Nutritional Supplementation and Enhanced Antioxidant Function by Dietary Intake of Selenoneine and Other Selenium Compounds in Red Seabream Pagrus major.

Selenoneine, 2-selenyl-Nα, Nα, Nα-trimethyl-L-histidine, is the major organic selenium compound in marine fish. To characterize biological antioxidant function of selenoneine in fish, the accumulation of selenoneine and other selenium compounds, i. e., sodium selenite and selenomethionine, in the muscle and other tissues of red seabream. We reared red seabream by feeding of 1% dry pellet containing of sodium selenite, selenomethionine, or selenoneine of body weight twice a day for 4 weeks. After that, we replaced to 1% of normal commercial dry pellet of body weight twice a day for 1 week from the selenium supplementation, and tissue distribution of total selenium was determined. Selenium supplementation with selenoneine, selenomethionine, and sodium selenite enhanced selenium accumulation in the white muscle, kidney, and hepatopancreas in comparison with the control group. By the dietary intake of selenoneine, total selenium concentrations were increased in the white muscle, heart, kidney, spleen, hepatopancreas, brain, and blood cells in a dose-dependent manner during the trials after 2 weeks. Dietary intake of selenoneine as well as sodium selenite and selenomethionine reduced oxidation-reduction potential (ORP). Selenoneine concentrations in the white muscle and blood cells were accumulated for 4 weeks by the selenoneine intake, whereas selenoneine concentration was not elevated by the intake of selenomethionine and sodium selenite, suggesting that tissue selenoneine levels might be derived from only selenoneine-containing diet. The uptake factor of selenoneine from the artificial feed containing selenoneine was calculated to be 0.0062 in the white muscle and 4.0 in the blood. The half-life of total selenium in the blood cells and white muscle were estimated to be 60 days in the white muscle and 30 days in the blood.

Selenoneine Ameliorates Hepatocellular Injury and Hepatic Steatosis in a Mouse Model of NAFLD.

Selenoneine is a novel organic selenium compound markedly found in the blood, muscles, and other tissues of fish. This study aimed to determine whether selenoneine attenuates hepatocellular injury and hepatic steatosis in a mouse model of non-alcoholic fatty liver disease (NAFLD). Mice lacking farnesoid X receptor (FXR) were used as a model for fatty liver disease, because they exhibited hepatomegaly, hepatic steatosis, and hepatic inflammation. Fxr-null mice were fed a 0.3 mg Se/kg selenoneine-containing diet for four months. Significant decreases in the levels of hepatomegaly, hepatic damage-associated diagnostic markers, hepatic triglycerides, and total bile acids were found in Fxr-null mice fed with a selenoneine-rich diet. Hepatic and blood clot total selenium concentrations were 1.7 and 1.9 times higher in the selenoneine group than in the control group. A marked accumulation of selenoneine was found in the liver and blood clot of the selenoneine group. The expression levels of oxidative stress-related genes (heme oxygenase 1 (Hmox1), glutathione S-transferase alpha 1 (Gsta1), and Gsta2), fatty acid synthetic genes (stearoyl CoA desaturase 1(Scd1) and acetyl-CoA carboxylase 1 (Acc1)), and selenoprotein (glutathione peroxidase 1 (Gpx1) and selenoprotein P (Selenop)) were significantly decreased in the selenoneine group. These results suggest that selenoneine attenuates hepatic steatosis and hepatocellular injury in an NAFLD mouse model.