Effects of soy protein isolate on LEC rats, a model of Wilson disease: mechanisms underlying enhancement of liver cell damage

Soy-protein isolate (SPI) enhances liver cell damage in Long-Evans rats with a cinnamon-like coat color (LEC rats), which have a defect in Atp7b, the Wilson disease gene. Animals administered an SPI-diet from an age of six weeks died significantly earlier than those administered a control-diet, AIN-...

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Bibliographic Details
Published in:Biochemical and biophysical research communications 2003-03, Vol.302 (2), p.271-274
Main Authors: Yonezawa, Kayo, Nakagama, Hitoshi, Tajima, Rie, Ushigome, Mitsunori, Ogra, Yasumitsu, Suzuki, Kazuo T, Yoshikawa, Kunie, Nagao, Minako
Format: Article
Language:English
Subjects:
Animals
Cation Transport Proteins
Copper
Ctr1 expression
Disease Models, Animal
Glutathione
Glutathione - metabolism
Glutathione Disulfide - metabolism
Hepatolenticular Degeneration - metabolism
Hepatolenticular Degeneration - pathology
LEC rats
Liver - drug effects
Liver - metabolism
Membrane Proteins - genetics
Membrane Proteins - metabolism
Metallothionein
Metallothionein - genetics
Metallothionein - metabolism
Rats
RNA, Messenger - drug effects
RNA, Messenger - metabolism
Soy-protein isolate
Soybean Proteins - isolation & purification
Soybean Proteins - pharmacology
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Summary:Soy-protein isolate (SPI) enhances liver cell damage in Long-Evans rats with a cinnamon-like coat color (LEC rats), which have a defect in Atp7b, the Wilson disease gene. Animals administered an SPI-diet from an age of six weeks died significantly earlier than those administered a control-diet, AIN-93G, from severe liver cell damage associated with jaundice. Since the liver copper level was higher with the SPI-diet than the control-diet, one of the reasons for SPI-toxicity to LEC rats might be due to the higher uptake of copper into liver cells. In the present study, liver levels of glutathione, and liver and intestinal mRNA and protein levels were determined for metallothionein, MT-1 and MT-2. Furthermore, liver and intestinal mRNA expression for the high affinity copper transporter, Ctr1, was determined. None of the parameters showed any significant differences between the SPI-diet and control-diet groups, except for Ctr1 mRNA levels in the liver. It is thus suggested that SPI enhances liver cell copper uptake through induction of Ctr1 expression and this might be the mechanism underlying increased liver damage in LEC rats.
ISSN:0006-291X
1090-2104
DOI:10.1016/S0006-291X(03)00159-1