CONICET | Buscador de Institutos y Recursos Humanos

Maternal diabetes generates a pro-inflammatory/pro-oxidant environment, which leads to embryo alterations. The mechanisms involved in these alterations and their prevention are not completely clarified.In this work, we aimed to evaluate the effect of idebenone, a structural analog of coenzyme Q10, on markers of pro-inflammatory/pro-oxidant processes, on the expression of genes involved in mitochondrial biogenesis and function, and on the apoptotic rate in embryos from control and mild diabetic rats. Control and diabetic pregnant rats were orally treated with idebenone until day 10.5 of gestation when the embryos were explanted. Embryos from mild diabetic rats showed increased levels of nitrated proteins, 4-hydroxynonenal, and matrix metalloproteinase 9 which were prevented by idebenone administration. We also found a decreased embryonic expression of cytochrome c oxidase and reduced mRNA levels of peroxisome proliferator activated receptor-gamma coactivator-1-alpha and nuclear respiratory factor-1, both of which were prevented by idebenone administration to the diabetic pregnant rats.Embryos from mild diabetic rats also showed an increased apoptotic rate, which was diminished by idebenone treatment.We conclude that maternal idebenone treatment ameliorates altered parameters related to the pro-oxidant/pro-inflammatory environment foundin embryos from mild diabetic rats, suggesting a putative treatment to prevent diabetes-induced embryo alterations.