PMID- 1316758
OWN - NLM
STAT- MEDLINE
DCOM- 19920625
LR  - 20191021
IS  - 0899-1987 (Print)
IS  - 0899-1987 (Linking)
VI  - 5
IP  - 3
DP  - 1992
TI  - Genetic linkage between copper accumulation and hepatitis/hepatoma development in 
      LEC rats.
PG  - 199-204
AB  - The concentration of copper in the livers of Long-Evans rats with cinnamon-like 
      coat color (LEC), in which hepatitis and then hepatomas develop spontaneously, 
      was recently found to be abnormally high. Therefore, we examined the copper 
      concentrations in the livers of LEC F1 backcrosses (LEC F1 x LEC) to determine 
      the linkage of copper accumulation with development of hepatitis. Consistent with 
      a previously reported ratio of rats with hepatitis to rats without hepatitis of 
      about 1:1, hepatitis developed in 14 of 30 F1 backcrosses. The copper 
      concentrations in the livers of all LEC F1 backcrosses with hepatitis were 
      abnormally high and comparable to those of LEC rats. In contrast, the 
      concentrations in all backcrosses without hepatitis were similar to those in 
      normal Long-Evans with agouti coat color or Brown-Norway rats. Copper 
      accumulation was shown to be closely linked with the development of hepatitis in 
      LEC rats and appeared to be a possible cause of hepatitis. The concentrations of 
      copper in the livers of Fischer 344 rats after carbon tetrachloride treatment 
      were in the range for normal liver, indicating that a high copper concentration 
      in the liver is specific to LEC rats and not a specific characteristic of 
      hepatitis. Furthermore, we found that the size and level of ceruloplasmin mRNA in 
      the livers of LEC rats were the same as those in LEA rats and that the size and 
      level of ceruloplasmin polypeptide in their livers and plasma were almost the 
      same as those in LEA rats. Therefore, these results suggest that the copper 
      accumulation is not due to alteration of expression or to gross alteration of the 
      ceruloplasmin gene.
FAU - Sone, H
AU  - Sone H
AD  - Carcinogenesis Division, National Cancer Center Research Institute, Tokyo, Japan.
FAU - Maeda, M
AU  - Maeda M
FAU - Gotoh, M
AU  - Gotoh M
FAU - Wakabayashi, K
AU  - Wakabayashi K
FAU - Ono, T
AU  - Ono T
FAU - Yoshida, M C
AU  - Yoshida MC
FAU - Takeichi, N
AU  - Takeichi N
FAU - Mori, M
AU  - Mori M
FAU - Hirohashi, S
AU  - Hirohashi S
FAU - Sugimura, T
AU  - Sugimura T
AU  - et al.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Mol Carcinog
JT  - Molecular carcinogenesis
JID - 8811105
RN  - 0 (RNA, Messenger)
RN  - 789U1901C5 (Copper)
RN  - EC 1.16.3.1 (Ceruloplasmin)
SB  - IM
MH  - Animals
MH  - Carcinoma, Hepatocellular/*genetics
MH  - Ceruloplasmin/analysis/*metabolism
MH  - Copper/*metabolism
MH  - Female
MH  - *Genetic Linkage
MH  - Hepatitis/*genetics/metabolism/pathology
MH  - Liver/*metabolism
MH  - Liver Neoplasms/*genetics
MH  - Male
MH  - RNA, Messenger/metabolism
MH  - Rats
MH  - Rats, Inbred Strains/genetics
MH  - Species Specificity
EDAT- 1992/01/01 00:00
MHDA- 1992/01/01 00:01
CRDT- 1992/01/01 00:00
PHST- 1992/01/01 00:00 [pubmed]
PHST- 1992/01/01 00:01 [medline]
PHST- 1992/01/01 00:00 [entrez]
AID - 10.1002/mc.2940050306 [doi]
PST - ppublish
SO  - Mol Carcinog. 1992;5(3):199-204. doi: 10.1002/mc.2940050306.