Effects of Dietary Copper Level on Blood and Tissue Copper Contents in Geese

In order to study the effect of dietary copper level on blood and tissue copper contents in geese, one-week Sichuan white geese were randomly divided in- to four groups, and the geese in the first, second, third and fourth groups were fed with diet with copper levels of 39.55, 127.60, 194.75 and 255.22 mg/kg, respective- ly. At the ages of 4, 6, 8, 10 and 12 weeks, the contents of copper in blood, liver, chest muscle and subcutaneous fat of the geese were determined. The effects of dietary copper level, age and sex on the blood and tissue copper contents of geese were analyzed by multivariate analysis of variance. The results showed that the di- etary copper level showed no significant effects on the blood and liver copper con- tents of geese （P〉0.05）; the chest muscle copper content of geese in the second group was significantly higher than that in the first group （P〈0.05）; the subcuta- neous fat copper content of geese in the fourth group was significantly higher than those in the other three groups （P〈0.01）; the age had significant effects on the blood, liver, chest muscle and subcutaneous fat copper contents of geese （P〈0.01）; and the sex showed no significant effects on the blood and tissue copper contents of geese （P〉0.05）.

Dietary copper triggers onset of fulminant hepatitis in the Long-Evans cinnamon rat model

AIM： To investigate the impact of dietary copper given at different time points on the onset of fulminant hepatitis. METHODS： The Long-Evans cinnamon （LEC） rat mod- el of Wilson＇s disease （WD） was used to study the im- pact of high dietary copper （hCu） on the induction of fulminant hepatitis at early or late time points of life. High Cu diet was started in rat pups or in adults （month 5） for three months. Animals that received reduced di- etary copper （rCu） throughout their lifetime served as a control. Hepatitis-associated serum markers （alanine aminotransferase, aspartate transaminase, bilirubin） were analyzed in animal groups receiving hCu or rCu. Liver copper content and liver histology were revealed at sacrifice. A set of 5 marker genes previously found to be affected in injured liver and which are related to angiogenesis （Vegfa）, fat metabolism （Srebf1）, ex- tracellular matrix （Timp1）, oxidative stress （Hmox1）, and the cell cycle （Cdknla） were analyzed by real-time polymerase chain reaction. RESULTS： Regardless of the time point when hCu was started, LEC rats （35/36） developed fulminant hepati- tis and died. Animals receiving rCu （36/36） remained healthy, did not develop hepatitis, and survived long term without symptoms of overt disease, although liver copper accumulated in adult animals （477 ± 75 μg/g）. With regard to start of hCu, onset of fulminant hepatitis was significantly （P 〈 0.001） earlier in adults （35±9 d） that showed pre-accumulation of liver copper as com- pared to the pup group （77±15 d）. Hepatitis-associ- ated serum markers, liver copper and liver histology, as well as gene expression, were affected in LEC rats re- ceiving hCu. However, except for early and rapid onset of hepatitis, biochemical and molecular markers were similar at the early and late time points of disease. CONCLUSION： Rapid onset of fulminant hepatitis in asymptomatic LEC rats with elevated liver copper sug- gests that there is a critical threshold of liver copper which is important to trigger the course of WD.