Cellular and molecular oxidative stress-related effects in uterine myometrial and trophoblast-decidual tissues after perigestational alcohol intake up to early mouse organogenesis

VENTUREIRA, MARTÍN RICARDO; COLL, TAMARA ANAHÍ; VENTUREIRA, MARTÍN RICARDO; COLL, TAMARA ANAHÍ; CEBRAL, ELISA; PÉREZ-TITO, LETICIA GABRIELA; CEBRAL, ELISA; PÉREZ-TITO, LETICIA GABRIELA; RÍOS DE MOLINA, MARÍA DEL CARMEN; CHAUFAN, GABRIELA; RÍOS DE MOLINA, MARÍA DEL CARMEN; CHAUFAN, GABRIELA

MOLECULAR AND CELLULAR BIOCHEMISTRY

SPRINGER

Año: 2017 vol. 440 p. 89 - 104

0300-8177

The placenta plays a major role in embryo-fetal defects and intrauterine growth retardation after maternal alcohol consumption. Our aims were to determine the oxidative status and cellular and molecular oxidative stress effects on uterine myometrium and trophoblast-decidual tissue following perigestational alcohol intake at early organogenesis. CF-1 female mice were administered with 10% alcohol in drinking water for 17 days prior to and up to day 10 of gestation. Control females received ethanolfree water. Treated mice had smaller implantation sites compared to controls (p 0.05), diminished maternal vascular lumen, and irregular/discontinuous endothelium of decidual vessels. The trophoblast giant cell layer was disorganized and presented increased abnormal nuclear frequency. The myometrium of treated females had reduced nitrite content, increased superoxide dismutase activity, and reduced glutathione (GSH) content (p�.05). However, the trophoblast-decidual tissue of treated femaleshad increased nitrite content (p 0.05), increased GSH level (p 0.001), increased thiobarbituric acid-reactive substance concentration (p�.001), higher 3-nitrotyrosine immunoreaction, and increased apoptotic index (p�.05) compared to controls. In summary, perigestational alcohol ingestion at organogenesis induced oxidative stress in the myometrium and trophoblast-decidual tissue, mainly affecting cells and macromolecules of trophoblast and decidual tissues around early organogenesis, in CF-1 mouse, and suggests that oxidative-induced abnormal early placental formation probably leads to risk of prematurity and fetal growth impairment at term.