PMID- 10588814
OWN - NLM
STAT- MEDLINE
DCOM- 20000214
LR  - 20190709
IS  - 0022-0795 (Print)
IS  - 0022-0795 (Linking)
VI  - 163
IP  - 3
DP  - 1999 Dec
TI  - Involvement of inducible nitric oxide synthase in stress-impaired testicular 
      steroidogenesis.
PG  - 409-16
AB  - The immobilization stress induces an acute inhibition of testicular 
      steroidogenesis that is mediated by the nitric oxide (NO) signaling pathway. Here 
      we compared the effects of 2-h immobilization stress on in vivo and in vitro rat 
      steroidogenesis at two time points, 0 h and 6 h after the end of the stress 
      session. As expected, serum androgens and human chorionic gonadotropin 
      (hCG)-stimulated progesterone and testosterone production by testicular tissue 
      were inhibited at 0 h, and also at the 6-h time point. Both the acute and 
      sustained inhibitions of in vitro steroidogenesis were accompanied by a 
      significant increase in nitrite, a stable oxidation product of NO. To clarify 
      which subtype of NO synthase (NOS) (constitutive (cNOS) or inducible (iNOS)) 
      participates in down-regulation of testicular steroidogenesis, aminoguanidine 
      hydrochloride (AG), a selective iNOS inhibitor, was employed. Intratesticular 
      injection of AG prevented the sustained, but not the acute, stress-induced 
      decrease in serum testosterone. When added in vitro, it also prevented the 
      sustained decrease in steroid production and increase in nitrite production by 
      testicular tissue, both in a dose-dependent manner and with EC microM. 
      Furthermore, AG added in vivo and in vitro effectively blocked the sustained 
      decrease in 3beta-hydroxysteroid dehydrogenase (3betaHSD) and 
      17alpha-hydroxylase/C17-20 lyase (P450c17) activities. In all concentrations 
      employed, AG did not affect serum androgens and in vitro steroid and nitrite 
      production in unstressed animals. These results indicate that the NO signaling 
      pathway participates in acute and sustained stress-induced down-regulation of 
      testicular steroidogenesis, presumably through its direct action on 3betaHSD and 
      P450c17. The acute NO production is controlled by cNOS and the sustained 
      production of this messenger is controlled by iNOS.
FAU - Kostic, T S
AU  - Kostic TS
AD  - Institute of Biology, Faculty of Sciences, University of Novi Sad, 21000 Novi 
      Sad, Yugoslavia. stankosf@helix.nih.gov
FAU - Andric, S A
AU  - Andric SA
FAU - Maric, D
AU  - Maric D
FAU - Stojilkovic, S S
AU  - Stojilkovic SS
FAU - Kovacevic, R
AU  - Kovacevic R
LA  - eng
PT  - Journal Article
PL  - England
TA  - J Endocrinol
JT  - The Journal of endocrinology
JID - 0375363
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Guanidines)
RN  - 0 (Nitrites)
RN  - 08J2K08A3Y (Dihydrotestosterone)
RN  - 3XMK78S47O (Testosterone)
RN  - 4G7DS2Q64Y (Progesterone)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type II)
RN  - EC 1.14.13.39 (Nitric Oxide Synthase Type III)
RN  - EC 1.14.13.39 (Nos2 protein, rat)
RN  - EC 1.14.13.39 (Nos3 protein, rat)
RN  - SCQ4EZQ113 (pimagedine)
SB  - IM
MH  - Animals
MH  - Dihydrotestosterone/metabolism
MH  - Enzyme Inhibitors/pharmacology
MH  - Guanidines/pharmacology
MH  - Male
MH  - Nitric Oxide Synthase/antagonists & inhibitors/*metabolism
MH  - Nitric Oxide Synthase Type II
MH  - Nitric Oxide Synthase Type III
MH  - Nitrites/metabolism
MH  - Progesterone/metabolism
MH  - Rats
MH  - Rats, Wistar
MH  - Restraint, Physical
MH  - *Signal Transduction
MH  - Statistics, Nonparametric
MH  - Stress, Psychological/*metabolism
MH  - Testis/*drug effects/metabolism
MH  - Testosterone/*metabolism
MH  - Time Factors
EDAT- 1999/12/10 09:00
MHDA- 2000/02/19 09:00
CRDT- 1999/12/10 09:00
PHST- 1999/12/10 09:00 [pubmed]
PHST- 2000/02/19 09:00 [medline]
PHST- 1999/12/10 09:00 [entrez]
AID - JOE03378 [pii]
AID - 10.1677/joe.0.1630409 [doi]
PST - ppublish
SO  - J Endocrinol. 1999 Dec;163(3):409-16. doi: 10.1677/joe.0.1630409.