• Biomedical Science Letters
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• v.8 no.4
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• pp.203-209
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• 2002

Serum $\alpha$-D-mannosidase isozyme activities were measured in rats with ethanol intoxication combined with extrahepatic cholestasis induced by common bile duct ligation for the manifestation of the biochemical background of drinking hazards under the hepatobiliary disease. When chronic ethanol intoxication was combine with extraheparlc cholestasis, the activities of the rat's serum cytosolic, Iysosomal and Golgi $\alpha$-D-mannosidase isozymes increased at a more significant rate than those of the cholestasis alone. However, when acute ethanol intoxication was combined with extrahepatic cholestasis, the activities of the above isozymes were seen in the cholestasis alone. The results suggested that the elevated activities of these isozymes in chronic ethanol intoxication with cholestasis rather than in cholestasis alone were indications of increased hepatic damages, which caused these isozymes to leak into the blood in great quantity. Accordingly, the resulting data supported the fact that alcoholic drinks were enzymologically harmful to the hepatobiliary disease.

• Biomedical Science Letters
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• v.10 no.2
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• pp.99-105
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• 2004

Liver and serum rhodanese activities were determined in acute ethanol intoxicated rats with extrahepatic cholestasis induced by common bile duct ligation (CBD) to manifest the biochemical background of alcohol drinking hazard under the hepatobiliary disease. Liver cytosolic and microsomal rhodanese activities and these Vmax values in CBD ligated rats with acute ethanol intoxication were found to be decreased much more than that in CBD ligation alone. However, the difference of Km value on above hepatic enzyme was not found between the experimental groups. On the other hand, serum rhodanese activity in CBD ligated rats with acute ethanol intoxication was greater increased more than that in CBD ligation alone. These results indicate that the biosynthesis of the hepatic rhodanese decreases and the serum rhodanese activity increases in cholestasis combined with acute ethanol intoxication, reflecting damage of aggravated hapatocytic membrane. Accordingly, the resulting data supported the fact that alcoholic drinks were enzymologically harmful to the hepatobiliary disease.

• BMB Reports
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• v.32 no.4
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• pp.331-338
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• 1999

Ethanol catabolism is thought to produce metabolic disorders resulting in alcoholic liver disease. To investigate the mutual effects of ethanol catabolism and cholestasis induced by common bile duct ligation on the activities of carboxylesterase, we have determined the enzyme activities in rat hepatic (cytosolic, mitochondrial, and microsomal) preparations as well as in rat serum using ten animal models: normal rats (group 1), sham-operated rats (group 2), common bile duct-ligated rats (group 3), ethanol-intoxicated rats (group 4), sham-operation plus chronic ethanol-intoxicated rats (group 5), common bile duct-ligated plus chronic ethanol-intoxicated rats at 1.5h and 24h (groups 7A and 7B), and duct-ligated and acute ethanol intoxicated rats at 1.5 h and 24 h (groups 8A and 8B). The $K_m$ and $V_{max}$ values of carboxylesterase from these hepatic preparations of cholestatic rat liver combined with chronic ethanol intoxication were also measured by using ethyl valerate as the substrate from the 14th day post-ligation. Carboxylesterase activities of all hepatic preparations and rat serum (group 3) showed significant decreases compared to the activities from the sham-operated control (group 2). Enzyme kinetic parameters indicated that $V_{max}$ of carboxylesterase from all the hepatic preparations in cholestatic rats (group 3) decreased significantly, although the $K_m$ values were about the same as in the sham-operated control (group 2). When cholestasis was combined with chronic ethanol intoxication (group 6), carboxylesterase activities showed further decrease in all the hepatic preparations and serum compared to the control activity (group 5). The $V_{max}$ also decreased significantly, although $K_m$ values did not change. When common bile duct ligation was combined with acute ethanol intoxication (group 8), the enzyme activities in the rat liver and serum showed significant decrease compared to the activity from acute ethanol-intoxicated rats (group 7). However, quite contrary to this, the activities of serum from acute ethanol intoxication 1.5 h (group 7A) increased significantly compared to the activities in the normal control (group 1). These results, therefore, suggest that the biosynthesis of hepatic carboxyl-esterase seems to decrease when cholestasis is combined with chronic and acute ethanol intoxication, and the decrease in activity is more significant than from cholestasis alone.

• Biomedical Science Letters
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• v.9 no.1
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• pp.21-27
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• 2003

Hepatic subcellular $\alpha$-D-mannosidases activities and its Km and Vmax values were determined in chronic ethanol intoxicated rats with extrahepatic cholestasis induced by common bile duct ligation to manifest the biochemical background of alcohol drinking hazard under the hepatobiliary disease. In case of extrahepatic cholestasis, chronic ethanol intoxication in animals led to the increased activities of liver Golgi and microsomal $\alpha$-D-mannosidase as well as the Vmax values of these enzymes. However, the difference of Km values on hepatic subcellular enzymes were not found between the experimental groups. Therefore, the results indicate that the liver Golgi and microsomal $\alpha$-D-mannosidase may be more induced in chronic ethanol intoxication animals in case of cholestasis. Accordingly, the resulting data supported the fact that alcoholic drinks may led to enhancement of the hepatobiliary liver damage.

• Biomedical Science Letters
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• v.10 no.1
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• pp.35-42
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• 2004

Liver and serum $\beta$-D-mannosidase activities were determined in ethanol intoxicated rats with extrahepatic cholestasis induced by common bile duct ligation (CBD) to manifest the biochemical background of alcohol drinking hazard under the hepatobiliary disease. Liver $\beta$-D-mannosidase activity and its Vmax value in CBD ligated rats with chronic ethanol intoxication were found to be significantly decreased than that in CBD ligation alone. However, the difference of Km value on above hepatic enzyme was not found between the experimental groups. On the other hand, serum $\beta$-D-mannosidase activity in CBD ligated rats with chronic ethanol intoxication was increased more than that in CBD ligation alone. These results indicate that the biosynthesis of the hepatic $\beta$-D-mannosidase decreases and the serum $\beta$-D-mannosidase activity increases in cholestasis combined with chronic ehtanol intoxication, reflecting damage of aggravated hapatocytic membrane. Accordingly, the resulting data supported the fact that alcoholic drinks were enzymologically harmful to the hepatobiliary disease.

• Proceedings of the Ginseng society Conference
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• 1984.09a
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• pp.63-74
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• 1984

Preventive effect of the saponin fraction extracted from Panax ginseng C.A. Meyer against ethanol intoxication of the liver has been investigated biochemically and morphologically. Previous work in this laboratory showed that the moderate amounts of ginseng sponins stimulated several enzymes including mitochondrial dehydrogenases and transaminases so far examined in vitro. It was also realized that the half life of the saponin in the liver was estimated approximately five hours and the saponin concentration in the liver was around $10^{-5}\%$ level at two hours after the saponin (1mg) administration orally. In this study, it was confirmed that ginseng saponins stimulated alcohol dehydrogenase, aldehyde dehydrogenase and microsomal ethanol oxidizing system in vivo as well as in vitro. It seemed likely that toxic aldehyde formed during ethanol oxidation in the body might be removed relatively quickly from the liver and the excess hydrogen was used for the biosynthetic work in the presence of the saponin, resulting in the liver protection from alcohol intoxication. Electron microscopic observation demonstrated that the hepatocytes of rats doses with $12\%$ ethanol instead of water for six days were found severely damaged while those of the ginseng saponin administered rats were not impaired suggesting that the sapcnin protected the liver against ethanol intoxication.

• Journal of Ginseng Research
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• v.9 no.1
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• pp.1-8
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• 1985

Preventive effect of ginseng saponin fraction against ethanol intoxication of the liver of rats fed width 12% ethanol instead of water for 6 days was investigated. Control group was dosed 12% ethanol instead of water (free access) for 6 days and test group was dosed 0.1% ginseng saponin fraction in the 12% ethanol instead of water for 6 days. Normal rats was given only water freely. It was observed that the activities of alcohol dehydrogenase (ADH) and Microsomal ethanol oxidizing system (MEOS) of both control and test groups were higher than those of normal group while the activity of aldehyde dehydrogenate (ALDH) of control and test groups were lower than that of normal rats, However, the ALDH activity decrease of test group was much less than that of control groups. Electron micrograph showed that severely swollen and disrupted mitochondria and dilated and vesiculated ER can be seen in control group while dilated or vesiculated ER are very few and swollen or disrupted mitochondria can not be seen in test group. From the above experimental result, it seems that ginseng saponin might stimulate ethanol oxidation and the removal of acetaldehyde resulting in the decrease of ethanol intoxication of the liver.

• Journal of the Korean Society of Food Science and Nutrition
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• v.23 no.2
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• pp.181-186
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• 1994

The present study was undertaken to clarify the effect of Puffer fish skin extract (PF) on the hepatic alcohol metabolism in rats. It was observed that alcohol concentration in blood had been markedly decreased by the pretreatment of PF for two weeks. Activities of alcohol dehydrogenase (ADH) and microsomal ethanol-oxidizing system (MEOS) were significantly incrased (more than 20% of control) by pretreatment of PF for two weeks and acute alcohol intoxication (5 g/kg) on final day. When rats were fed with subacute toxic state by alcohol (25v/v % , once a day for six weeks), activities of ADH and MEOS were significantly increased by additional treatments of PF for final two weeks. But the catalase activity was not affected by any of both case. And also activities of ADH and MEOS in vitro were not changed . These results suggest that PF treatemnt prompted the recovery from alcohol intoxication.

• Journal of the Korean Society of Food Science and Nutrition
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• v.43 no.8
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• pp.1139-1147
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• 2014

We investigated whether or not Schisandra chinensis (SC), a traditional herbal medicine, has protective effects against alcohol-induced fatty liver and blood alcohol clearance. Two tests focused on acute intoxication and chronic ethanol treatment were carried out. For the chronic ethanol treatment test, rats were fed ethanol by intragastric administration everyday for 8 weeks to induce alcoholic fatty liver. Ethanol treatment significantly increased blood alcohol concentration at 90 min after acute ethanol intoxication. Compared with the two ethanol-treated groups, rats administered ethanol along with SC extracts showed an approximately 13% increased blood alcohol clearance rate at 360 min. Chronic ethanol treatment significantly increased serum and hepatic triglyceride (TG) levels, and caused fatty degeneration of liver. Ethanol treatment also elevated the serum total-cholesterol (TC) level. However, after feeding of ethanol plus SC extracts, ethanol-induced elevation of hepatic TG levels reversed, whereas elevation of serum TG and TC levels was not observed after treatment with SC extracts. Ethanol treatment significantly increased ${\gamma}$-GT, aspartate aminotransferase, and alanine aminotransferase activities after 8 weeks. Compared with the ethanol-fed group, rats administered ethanol plus SC extracts for 4 weeks showed attenuated fatty degeneration as well as decreased hepatic function test values. SC administration also significantly increased intracellular lipid accumulation in hepatocytes and reduced steatosis score and hepatic TG levels, as measured by biochemical and histolopathological analyses. Our results indicate that the protective effects of SC are accompanied by a significant decrease in hepatic TG levels, thereby suggesting SC has the ability to prevent ethanol-induced fatty liver, by reducing hepatic TG and enzyme levels in alcoholic rats.

• Journal of Veterinary Clinics
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• v.4 no.1
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• pp.423-432
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• 1987

The present studies were undertaken in attempt to investigate the therapeutic effect of ethanol in dogs intoxicated with ethylene glycol Three dogs treated with ethylene glycol and other three dogs with ethylene glycol plus 20% ethanol orally were examined on clinical signs, endoscopic views, histopathological findings, and autopsy findings respectively. The results obtained were summarized as fellows : 1. The clinical sings and their severity of dogs intoxicated with ethylene glycol were time related and progressed from vomiting, depression, thirsty, tachycardia, tachypnea, convulsiot ataxia, melena, uremia and coma, but clinical signs of dogs treated with ethylene glycol and ethanol simultaneously only stowed vomiting and thirsty. 2. In the gastroscopic view, the dogs intoxicated with ethyelne glycol showed edematous, hyperemia, errosive and ulcerative lesions in the fundus and body area but the dogs treated with ethylene glycol and ethanol simultanously showed edematous and hyperemic lesions. 3. Oral treatment of ethanol with ethylene glycol simultaneously have reduced the signs of EG intoxications in dogs.