Abstract
The LEC rats with hereditary hepatitis show an abnormal accumulation of copper in various organs such as liver, kidney, and brain, together with a marked decrease in the level of serum or plasma ceruloplasmin (Cp) [1]. Cp is a copper-binding protein primarily involved in the transport of copper from the liver [2]. The apoprotein is synthesized in the liver [3], and then binds from six to eight atoms of copper per Cp molecule [4, 5]. Most of the copper in plasma is present as the Cp-bound form. Thus, impaired copper metabolism may bear an etiological significance for the hepatic lesions in LEC rats, although the basic defect involved in the occurrence of hepatitis still remains obscure.
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© 1991 Springer-Verlag Tokyo
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Ono, T., Abe, S., Yoshida, M.C. (1991). Hereditary Low Levels of Plasma Ceruloplasmin in LEC Rats. In: Mori, M., Yoshida, M.C., Takeichi, N., Taniguchi, N. (eds) The LEC Rat. Springer, Tokyo. https://doi.org/10.1007/978-4-431-68153-3_14
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DOI: https://doi.org/10.1007/978-4-431-68153-3_14
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