Please use this identifier to cite or link to this item: http://hdl.handle.net/10637/14544

Prevention of Teratogenesis in Pregnancies of Obese Rats by Vitamin E Supplementation

Title: Prevention of Teratogenesis in Pregnancies of Obese Rats by Vitamin E Supplementation
Authors : Alcalá Díaz-Mor, Martín
Bolado García, Victoria Eugenia
Sánchez Vera, Isabel
Clapés, Sonia
Dasí, Francisco
Sáez, Guillermo
Carrera Puerta, Esther
Álvarez Gallego, Fabiola
Loeken, Mary R.
Viana Arribas, Marta
Keywords: Embryo malformationTeratogenesisOxidative stressGlutathioneVitamin EObesity
Publisher: MDPI
Citation: Alcala, M.; Bolado, V.E.; Sánchez-Vera, I.; Clapés, S.; Dasí, F.; Sáez, G.; Carrera, E.; Alvarez-Gallego, F.; Loeken, M.R.; Viana, M. Prevention of Teratogenesis in Pregnancies of Obese Rats by Vitamin E Supplementation. Antioxidants 2021, 10, 1173. https://doi.org/10.3390/ antiox10081173
Abstract: Congenital malformations are a common adverse outcome in pregnancies complicated by pregestational obesity, although the underlying mechanisms are still unrevealed. Our aim was to study the effect of oxidative stress in obesity-induced teratogenesis. Wistar rats were fed a high-fat diet for 13 weeks, with (OE group) or without (O group) vitamin E supplementation. Then, rats were mated and sacrificed at day 11.5 of gestation. Embryos from O dams presented a 25.9 3.5% rate of malformations (vs. 8.7 3.4% in C rats), which was reduced in the OE group (11.5 2.3%). Pregestational obesity induced hepatic protein and DNA oxidation and a decline in antioxidant enzymes. Importantly, glutathione content was also decreased, limiting the availability of this antioxidant in the embryos. Vitamin E supplementation efficiently maintained glutathione levels in the obese mothers, which could be used in their embryos to prevent oxidation-induced malformations. To test the effect of decreasing glutathione levels alone in a cell culture model of neuroepithelium, murine embryonic stem cells (ESC) were induced to form neuronal precursors and glutathione synthesis was inhibited with the gamma–glutamylcysteine synthesis inhibitor, buthionine sulfoximine (BSO). BSO inhibited the expression of Pax3, a gene required for neural tube closure that is also inhibited by oxidative stress. Taken together, our data indicate that obesity causes malformations through the depletion of maternal glutathione, thereby decreasing glutathione-dependent free radical scavenging in embryos, which can be prevented by vitamin E supplementation.
URI: http://hdl.handle.net/10637/14544
Rights : http://creativecommons.org/licenses/by-nc-nd/4.0/deed.es
openAccess
Issue Date: 23-Jul-2021
Center : Universidad San Pablo-CEU
Appears in Collections:Facultad de Farmacia





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