Effect of liver hydrolysate on ethanol- and acetaldehyde-induced deficiencies

• Published in: Nihon yakurigaku zasshi Vol. 111; no. 2; p. 117
• Main Authors: Washizuka, M, Hiraga, Y, Furuichi, H, Izumi, J, Yoshinaga, K, Abe, T, Tanaka, Y, Tamaki, H
• Format: Journal Article
• Language: Japanese
• Published: Japan 01.02.1998
• Subjects: Acetaldehyde - toxicity; Alanine Transaminase - blood; Alcoholic Intoxication - drug therapy; Alcoholic Intoxication - physiopathology; Animals; Aspartate Aminotransferases - blood; Cattle; Disease Models, Animal; Dose-Response Relationship, Drug; Eating - drug effects; Ethanol - toxicity; Liver - chemistry; Male; Mice; Mice, Inbred ICR; Motor Activity - drug effects; Protein Hydrolysates - therapeutic use; Rats; Rats, Inbred F344; Tissue Extracts - therapeutic use
• ISSN: 0015-5691
• DOI: 10.1254/fpj.111.117

Since it has been reported that amino acids have alleviating effects on ethanol- and acetaldehyde-induced toxicity, we investigated the effect of liver hydrolysate derived from bovine liver on ethanol- or acetaldehyde-induced toxicity and deficiency models of mice and rats in the present study. Liver hydrolysate improved the deficiencies of beam walking and food intake of mice in a dose-dependent fashion when challenged with ethanol at the dose of 5 ml/kg, p.o. According to the analysis using selective inhibitors for alcohol dehydrogenase and acetaldehyde dehydrogenase, it has been suggested that this improvement effect of liver hydrolysate is mainly due to the reduction of acetaldehyde toxicity. No effect of liver hydrolysate was found in coma and death produced by orally treated ethanol at 10 ml/kg. In contrast, liver hydrolysate dose-dependently decreased the coma and death of mice administered acetaldehyde at 1.8 ml/kg, p.o. Furthermore, an increase in serum GPT activity, which was caused by twice oral administration of acetaldehyde at 1.2 ml/kg at interval of 1 hr, was inhibited by liver hydrolysate. These results suggest that liver hydrolysate has a protective effect against ethanol- and acetaldehyde-induced toxicity.