The role of Folic acid and Selenium against oxidative ethanol damage in early life programming: a review

Several disorders in children, called Fetal Alcohol Spectrum Disorders (FASD), occur as result of alcohol consumption during pregnancy and lactation. They appear, at least in part, to be related to the oxidative stress that this drug generates. Ethanol metabolism generates reactive oxygen species and causes a depletion of the antioxidant molecule glutathione (GSH) leading to oxidative stress and lipid and protein damage which are related to growth retardation and neurotoxicity, increasing the incidence of FASD. Furthermore, prenatal and postnatal ethanol exposure in dams, as well as increasing oxidation in offspring, causes malnutrition of several micronutrients such as the antioxidant Folic acid and Selenium (Se), affecting their metabolism and body distribution. Despite alcohol abstinence being the only way to prevent FASD, it is possible to reduce its harmful effects with a maternal dietary antioxidant therapy. In this review Folic acid and Se have been chosen to be analyzed as antioxidant intervention systems related to FASD since, like ethanol, they act on the methionine metabolism cycle, being related to the endogenous antioxidants glutathione (GSH) and glutathione peroxidase. Moreover, several birth defects are related with a poor folate and Se status.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author