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Galactosamine Hepatitis, Endotoxemia, and Lactulose
Author(s) -
Vugt Hendrina Van,
Van Gool Jacobus,
Thomas Lambert L. M.
Publication year - 2007
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.1840030217
Subject(s) - lactulose , galactose , sorbitol dehydrogenase , galactosamine , chemistry , transaminase , sorbitol , medicine , toxicity , biochemistry , enzyme
Studies by Liehr et al. suggest that endotoxins are important in the pathogenesis of galactosamine hepatitis (Gal‐N hepatitis) in rats. Lactulose (9.1 gm per kg per day) prevents hepatic lesions induced by Gal‐N; an antiendotoxin effect of lactulose is postulated. However, commercial preparations of lactulose are contaminated with galactose, which shows a competitive action to Gal‐N. To analyze the effect of galactose, male Wistar rats were pretreated with lactulose (Duphalac®, 9.1 gm per kg per day) and given Gal‐N (375 mg per kg i.p.). After 24 hr, serum was analyzed for glutamic pyruvate transaminase, glutamate dehydrogenase, and sorbitol dehydrogenase activities. Pretreatment with Duphalac®, even 1 hr before Gal‐N, abolished toxicity. Duphalac® contains 10 gm galactose per 100 ml. Galactose was given in a similar concentration and similar inhibition occurred. Pretreatment with purified lactulose (9.1 gm per kg for 5 days) diminished the effects of Gal‐N but did not normalize enzyme concentrations. Because small doses of galactose (80 and 300 mg per kg) showed similar inhibitory effects, we conclude that the protective effect of commercial lactulose preparations is mainly due to galactose contamination and not to an antiendotoxin effect.