the mechanism of calcium mobilization. These results suggested that the intermittent hypoxia stimulated the secretion of testosterone at least in part via stimulatory actions on the activities of adenylyl cyclase, cAMP, L-type calcium channel, and steroidogenic enzymes.

Author-supplied keywords

  • 17-Hydroxysteroid Dehydrogenases
  • 17-Hydroxysteroid Dehydrogenases: metabolism
  • 8-Bromo Cyclic Adenosine Monophosphate
  • 8-Bromo Cyclic Adenosine Monophosphate: pharmacolo
  • Animals
  • Calcium Channel Blockers
  • Calcium Channel Blockers: pharmacology
  • Calcium Channels, L-Type
  • Calcium Channels, L-Type: metabolism
  • Cell Hypoxia
  • Cell Hypoxia: physiology
  • Cell Separation
  • Cholesterol Side-Chain Cleavage Enzyme
  • Cholesterol Side-Chain Cleavage Enzyme: metabolism
  • Chorionic Gonadotropin
  • Chorionic Gonadotropin: pharmacology
  • Cyclic AMP
  • Cyclic AMP: metabolism
  • Forskolin
  • Forskolin: pharmacology
  • Gonadotropins
  • Gonadotropins: metabolism
  • Leydig Cells
  • Leydig Cells: metabolism
  • Male
  • NADP
  • NADP: analogs & derivatives
  • NADP: pharmacology
  • Radioimmunoassay
  • Rats
  • Rats, Sprague-Dawley
  • Testosterone
  • Testosterone: blood
  • Testosterone: metabolism

Get free article suggestions today

Mendeley saves you time finding and organizing research

Sign up here
Already have an account ?Sign in

Find this document


  • Guey-Shyang Hwang

  • Szu-Tah Chen

  • Te-Jung Chen

  • Shyi-Wu Wang

Cite this document

Choose a citation style from the tabs below

Save time finding and organizing research with Mendeley

Sign up for free