Hepatic GPx1 and GIT1 expression altered by ethanol exposure during third trimester-equivalent development [version 1; peer review: awaiting peer review]

• Published in: F1000 research Vol. 13; p. 1293
• Main Authors: JOTTY-Arroyo, KARICK, Díaz--Castillo, Albert, Gomez--Estrada, Harold, Pineda--Aleman, Rafael
• Format: Journal Article
• Language: English
• Published: 2024
• Subjects: Ethanol-exposed; GPx1-antioxidant; GIT1; Hepatic
• ISSN: 2046-1402; 2046-1402
• DOI: 10.12688/f1000research.155941.1

Background Ethanol (EtOH) exposure throughout gestation and breastfeeding leads to multiple adverse outcomes in the hepatic system. Under oxidative stress, alterations in the liver are related to the inhibition of induced nitric oxide synthase activity in sinusoidal cells as a consequence of low expression of G-protein-coupled receptor (GPCR)-kinase interacting (GIT1). Here, we hypothesized that both glutathione peroxidase 1 (GPx1) and GIT1 could be altered by EtOH exposure during the third trimester of human equivalent development. Methods We exposed rats during the third trimester equivalent [postnatal days (PD) 2-8] to moderate levels of maternal EtOH (20%). GPx1 and GIT1 expression was detected by western blotting, and the antioxidant activity of glutathione peroxidase GPx and the concentration of hepatic carbonyl groups (CG were determined by spectrophotometry. Serum biochemistry parameters such as alanine aminotransferase (ALT), glucose (gluc), cholesterol (chol), and triglycerides (TG) were also measured. Results We found that ethanol decreased both GIT1 and GPx1 selenoprotein expression, affecting GPx antioxidant activity and increasing protein oxidation. Conclusions 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 decrease in GIT1 expression [1].