Hilton J W, Hodson P V
J Nutr. 1983 Jun;113(6):1241-8. doi: 10.1093/jn/113.6.1241.
Juvenile trout were reared on either a high available carbohydrate (HC) or low available carbohydrate (LC) diet supplemented with from 0 to 10 micrograms selenium per gram of diet for 16 weeks, to determine if excess liver glycogen deposition affected the metabolism and toxicity of dietary selenium. Trout reared on the HC diet with 10 micrograms selenium per gram diet first demonstrated signs of selenosis and had significantly higher (P less than 0.05) liver selenium levels than trout reared on the LC diet with 10 micrograms selenium per gram diet after 16 weeks, indicating that excess dietary carbohydrate enhances dietary selenium toxicity in trout. The mechanism of the interaction is unclear since neither selenium elimination rates nor carcass and kidney selenium levels were affected by the dietary carbohydrate level. Trout reared on high dietary selenium diets (10 micrograms/g) had an increased incidence of renal calcinosis. In addition, liver copper levels were significantly affected by both dietary selenium and liver glycogen content indicating a significant copper-selenium and copper-glycogen interaction in trout. The development of renal calcinosis and the copper interactions suggest a variety of toxic effects of selenium on trout that may all be responsible for the observed changes in growth and feed efficiency.
将幼鳟饲养在每克饲料添加0至10微克硒的高可利用碳水化合物（HC）或低可利用碳水化合物（LC）饲料上，为期16周，以确定肝脏糖原过量沉积是否会影响饲料硒的代谢和毒性。在每克饲料含10微克硒的HC饲料上饲养的鳟鱼首先出现硒中毒迹象，并且在16周后，其肝脏硒水平显著高于（P<0.05）在每克饲料含10微克硒的LC饲料上饲养的鳟鱼，这表明过量的饲料碳水化合物会增强鳟鱼对饲料硒的毒性。由于饲料碳水化合物水平既不影响硒的消除率，也不影响鱼体和肾脏的硒水平，因此这种相互作用的机制尚不清楚。在高饲料硒（10微克/克）日粮中饲养的鳟鱼肾钙化发病率增加。此外，肝脏铜水平受到饲料硒和肝脏糖原含量的显著影响，这表明鳟鱼体内存在显著的铜-硒和铜-糖原相互作用。肾钙化的发展和铜的相互作用表明，硒对鳟鱼有多种毒性作用，这些作用可能都是观察到的生长和饲料效率变化的原因。
