Study of Molecular Mechanisms involved in the ethiology of embryo.fetal losses associated to immunological and hematological processes

GUTIERREZ, GABRIELA; DUBINSKY V; JUNOVICH G; PASQUALINI S.; GENTILE TERESA

Sgo de Chile, Chile

Congreso; II Latin-American Symposium on feto-maternal interaction and Placenta; 2006

Placenta Association of the Americas. International Federation of Placenta Associations

During last years, Immunology and Hematology has been approached to Reproductive Medicine in other to explain mechanisms implicated in endothelial injury causing abortion. Current research has been focused on inflammatory process leading to coagulation involved in causation of fetal death by ischemia. Cytokine provoking vascular damage rather than direct action on trophoblast may explain abortion of genetically normal embryos. We have been demonstrated that inoculation of rIL-6 or low-molecular weight heparin was able to diminish abortion rate in a murine model. In the present work, the hypothesis that antioxidant supplementation is able to counteract toxic effect of oxidative stress on pregnancy has been postulated. We studied the effect of Vitamin E oral supplementation of CBA/J x DBA/2 pregnant females on abortion rate (IR), TNF-a, IL-6, IL-10 placental levels, as well as placental NO production. Methods: Different doses of natural Vitamin E were administered orally on CBA/J x DBA/2 females on days 0.5 up to 12.5 of pregnancy. Feto-Placental units were scored at 14.5 days of pregnancy and IR was scored. Cytokine concentration was determined by ELISA. Placental NO levels were measured by colorimetric procedure described by Griess. Results: 0,5mg/g of Vitamin E decreases IR up to 93% (p<0,0001) whereas increases placental IL-6 levels up to 23.6pg/mL with regards to 10.9 pg/mL of non-treated animals (p=0,0004). No differences were found on IL-10, TNF-a or NO levels. Conclusions: Vitamin E is able not only to prevent fetal wastage but also to modulate anti-inflammatory IL-6 placental levels. This protective effect seems to be independent of the antioxidant function. Supported by B 094 UBA 2004-2007.