posted on 2010-06-23, 09:12authored byPushpa Patel, Manu Vatish, John Heptinstall, Rui Wang, Ray J. Carson
Background: Hydrogen sulphide is a gas signalling molecule which is produced endogenously from
L-cysteine via the enzymes cystathionine beta-synthase (CBS) and cystathionine gamma-lyase
(CSE). The possible role of hydrogen sulphide in reproduction has not yet been fully investigated.
It has been previously demonstrated that hydrogen sulphide relaxes uterine smooth muscle in
vitro. The aim of the present study was to investigate the endogenous production of hydrogen
sulphide in rat and human intrauterine tissues in vitro.
Methods: The production of hydrogen sulphide in rat and human intrauterine tissues was
measured in vitro using a standard technique. The expression of CBS and CSE was also investigated
in rat and human intrauterine tissues via Western blotting. Furthermore, the effects of nitric oxide
(NO) and low oxygen conditions on the production rates of hydrogen sulphide were investigated.
Results: The order of hydrogen sulphide production rates (mean +/- SD, n = 4) for rat tissues
were: liver (777 +/- 163 nM/min/g) > uterus (168 +/- 100 nM/min/g) > fetal membranes (22.3 +/-
15.0 nM/min/g) > placenta (11.1 +/- 4.7 nM/min/g), compared to human placenta (200 +/- 102 nM/
min/g). NO significantly increased hydrogen sulphide production in rat fetal membranes (P < 0.05).
Under low oxygen conditions the production of hydrogen sulphide was significantly elevated in
human placenta, rat liver, uterus and fetal membranes (P < 0.05). Western blotting (n = 4) detected
the expression of CBS and CSE in all rat intrauterine tissues, and in human placenta, myometrium,
amnion and chorion.
Conclusion: Rat and human intrauterine tissues produce hydrogen sulphide in vitro possibly via
CBS and CSE enzymes. NO increased the production of hydrogen sulphide in rat fetal membranes.
The augmentation of hydrogen sulphide production in human intrauterine tissues in a low oxygen
environment could have a role in pathophysiology of pregnancy.
History
Citation
Reproductive biology and endocrinology, 2009, 7(10).