• Proceedings of the Ginseng society Conference
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• 1980.09a
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• pp.131-135
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• 1980

The influence of Panax ginseng on alcohol-induced hyperuricemia were observed. Changes of uric acid blood levels and hepatic xanthine oxidase activities were studied by means of treating alcohol intoxication with ginseng. It was found that a single dose (4 mg/Kg) of ginseng saponin administered intraperitoneally significantly inhibits the hepatic xanthine oxidase activities and decrease urate blood levels in ethanol-induced hyperuricemic mice. It was also observed that there were some difference in pharmacological aspect between Panax ginseng and allopurinol which is a potent inhibitor of xanthine oxidase from any sources.

• Biomolecules & Therapeutics
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• v.6 no.4
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• pp.345-350
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• 1998

The adverse effects of ethanol on cell proliferation have been described for a variety of tissues and cells. In the present study, we investigated whether chronic ethanol intoxication impairs the cell proliferation and DNA synthesis induced by oncogenic $H-ras^{V12}$ - and $v-K-ras^{V12}$-transformed cells. Ethanol treatment inhibited the cell proliferation and the DNA synthesis of control parental fibroblasts in a time- and dose-dependent manner. In contrast, ethanol did not suppress the proliferation of either oncogenic $H-ras^{V12}$ - or $v-K-ras^{V12}$ -transformed fibroblasts. Microinjection of oncogenic $H-Ras^{V12}$ protein induces DNA synthesis and ethanol treatment did not interfere with the DNA synthesis. The antiproliferative toxicity of ethanol was rescued by antioxidants, such as N-acetylcysteine and 4-methlpyrazole. These results indicate that the antiproliferative action site of ethanol toxicity lies upstream or is independent of Ras and ethanol exerts its toxicity through a free radical formation.

• Journal of The Korean Society of Clinical Toxicology
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• v.10 no.1
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• pp.15-21
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• 2012

Purpose: Toxic alcohols are responsible for accidental and suicide motivated poisonings, resulting in death or permanent sequelae for the afflicted patients. Major therapeutic modalities in these cases include treatment with alcohol dehydrogenase inhibitors and extracorporeal elimination. There have been a number of case reports of toxic alcohol intoxication in Korea. The purpose of this study was to review the clinical characteristics of patients suffering toxic alcohol intoxication. Methods: We retrospectively reviewed the medical records of patients who presented with toxic alcohol intoxication at 8 emergency departments (ED) from Jun 2005 to Nov 2011. Patients who ingested methanol, isopropyl alcohol, ethylene glycol, and other alcohols except ethanol, were included in this study. The clinical characteristics of these patients were analyzed to include anion and osmolar gap, and estimated concentration of alcohol in the body. Results: During the study period, 21 patients were identified who had ingested toxic alcohol (methanol; 12 patients, ethylene glycol; 9 patients). At ED arrival, the mean anion gap was $18.7{\pm}6.9$ and the osmolar gap was elevated in 13 patients. Oral and IV ethanol were administrated to 11 patients in order to inhibit alcohol dehydrogenase. Extracorporeal elimination procedures such as hemodialysis were performed in 9 patients. There were no fatalities, but the one patient suffered permanent blindness. Conclusion: This study found that ethylene glycol and methanol were the substances ingested which produced toxic alcohol intoxication. The patients presented with high anion gap metabolic acidosis and were typically treated with oral ethanol and hemodialysis.

• BMB Reports
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• v.42 no.8
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• pp.482-485
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• 2009

The effect of water dropwort (Oenanthe javanica DC) extract in eliminating ethanol was evaluated in New Zealand white rabbit and ICR mice. When a hot-water extract of water dropwort extract and ethanol was injected into New Zealand white rabbit, the plasma ethanol level was rapidly reduced, similar to metadoxine treatment. Specifically, the n-butanol fraction of hot-water extract was the strongest in eliminating plasma alcohol in ICR mice. When ethanol was orally ingested, administration of the hot-water extract eliminated up to 44% of the plasma ethanol in mice while the n-butanol fraction eliminated around 70%. Alcohol removal behaved in a dose-dependent manner in response to 50-200 mg/kg of n-butanol fraction. These data show O. javanica extract is effective in overcoming alcohol intoxication by the accelerating ethanol metabolism.

• Journal of the Korean Society of Food Science and Nutrition
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• v.25 no.1
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• pp.46-52
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• 1996

The present study was undertaken to investigate the effect of the water extract of the puffer fish Fugu xanthopterus(FXH) on the alcohol induced hyperuricemia. The normal group and the FXH treated group showed no sigbificant changes in the levels of blood uric acid but, the blood uric acid significantly decreased in the FXh treated rats with 100mg/kg for two weeks compared to the ethanol treated group. There were no significant changes in the activities of uricase, adenosine deaminase, guanine deaminase, and purine uncleoside phosphorylase, among all the test group. But the activitis of liver xanthine oxidase were recovered to the normal level in ethanol +FXH treated group comparing to the ethanol treated group. Furthermore, ethanol+FXH treated rats showed the similar pattern in the levels of blood uric acid and urinary allantoin with normal group. These results indicate that the decreased blood uric acid by the FXH treatment of the alcohol induced hyperuricemia rats may result from decreased activity of hepatic xanthine oxidase.

• YAKHAK HOEJI
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• v.28 no.1
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• pp.49-51
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• 1984

After pretreatment with ginseng followed by induction of acute intoxication of alcohol, the activities of alcohol dehydrogenase (ADH), microsomal ethanol-oxidizing system (MEOS) and aldehyde dehydrogenase(Ald DH) increased respectively compared to the groups treated with alcohol alone. In case that ginseng was given to rats fed with 5% alcohol instead of water for 60 days, the activities of ADH and MEOS increased compared to the groups treated. On the contrary, the activity of Ald DH in mitochondrial fraction decreased to an extent of about 35% in chronic alcoholism, but after pretreatment of ginseng the activity was restored to the control level. On the other hand, the catalase activity was not significantly affected by either treatment. Ginseng butanol fraction significantly increased the serum isocitrate dehydrogenase activity which is inhibited by alcohol-treated in rat. Alcohol-induced lactate dehydrogenase activity was decreased to control level in liver by ginseng treatment. And the serum level of lactic acid also decreased by ginseng treatment in alcohol-intoxicated rat. Ginseng butanol fraction markedly decreased the xanthine oxidase activity in the ethanol-treated rat liver. It was also observed that ginseng reduced the blood concentration of uric acid on experimentally reduced hyperuricemia by alcohol treatment. Uricase activity was not affected by either treatment. Ginseng butanol fraction decreased the hepatic aniline hydroxylase activity which was induced by alcohol-treated rat. These results suggest that the treatment with ginseng can be promoted the recovery from alcohol intoxication and some therapeutic effect on alcoholinduced metabolic disease.

• The Korean Journal of Physiology and Pharmacology
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• v.10 no.6
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• pp.303-307
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• 2006

The effects of ethanol on corticostriatal synaptic transmission were examined, using extracellular recording and analysis of population spike amplitudes in rat brain slices, to study how acute ethanol intoxication impairs striatal function. Ethanol caused a decrease in population spike amplitudes in a dose dependent manner ($50{\sim}200mM$). Pretreatment with picrotoxin, a ${\gamma}-amino$ butyric acid $(GABA)_{A}$ receptor antagonist, increased the population spikes but ethanol (100 mM) was still effective in decreasing the population spikes under this condition. In the presence of $_{(DL)}-2-amino-5-phosphonovaleric$ acid (APV), N-methyl-D-aspartate (NMDA) receptor antagonist, the inhibitory action of ethanol on population spikes was not shown. These results suggest that ethanol inhibits the glutamatergic corticostriatal synaptic transmission through blockade of NMDA receptors.

• The Journal of Internal Korean Medicine
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• v.18 no.1
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• pp.15-25
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• 1997

Chunggansan was tested for the effects on detoxication mechanism of alcohol. Chunggansan was treated firstly into samples, and then ethanol intoxicated animal models were set with them. The administration of Chunggansan to the rats increased proportionally in alcohol dehydrogenase activities in liver in relation to the level of concentration and days of treatment. Especially, the alcohol dehydrogenase was the most active when the concentration of extract was 200mg/kg and it was 7th day. The enzyme activities of alcohol dehydrogenase and aldehyde dehydrogenase in liver highly increased in Chunggansan pre-medicating group compared to that of ethanol treated group. Also, the blood ethanol concentration in rats was considerably decreased. In conclusion, Chunggansan recovers the damage of liver due to acute alcohol intoxication by the increased enzyme activities of alcohol dehydrogenase and aldehyde dehydrogenase.

• Natural Product Sciences
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• v.21 no.1
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• pp.54-58
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• 2015

The protective effect of EtOAc fraction of Limonium tetragonum extract (EALT) against alcohol-induced hepatotoxicity was assessed following acute ethanol intoxication in Spraque-Dawley rats. EALT (200 mg/kg p.o.) was administrated once before alcohol intake (8 g/kg, p.o.). Blood ethanol concentration, and the activities of alcohol metabolic enzymes, alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) in the liver were measured. Also, the formation of malondialdehyde (MDA) and the activities of antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GSH-px), catalase were determined after acute alcohol exposure. Pretreatment of rats received ethanol with EALT significantly decreased blood ethanol concentration and elevated the activities of ADH and ALDH in liver. The increased MDA level was decreased, and the reduced activities of SOD, GSH-px and catalase were markedly preserved by the treatment with EALT. This study suggests that EALT prevent hepatic injury induced by acute alcohol which is likely related to its modulation on the alcohol metabolism and antioxidant enzymes activities.

• Journal of the Korean Society of Food Science and Nutrition
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• v.45 no.5
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• pp.625-633
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• 2016

Allium hookeri is known as a healthy food since it contains larger amounts of sulfur compounds than commonly known alliaceous plants. The antioxidant and anti-inflammatory effects of A. hookeri were compared between two types of extracts, $80^{\circ}C$ water and 95% ethanol extracts of A. hookeri roots. A. hookeri root 95% ethanol extracts displayed superior total polyphenol content, antioxidant activity [1,1-diphenyl-2-picrylhydrazyl and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonate) radical scavenging activity], and anti-inflammation activity than those of water extracts (P<0.05). We studied the effects of A. hookeri root 95% ethanol extracts (95% ethanol extracts group: AHE) on acute alcohol-induced intoxication in mice. AHE [250, 500, and 1,000 mg/kg body weight (BW)/d] was orally administered to the study group once a day for 1 week. On the last day of AHE treatment, 40% ethanol (10 mL/kg BW) was orally administered to induce acute liver injury. The blood alcohol concentration of mice treated with AHE was significantly lower compared to the control group (P<0.05). The levels of hepatic aspartate aminotransferase and alanine aminotransferase were lower in the AHE-treated group than the control group (P<0.05). The RT-PCR results for alcohol dehydrogenase and aldehyde dehydrogenase measured based on mRNA in liver tissues showed that enzyme activities were higher in the AHE-treated group than in the control group at a low blood alcohol concentration.