Ojeda María Luisa, Rua Rui Manuel, Murillo María Luisa, Carreras Olimpia, Nogales Fátima
Department of Physiology, Faculty of Pharmacy, Seville University, Seville, Spain.
Alcohol Clin Exp Res. 2015 May;39(5):818-26. doi: 10.1111/acer.12707. Epub 2015 Apr 10.
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.
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).
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.
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.
暴饮（BD）是青少年中最常见的乙醇（EtOH）摄入模式，但对其对肝脏的影响知之甚少。在肝脏代谢过程中，急性酒精暴露会产生大量活性氧，这会导致酒精性肝损伤。硒（Se）在抗氧化防御中起关键作用，因为它是硒蛋白的一部分，如主要在肝脏中合成的抗氧化谷胱甘肽过氧化物酶（GPxs）或硒蛋白P（SelP）。长期摄入EtOH会减少硒的沉积以及该组织的抗氧化活性。
在青春期大鼠中使用两种BD给药途径（口服和腹腔内）来分析硒稳态；主要肝脏硒蛋白的表达：GPx1、GPx4和SelP，以及它们与氧化相关的生物学作用。还通过分析转录因子核因子-κB（NF-κB）的表达来确定它们与炎症过程的关系。
首次证明，青少年中的BD会改变硒稳态，无论采用何种给药途径，尽管BD口服组饮食中摄入的硒较少。血清和肝脏中硒的减少与血清GPx3和肝脏GPx1活性的降低直接相关，导致发现的氧化失衡。肝脏中检测到的硒耗竭会影响GPx1的表达，令人惊讶的是，也会影响GPx4的表达。这可能与肝脏中转录因子NF-κB的较低表达有关，NF-κB是炎症过程调节中的关键参与者。
基于上述情况，为了探究补充硒疗法是否能改善这些情况，更深入地探索硒、BD青少年中发现的高氧化状态以及报道的免疫反应抑制之间的关系将是很有意义的。
