title: Binge drinking during adolescence disrupts Se homeostasis and its main hepatic selenoprotein expression.
abstract: BACKGROUND
  Binge drinking (BD) is the most common ethanol (EtOH) intake consumption model among teenagers, but little is known about its effects on the liver. During its hepatic metabolism, acute alcohol exposure produces a great amount of reactive oxygen species which contributes to alcohol-induced liver injury. Selenium (Se) plays a key role in antioxidant defense as it forms part of selenoproteins, such as the antioxidant glutathione peroxidases (GPxs) or the selenoprotein P (SelP), synthesized mainly in liver. Chronic EtOH consumption decreases both Se deposits and this tissue's antioxidant activity.
  
  
  METHODS
  Two BD administration routes (oral and intraperitoneal) were used in adolescent rats to analyze Se homeostasis; the main hepatic selenoproteins' expression: GPx1, GPx4, and SelP, and their biological roles related to oxidation. Their relationship with inflammatory processes was also determined by analyzing the expression of the transcriptional factor nuclear factor-kappa beta (NF-κB).
  
  
  RESULTS
  It has been demonstrated for the first time that BD in adolescents alters Se homeostasis regardless of the administration route employed, despite the fact that the BD oral group ingested less Se in diet. This decrease of Se in serum and liver is directly related to a decrease in serum GPx3 and hepatic GPx1 activity, contributing to the oxidative imbalance found. The depletion of Se detected in liver affects GPx1 expression and, surprisingly, GPx4 expression. This could be related to the lower expression of the transcriptional factor NF-κB in the liver, a key player in the regulation of inflammatory processes.
  
  
  CONCLUSIONS
  Due to the above, and to find whether a Se supplementation therapy improves these situations, it would be interesting to explore in more depth the relationship between Se, the high oxidation found, and the depressed immune response reported in BD adolescents.
authors: Department of Physiology, Faculty of Pharmacy, Seville University, Seville, Spain.
authors: María Luisa
authors: ML
authors: Ojeda
authors: Rui Manuel
authors: RM
authors: Rua
authors: María Luisa
authors: ML
authors: Murillo
authors: Olimpia
authors: O
authors: Carreras
authors: Fátima
authors: F
authors: Nogales
mesh_terms: D000284:Administration, Oral; D000367:Age Factors; D000818:Animals; D063425:Binge Drinking / Q000378:metabolism*; D000431:Ethanol / Q000008:administration & dosage* / Q000494:pharmacology*; D005243:Feces / Q000737:chemistry; D005979:Glutathione Peroxidase / Q000096:biosynthesis / Q000097:blood; D006706:Homeostasis / Q000187:drug effects*; D007263:Infusions, Parenteral; D008099:Liver / Q000378:metabolism*; D008297:Male; D016328:NF-kappa B / Q000096:biosynthesis; D018384:Oxidative Stress / Q000187:drug effects; D000080662:Phospholipid Hydroperoxide Glutathione Peroxidase; D051381:Rats; D012643:Selenium / Q000032:analysis / Q000097:blood / Q000378:metabolism* / Q000652:urine; D051149:Selenoprotein P / Q000096:biosynthesis*; D000094765:Glutathione Peroxidase GPX1
chemical_list: D016328:NF-kappa B; D051149:Selenoprotein P; D000431:Ethanol; C505355:GPX3 protein, rat; D000080662:Phospholipid Hydroperoxide Glutathione Peroxidase; D005979:Glutathione Peroxidase; C523860:glutathione peroxidase 4, rat; D012643:Selenium; D000094765:Glutathione Peroxidase GPX1; C000722069:Gpx1 protein, rat
keywords: Adolescence; Binge Drinking; GPx Activity; Liver; NF-κB; Selenoproteins