Effects of Hypoxia on Testosterone Release in Rat Leydig cells

  • Hwang G
  • Jian C
  • Chen T
 et al. 
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Abstract

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%O2 + 88%N2, 1.5 l/ml) for 8 h daily for 4 days. Normoxic rats were used as control. In an in vivo experiment, hypoxic and normoxic rats were sacrificed and the blood samples were 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(-)5M), and NAADP (calcium signaling messenger causing release of calcium from intracellular stores, 10(-6)10(-4)M). The concentrations of testosterone in plasma and media were measured by radioimmunoassay (RIA). 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 17beta-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 Key words: Hypoxia, Testosterone, Leydig cell

Author-supplied keywords

  • Calcium
  • Calcium Signaling
  • Forskolin
  • In Vitro
  • Male
  • Nimodipine
  • Progesterone
  • Radioimmunoassay
  • Rats
  • Testosterone
  • biosynthesis
  • blood
  • secretion

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Authors

  • G S Hwang

  • C Y Jian

  • T J Chen

  • S T Chen

  • S W Wang

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