Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The natural history of hereditary hepatitis in long-survived LEC rats was reported. Among 56 (female: male, 28:28) LEC rats of F30, 16 (8:8) (29%) died of fulminant hepatitis approximately four months after birth. The remaining 40 (20:20) rats that survived more than one year developed chronic hepatitis and subsequent hepatic lesions including hepatocellular carcinomas. Further study made with 32 F31 rats killed at the age of five months revealed that hepatitis occurred in all of these rats. Genetic analysis performed by various crosses of LEC and LEJ rats confirmed the previous result that hereditary hepatitis was caused by a single autosomal recessive gene. F1 hybrid rats never developed hepatitis, showing normal histology of the liver. Histological features of hepatitis in F2 (F1 X F1) and backcross (F1 X LEC) rats were the same as those observed in the LEC rats. The preneoplastic foci also appeared in some of these hybrid rats at the age of eight months. We propose a gene symbol hts to designate the present hepatitis which is assumed to be homozygous in LEC strain rats.
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PMID:Hereditary hepatitis of LEC rats is controlled by a single autosomal recessive gene. 339 51

A new mutant causing hereditary hepatitis associated with severe jaundice has been discovered in the LEC strain of rats. Hepatitis appears suddenly in adult rats three to four months after birth. The clinical signs of hepatitis are characterized by severe jaundice, subcutaneous bleeding, oliguria, and loss of body weight. The affected rats showed a high lethality and histological changes of the liver with focal necrosis of enlarged hepatocytes without inflammatory cell response. Genetic tests indicate that at least a single autosomal recessive gene is responsible for the major cause of hepatitis. Furthermore, liver cancer appears in long survived rats after recovery from jaundice as well as a few asymptomatic rats without jaundice. The LEC rats thus provide an animal model useful for the basic and clinical studies of hepatitis and liver cancer, including their pathogenesis, prevention, and treatment.
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PMID:New mutation causing hereditary hepatitis in the laboratory rat. 342 43

LEC strain rats (LEC rats), which are known to develop hereditarily spontaneous fulminant hepatitis 4-5 months after birth, were highly sensitive to whole-body X-irradiation when compared to WKAH strain rats. The radiosensitivity of F1 hybrids of LEC and WKAH rats was similar to that of WKAH rats and significantly lower than that of LEC rats. Segregation data of backcross hybrids (F1 x LEC and LEC x F1) suggested that the hypersensitivity of LEC rats to whole-body irradiation is controlled by a single autosomal recessive gene. The radiosensitivity of fibroblasts from LEC rats was higher than that of fibroblasts from WKAH rats. The repair process of DNA double-strand breaks in LEC cells was slower than that in WKAH cells. LEC rats could provide a useful animal model to assist in understanding the mechanism of radiation-induced DNA damage and repair.
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PMID:Radiation hypersensitivity of LEC strain rats controlled by a single autosomal recessive gene. 751 Mar 63

LEC strain rats, which have been known to develop hereditarily spontaneous fulminant hepatitis 4 to 5 months after birth, are highly sensitive to whole-body X-irradiation when compared to WKAH strain rats. The present results showed that the frequencies of all types of chromosome aberrations induced by X-irradiation in the bone marrow cells of LEC rats were approximately 2- to 3-fold higher than those of WKAH rats, though no significant difference was observed in the frequency of spontaneous chromosome aberrations between LEC and WKAH rats.
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PMID:A high frequency of induction of chromosome aberrations in the bone marrow cells of LEC strain rats by X-irradiation. 751 41

The role of hepatocyte growth factor (HGF) in LEC rats were investigated at various phases of liver diseases by the detection of HGF expression, using ELISA assay, mRNA analysis and immunohistochemistry. Levels of plasma HGF increase in the fulminant hepatitis phase, decreased during chronic/cholangiofibrosis phase, and in some LEC rats, high levels of HGF were observed in hepatoma phase. HGF mRNA level in the liver was very high in fulminant hepatitis phase and low in chronic hepatitis phase. In hepatoma phase, HGF mRNA level was intermediate or high in the liver. In fulminant hepatitis phase, HGF mRNA level in the lung was slightly increased, while it was almost stable in the kidney in all the conditions studied. Immunohistochemical studies revealed that the frequency of HGF positive cells increased remarkably in fulminant hepatitis phase, and that many of them were located at the portal triads. Fewer HGF-positive cells were found in chronic hepatitis phase and were not found in the tissue of cholangiofibrosis. HGF was found in the surface of hepatocellular carcinoma cells and in the cytoplasm of the non-epithelial cells in cancerous liver tissues. HGF-positive cells appeared 24h after partial hepatectomy, diffusely, and HGF mRNA increased earlier in the kidney and lung than in the liver. Moreover, HGF mRNA level was higher in the lung than in the liver. These results suggest that in the natural course of spontaneous hepatitis and hepatoma in LEC rats, HGF is expressed mainly in the liver and that HGF may play an important role in the regeneration of hepatocytes in a paracrine manner. In contrast, after partial hepatectomy, HGF produced in the lung may be effective for liver regeneration in an endocrine manner.
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PMID:[Expression of hepatocyte growth factor (HGF) in LEC rats at various phases of hepatitis and hepatoma]. 759 Jun 6

Using anti-rat hepatocyte growth factor (HGF) antibody, we investigated the distribution of HGF-positive cells in the liver tissues of LEC rats at various phases of liver diseases. During the phase of fulminant hepatitis, HGF-positive cells increased remarkably, and many of them were localized at the portal triads; these cells were identified from their shape as non-epithelial cells. A reduced number of HGF-positive cells was observed during the phase of chronic hepatitis, while no HGF-positive cells were seen in the tissue of cholangiofibrosis. During the phase of carcinoma, staining revealed that both the hepatocellular carcinoma cells and the non-epithelial cells in cancerous liver tissue were HGF-positive. These results suggest that, in LEC rats, HGF may play an important role in the regeneration of hepatocytes as well as in the development of hepatocellular carcinoma.
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PMID:Differing distribution of hepatocyte growth factor-positive cells in the liver of LEC rats with acute hepatitis, chronic hepatitis and hepatoma. 773 10

LEC rats develop disorder of cooper metabolism and hepatitis similar to those of human Wilson's disease. We recently demonstrated that the gene responsible for hepatitis (hts) of LEC rats is homologous to Wilson's disease gene (WD). The present study showed a deletion of at least 90 base pair of WD cDNA in LEC rats, which corresponds to nucleotides 3981 to 4071 in human WD cDNA sequence. This deletion was linked with hepatic copper accumulation and hepatitis, and considered to be a primary mutation for hepatic disorder in the LEC rat. The WD gene was assigned to rat chromosome 16 at band q12.2-q12.4 by fluorescence in situ hybridization (FISH).
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PMID:Deletion of the Wilson's disease gene in hereditary hepatitis LEC rats. 777 79

LEC rats develop an autosomal recessive hepatitis and subsequently liver cancer associated with copper accumulation in the liver similar to that of Wilson's disease. Using 71 backcross [(WKAH x LEC) x LEC] rats, linkage analysis of the hepatitis with the WD gene for Wilson's disease revealed identical segregation and no recombination event between these two genes. This result indicates that the WD gene is a prime candidate for the hts gene responsible for the hepatitis of LEC rats, and suggests that the hepatitis of LEC rats may be caused by a defect in a copper-transporting ATPase expressed in the liver.
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PMID:The WD gene for Wilson's disease links to the hepatitis of LEC rats. 792 21

The LEC rat is a mutant strain that has been established as a model of hepatitis and hepatoma. In addition to hepatic disorders, it has been found that this strain has a defect in T cell maturation, and has low levels of serum IgG. Sodium dodecylsulfate polyacrylamide gel electrophoresis (SDS-PAGE) and immunoblot analysis showed that low levels of serum IgG were largely due to reduction of the IgG2a subclass. Quantitative determination of IgG subclasses by enzyme-linked immunosorbent assay (ELISA) using subclass-specific antibodies indicated that IgG2b and IgG2c subclasses were increased during development in this strain, whereas the IgG2a subclass was markedly decreased. These results suggest that dysfunction of some helper T cells in LEC rats selectively suppress synthesis of the IgG2a subclass during development but not affect production of IgG2b and IgG2c.
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PMID:Selective suppression of IgG2a subclass in LEC rats during development. 806 13

A mutant strain of LEC rats (Long-Evans rats with a cinnamon-like coat color) develop spontaneous hepatic injury associated with severe jaundice about 4 months after birth. Recently, we obtained evidence which shows an unusual accumulation of copper (Cu) in the liver of LEC rats, followed by the finding of copper-metallothionein (Cu-MT) induction. To know the mechanism for the development of hepatitis in LEC rats, in relation to induced Cu-MT, we examined whether the generation of active oxygen species is observed. When the Cu-MT was treated with H2O2, which is formed by dismutation of superoxide anion radicals or NADPH oxidases in living systems, strong ESR signals due to Cu(II) state appeared when measured at 77K. On the same system, ESR signals due to the spin trapped hydroxyl radicals were observed at room temperature when DMPO (5,5-dimethyl-pyrroline-1-oxide) was used as a spin-trapping agent. The present results suggested that Cu-MT of LEC rat has an important pathogenic role by generating hydroxyl radicals, when hydrogen peroxide is produced in cells or tissues.
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PMID:Unusual generation of hydroxyl radicals in hepatic copper-metallothionein of LEC (Long-Evans cinnamon) rats in the presence of hydrogen peroxide. 812 29


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