The Production of hydrogen Sulphide and the Effects of Nitric Oxide (NO) and Low Oxygen Conditions in Intrauterine Tissues in Rats

Document Type : Original Article

Authors

1 Biochemistry Dept. Faculty ofMedicine, Minia University

2 Obstetric and Gyncology Dept. Zagazig University

3 Biochemistry Dept. Faculty of Vet. Medicine, Zagazig University

Abstract

Hydrogen sulphide (H2S) is a gas signaling molecule which is produced
endogenously from L-cysteine via the enzymes cystathionine beta-synthase (CBS) and
cystathionine gamma-lyase (CSE). H2S may mediate hypoxic responses in vascular
smooth muscle. H2S also appears to be a signaling molecule in mammalian non-vascular smooth muscle. Hypoxia is associated with pre-eclampsia where poor
placental function can reduce the supply of oxygen and nutrients to the fetus resulting
in intrauterine growth restriction (IUGR) and other placental dysfunctions. Hypoxia
can also bring about other pre-eclamptic features such as the release of pro-inflammatory cytokines and oxidative stress.Hypoxic conditions can also reduce the
uteroplacental perfusion, which may lead to inflammatory conditions i.e. oxidative
stress. However, there are no reports to date on the production of H2S in reproductive
tissues and 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. We investigated the endogenous production of H2S in
rat intrauterine tissues and the effectof NO and low oxygen condition on H2S
production in intrauterine tissues. The production of H2S in rat intrauterine tissues
was measured in vitro using a standard technique. The expression of CBS and CSE
was also investigated in rat 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. The order of H2S production rates for rat
tissues were: liver (488±28.9 nM/min/g) > uterus (310±36.7 nM/min/g) > fetal
membranes (88.2±3.8 nM/min/g)> placenta (42.7± 6.8 nM/min/g). Under the effect of
NO donor, NO significantly increased H2S production in rat fetal membranes only
(from 88.2±3.8 nM/min/g to 103.2±7.4 nM/min/g). Under low oxygen conditions,
production of H2S was significantly increased compared to room air oxygen
conditions for rat liver (from 422±31.6 nM/min/g to 583±38.7 nM/min/g), uterus
(from 328±11.8 nM/min/g to 5913±21.8 nM/min/g) and fetal membranes (from
78.2±9.1 to 189±17.1) , but not rat placenta. Western blotting detected the expression
of CBS and CSE in all rat intrauterine tissues. Rat intrauterine tissues produce H2S in
vitro possibly via CBS and CSE enzymes.