Biliary excretion of copper in fischer rats treated with copper salt and in long-evans cinnamon (LEC) rats with an inherently abnormal copper metabolism

1994 ◽  
Vol 46 (1-2) ◽  
pp. 125-134 ◽  
Author(s):  
Naoki Sugawara ◽  
Dan Li ◽  
Michihiro Katakura ◽  
Chieko Sugawara
2003 ◽  
Vol 90 (3) ◽  
pp. 573-579 ◽  
Author(s):  
Hong Xu ◽  
Shoji Sakakibara ◽  
Masashi Morifuji ◽  
Quazi Salamatulla ◽  
Yoritaka Aoyama

Long-Evans Cinnamon (LEC) rats spontaneously develop fulminant hepatitis, associated with excess Cu accumulation in the liver: thus, they are considered an animal model of Wilson's disease. In the present study, we investigated the ability of excess dietary histidine to reduce the excess accumulation of liver Cu in LEC rats by comparing them with Fischer rats. The results clearly showed that the excess-histidine diet markedly stimulated the Cu excretion in urine, and significantly decreased the liver Cu content in LEC rats by 47·5%. The serum Cu content in LEC rats was not influenced by excess dietary histidine. We also compared the effects of excess dietary histidine on some liver antioxidant enzyme activities, liver and serum lipid levels and serum alanine aminotransferase activity of LEC and Fischer rats. Dietary histidine decreased the activities of total and Cu, Zn-superoxide dismutase in the liver of both strains. In LEC rats, the liver cholesterol content decreased, and serum cholesterol and phospholipids levels increased on feeding the excess-histidine diet. When fed on the basal diet, the serum alanine aminotransferase activity was higher in LEC rats than in Fischer rats, but a significant decrease in serum alanine aminotransferase activity of LEC rats was observed on feeding the excess-histidine diet. These results suggest that excess dietary histidine is effective in removing Cu ions from the liver of LEC rats. Thus, it may be of benefit in the prevention or treatment of liver injury in LEC rats and in patients with Wilson's disease.


Toxicology ◽  
1996 ◽  
Vol 108 (1-2) ◽  
pp. 1-7 ◽  
Author(s):  
Naoki Sugawara ◽  
Yu-Rong Lai ◽  
Chieko Sugawara

1996 ◽  
Vol 17 (12) ◽  
pp. 448-448
Author(s):  
Philip O. Ozuah

Wilson disease (hepatolenticular degeneration) is an autosomal recessive, inherited disorder of copper metabolism resulting in excessive accumulation of copper in the liver, brain, and other organs of the body. The manifestations of the disease are related directly to this accumulation of copper. Copper homeostasis normally is a product of the balance between intestinal absorption of dietary copper and hepatic biliary excretion of excess copper. In Wilson disease, incorporation of hepatic copper into ceruloplasmin is defective and excretion of copper in the bile is reduced. A low level of ceruloplasmin, which until a few years ago was erroneously considered to be the basis for the disease, is a consequence of the underlying metabolic defect.


2012 ◽  
Vol 37 (1) ◽  
pp. 169-175 ◽  
Author(s):  
Kyoumi Nakazato ◽  
Katsuyuki Nakajima ◽  
Takamitsu Nakano ◽  
Tsukasa Kodaira ◽  
Kenji Nakayama ◽  
...  
Keyword(s):  
Lec Rats ◽  

1999 ◽  
Vol 120 (4) ◽  
pp. 333-346 ◽  
Author(s):  
J. Yamate ◽  
D. Kumagai ◽  
K. Tsujino ◽  
S. Nakatsuji ◽  
M. Kuwamura ◽  
...  

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