Binge Drinking During Adolescence Disrupts Se Homeostasis and Its Main Hepatic Selenoprotein Expression

Ojeda, María Luisa; Rua, Rui Manuel; Murillo, María Luisa Ojeda; Carreras, Olimpia; Nogales, Fátima

doi:10.1111/acer.12707

Cited by 13 publications

(7 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, BD rats presented high ALT and AST serum values; this increase in transaminases indicates that hepatic damage is taking place [ 35 ]. The same results of transaminases and hepatic damage are described in clinical trials in adolescents exposed to intensive alcohol consumption [ 36 ] and in experimental BD-exposed animals [ 37 , 38 ]. When FA is supplemented, these values decrease, particularly ALT values.…”

Section: Discussionmentioning

confidence: 59%

Folic Acid Homeostasis and Its Pathways Related to Hepatic Oxidation in Adolescent Rats Exposed to Binge Drinking

et al. 2022

Self Cite

View full text Add to dashboard Cite

Chronic ethanol consumption and liver disease are intimately related to folic acid (FA) homeostasis. Despite the fact that FA decreases lipid oxidation, its mechanisms are not yet well elucidated. Lately, adolescents have been practising binge drinking (BD), consisting of the intake of a high amount of alcohol in a short time; this is a particularly pro-oxidant form of consumption. The aim of this study is to examine, for the first time, FA homeostasis in BD adolescent rats and its antioxidant properties in the liver. We used adolescent rats, including control rats and rats exposed to an intermittent intraperitoneal BD model, supplemented with or without FA. Renal FA reabsorption and renal FA deposits were increased in BD rats; hepatic deposits were decreased, and heart and serum levels remained unaffected. This depletion in the liver was accompanied by higher transaminase levels; an imbalance in the antioxidant endogenous enzymatic system; lipid and protein oxidation; a decrease in glutathione (GSH) levels; hyper-homocysteinemia (HHcy); an increase in NADPH oxidase (NOX) 1 and NOX4 enzymes; an increase in caspase 9 and 3; and a decrease in the anti-apoptotic metallopeptidase inhibitor 1. Furthermore, BD exposure increased the expression of uncoupled endothelial nitric oxide synthase (eNOS) by increasing reactive nitrogen species generation and the nitration of tyrosine proteins. When FA was administered, hepatic FA levels returned to normal levels; transaminase and lipid and protein oxidation also decreased. Its antioxidant activity was due, in part, to the modulation of superoxide dismutase activity, GSH synthesis and NOX1, NOX4 and caspase expression. FA reduced HHcy and increased the expression of coupled eNOS by increasing tetrahydrobiopterin expression, avoiding nitrosative stress. In conclusion, FA homeostasis and its antioxidant properties are affected in BD adolescent rats, making it clear that this vitamin plays an important role in the oxidative, nitrosative and apoptotic hepatic damage generated by acute ethanol exposure. For this, FA supplementation becomes a potential BD therapy for adolescents, preventing future acute alcohol-related harms.

show abstract

Section: Discussionmentioning

confidence: 59%

Folic Acid Homeostasis and Its Pathways Related to Hepatic Oxidation in Adolescent Rats Exposed to Binge Drinking

et al. 2022

Self Cite

View full text Add to dashboard Cite

show abstract

“…Clinical and research studies have demonstrated that acute or chronic alcohol consumption alters Se bioavailability and its antioxidant function by affecting selenoprotein tissue expressions [ 146 , 147 ]. Nonetheless, few studies analyze Se homeostasis during pregnancy after EtOH exposure [ 148 ] in the mother or fetus; however, an impairment of the selenoprotein GPx in FASD during the embryonic period in different tissues is well described [ 149 , 150 , 151 , 152 , 153 ].…”

Section: Oxidative Stress-programming Pathologies and Sementioning

confidence: 99%

Fetal Programming Is Deeply Related to Maternal Selenium Status and Oxidative Balance; Experimental Offspring Health Repercussions

et al. 2021

Self Cite

View full text Add to dashboard Cite

Nutrients consumed by mothers during pregnancy and lactation can exert permanent effects upon infant developing tissues, which could represent an important risk factor for diseases during adulthood. One of the important nutrients that contributes to regulating the cell cycle and tissue development and functionality is the trace element selenium (Se). Maternal Se requirements increase during gestation and lactation. Se performs its biological action by forming part of 25 selenoproteins, most of which have antioxidant properties, such as glutathione peroxidases (GPxs) and selenoprotein P (SELENOP). These are also related to endocrine regulation, appetite, growth and energy homeostasis. In experimental studies, it has been found that low dietary maternal Se supply leads to an important oxidative disruption in dams and in their progeny. This oxidative stress deeply affects gestational parameters, and leads to intrauterine growth retardation and abnormal development of tissues, which is related to endocrine metabolic imbalance. Childhood pathologies related to oxidative stress during pregnancy and/or lactation, leading to metabolic programing disorders like fetal alcohol spectrum disorders (FASD), have been associated with a low maternal Se status and intrauterine growth retardation. In this context, Se supplementation therapy to alcoholic dams avoids growth retardation, hepatic oxidation and improves gestational and breastfeeding parameters in FASD pups. This review is focused on the important role that Se plays during intrauterine and breastfeeding development, in order to highlight it as a marker and/or a nutritional strategy to avoid diverse fetal programming disorders related to oxidative stress.

show abstract

“…From a nutritional point of view, neither BD nor Se supplementation affects Kcal intake or body weight. With regard to liver, previous research in this laboratory has described hepatic damage associated to BD exposition during adolescence 37,41,42 . Moreover, this lab has previously described that Se plays an important role in the liver of BD exposed animals, since BD deeply affects hepatic selenoprotein expression; and when selenite is supplied, hepatic selenoproteins expression increased, leading to a better oxidative, inflammatory and apoptotic liver profile 3 .…”

Section: Nutritional and Hepatic Parametersmentioning

confidence: 99%

Selenite supplementation modulates the hepatic metabolic sensors AMPK and SIRT1 in binge drinking exposed adolescent rats by avoiding oxidative stress

et al. 2021

Self Cite

View full text Add to dashboard Cite

show abstract

Binge Drinking During Adolescence Disrupts Se Homeostasis and Its Main Hepatic Selenoprotein Expression

Abstract: 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.

Cited by 13 publications

References 49 publications

Folic Acid Homeostasis and Its Pathways Related to Hepatic Oxidation in Adolescent Rats Exposed to Binge Drinking

Folic Acid Homeostasis and Its Pathways Related to Hepatic Oxidation in Adolescent Rats Exposed to Binge Drinking

Fetal Programming Is Deeply Related to Maternal Selenium Status and Oxidative Balance; Experimental Offspring Health Repercussions

Selenite supplementation modulates the hepatic metabolic sensors AMPK and SIRT1 in binge drinking exposed adolescent rats by avoiding oxidative stress

Contact Info

Product

Resources

About