Nitric oxide synthase distribution and nitric oxide levels in murine myometrium and decidua after maternal alcohol intake

COLL ,T.A.; HOFMANN ORSETTI C.; SOBARZO C; FONTANA V; CEBRAL E

Cordoba

Congreso; Latin American Symposium on Maternal-Fetal Interaction and Placenta: Basic and Clinic Research (SLIMP; 2007

SLIMP

We had studied the prostaglandin (PG) synthesis and its modulation by nitric oxide (NO) in implantation site (IS) after alcohol intake. To evaluate the perigestational alcohol effects on placentation and regulatory factors, we assessed the altered IS % and analyzed the decidual (De) and myometrial (M) endothelial, inducible and neuronal nitric oxide synthase (eNOS, iNOS, nNOS) distribution, the NO production and its regulation by PGs. Female mice were treated with 10% ethanol for 15 days before and during gestation up to day 10 of pregnancy (T). Controls (C) received water. The majority of T-IS had low De-decidualization, reduced villi growth, collapsed intervillous space and abnormal trophoblast giant cells (TGC). The % of eNOS immunoreactive T-IS was reduced vs C-IS. A very weak eNOS labeling in De, TGC, villi “core” and mononuclear trofoblast which had delocalized immunostain near to the apical cell region, was detected in T-IS. Negative eNOS reactivity appeared in T-IS without villi or collapsed spaces. Differential alterations in nNOS and iNOS immunostain were also seen. T-M had reduced NOS immunoreaction. Endogenous nitrite (Ns) production (Griess) and NADPH-diaphorase stain was similar in C and T-De/M. In-vitro Ns levels were lower in T vs C-tissues, and meloxicam or indomethacin incubation reduced Ns in C-De and/or M. The PGF2 significantly increased the Ns levels of De and M from C and T.The perigestational alcohol induced-defective placentation resulted associated with abnormal NOS villi distribution, partial NOS activity inhibition and dysregulation of PG-NO pathway.