| Budget Amount *help |
¥6,700,000 (Direct Cost: ¥6,700,000)
Fiscal Year 1990: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1989: ¥5,700,000 (Direct Cost: ¥5,700,000)
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| Research Abstract |
Both in human and rat alcoholic liver injury (ALI), transferrin (TF) was strongly stained in the ballooned hepatocytes. This change was related to the appearance of microheterogeneity (MCHT) of serum TF. By immunoelectron microscopy, Tf retained in the Golgi apparatus. Incorporation rate of ^<14>C-fucose and ^3H-leucine, especially fucose, to serum Tf decreased, and secretion of these labels from the Golgi apparatus delayed in ALI. By the Pulse-chase labeling analysis in cultured hepatocytes using ^<35>S-methionine, it was suggested that maturation of Tf may be retarded in ALI. MCHT of serum Tf and alphal-antitrypsin, but not other glycoproteins, was clearly detected by Western blotting. MCHT disappeared by the treatment of sialidase, indicating that MCHT of TF was caused by changes in silalic acid. In severe liver disease, such as decompensated liver cirrhosis, MCHT of TF was also found. However, the isoelectric focusing pattern of such disease was different from that of ALI. The differences was found even in the sialic acid-treated serum, suggesting that MCHT of Tf may not be related to the decrease of asialo-glycoprotein receptor on the hepatocyte membrane. A simple method to detect MCHT of serum TF was developed. Using this method, MCHT of TF was found in 73 % of 100 patients with ALI. MCHT was more frequently found in severe type of ALI. However, MCHT of TF could not found in any case of alcoholic pancreatitis and heavy drinkers without liver disease. These results suggest that MCHT is a marker of alcohol specific liver injury, but not chronic alcoholism.
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