<b>Hepatic GPx1 and GIT1 Expression Altered by Ethanol Exposure During Third Trimester-Equivalent Development</b>

Ethanol (EtOH) exposure throughout gestation and breastfeeding periods leads to multiples adverse outcomes in the hepatic system. Under oxidative stress, alterations in liver are related to the inhibition of induced nitric oxide synthase activity in sinusoidal cells as a consequence of the G-protein-coupled receptor (GPCR)-kinase interacting (GIT1) low expression. Here, we hypothesized that both glutathione peroxidase 1 (GPx1) and GIT1 could be altered by EtOH exposure during the third trimester human equivalent development. Therefore, we ex-posed rats during the third trimester-equivalent [postnatal days (PD) 2-8] to moderate levels of maternal EtOH (20%). GPx1 and GIT1 expressions were detected by western blotting, antioxidant activity of GPx and concentration of hepatic carbonyl groups (PC) were determined by spectrophotometry. Serum biochemistry parameter, such as alanine aminotransferase (ALT), glucose (gluc), cholesterol (chol), and triglycerides (TG) were also measured. We found that ethanol de-creases both GIT1 and GPx1 selenoprotein expression, affecting the GPx antioxidant activity and conversely increasing the protein oxidation. These results demonstrate, for the first time that the GPx antioxidant system altered by EtOH exposure during the third trimester of development is related to a parallel decreased expression of the GIT1.