Effect of an Acute Ethanol Administration of Rat Liver Alcohol Dehydrogenase

Kim, Moon-Hee,Kwon, Oh-Hyep,Park, Chan-Koo 생화학분자생물학회 1993 한국생화학회지 Vol.26 No.5

Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are the main enzymes responsible for ethanol metabolism in the liver. In the present study, effect of an acute administration of ethanol on activities of hepatic ADH and ALDH was investigated in starved rats fed ethanol at a dose of 3 g/kg body weight (bw). ADH and ALDH activities were measured at 1, 2, 4, and 6 h after the ethanol treatment. The acute administration of ethanol caused an inhibition of cytosolic ADH enzyme in the liver at 1 h, and this inhibition remained until 6 h after the ethanol intake. In contrast to ADH, mitochondrial ALDH activity was not affected by ethanol at early times. However, it was slightly reduced at 6 h after ethanol intake. Factors that may regulate ADH activity in ethanol-fed rats were examined. ADH activity was measured in the presence of various concentrations of ethanol or acetaldehyde in assay mixture containing hepatic cytosolic fraction prepared from rats fed a chow diet, in order to determine whether the substrate (ethanol) or the product (acetaldehyde) of this enzyme inhibits ADH. Both ethanol and acetaldehyde inhibited ADH enzyme at high concentrations. However, ADH inhibition by acetaldehyde disappeared after dialysis. An ethanol disappearance curve was constructed to determine the elimination rate constant for ethanol, $k^{el}$, and the blood lactate/pyruvate (L/P) ratio was measured to estimate the redox state in the liver during ethanol metabolism. The $k^{el}$, value was calculated to be 0.092/min and the blood L/P ratio increased 16.6% by ethanol treatment. The combined data suggest that the decrease in hepatic ADH activity observed in rats fed ethanol is probably due to an inhibition caused by local, high concentrations of ethanol and acetaldehyde in the cytosol of the liver and that the inhibition of ADH by acetaldehyde is reversible.

Effect of an Acute Ethanol Administration of Rat Liver Alcohol Dehydrogenase

Moon Hee Kim,Oh Hyep Kwon,Chan Koo Park 생화학분자생물학회 1993 BMB Reports Vol.26 No.5

Alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) are the main enzymes responsible for ethanol metabolism in the liver. In the present study, effect of an acute administration of ethanol on activities of hepatic ADH and ALDH was investigated in starved rats fed ethanol at a dose of 3 g/㎏ body weight (bw). ADH and ALDH activities were measured at 1, 2, 4, and 6 h after the ethanol treatment. The acute administration of ethanol caused an inhibition of cytosolic ADH enzyme in the liver at 1 h, and this inhibition remained until 6 h after the ethanol intake. In contrast to ADH, mitochondrial ALDH activity was not affected by ethanol at early times. However, it was slightly reduced at 6 h after ethanol intake. Factors that may regulate ADH activity in ethanol-fed rats were examined. ADH activity was measured in the presence of various concentrations of ethanol or acetaldehyde in assay mixture containing hepatic cytosolic fraction prepared from rats fed a chow diet, in order to determine whether the substrate (ethanol) or the product (acetaldehyde) of this enzyme inhibits ADH. Both ethanol and acetaldehyde inhibited ADH enzyme at high concentrations. However, ADH inhibition by acetaldehyde disappeared after dialysis. An ethanol disappearance curve was constructed to determine the elimination rate constant for ethanol, k^(el), and the blood lactate/pyruvate (L/P) ratio was measured to estimate the redox state in the liver during ethanol metabolism. The k^(el), value was calculated to be 0.092/min and the blood L/P ratio increased 16.6% by ethanol treatment. The combined data suggest that the decrease in hepatic ADH activity observed in rats fed ethanol is probably due to an inhibition caused by local, high concentrations of ethanol and acetaldehyde in the cytosol of the liver and that the inhibition of ADH by acetaldehyde is reversible.

Relationship of Hepatic Triglyceride Accumulation by Ethanol to Activities of Lipogenic Enzymes in Rat Liver

김문희,권오협,Kim, Moon-Hee,Kwon, Oh-Hyep 생화학분자생물학회 1992 한국생화학회지 Vol.25 No.6

에탄올은 간에서 중성지방 축적을 일으킨다. 쥐 간 glucose-6-phosphate dehydrogenase(G6PD)와 6-phosphogluconate dehydrogenase(6PGD)는 lipogenic enzymes이며, 이들의 활성은 간에서 지방산 합성속도와 비례한다. 절식한 쥐에 에탄올을 체중 kg당 3g을 먹인 후 간 G6PD와 6PGD의 활성과 간 중성지방 level을 측정함으로써, 간 중성지방 level과 관련하여 에탄올의 지방산 합성에 미치는 영향을 고찰하였다. 에탄올의 급성 투여는 에탄올 처리 후 6시간 동안 간 중성지방 level을 증가시켰으며, 투여 후 4시간에는 2.2배의 증가를 나타내었다. 그 밖에 혈청 중성지방 level에 대한 time course를 수행하였다. 혈청 중성지방 level의 변화 크기와 패턴은 간 중성지방 level의 경우와 유사하였다. 에탄올의 일회 투여는 간에서 중성지방 축척을 일으키는 조건하에서 lipogenic enzyme의 활성에 아무런 영향을 미치지 않았다. 결론적으로, 위 결과들은 에탄올 섭취로 인한 간 중성지방 level의 증가가 간에서 지방산 합성의 증가에 기인하지 않는다는 것을 나타내 주고 있다. Ethanol causes the accumulation of triglycerides in the liver. Rat liver glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD) are lipogenic enzymes whose activities are positively correlated with the rate of hepatic fatty acid synthesis. The effect of ethanol on fatty acid synthesis in relation to levels of triglycerides in the liver was investigated by assessing activities of hepatic G6PD and 6PGD and levels of hepatic triglycerides in starved rats fed ethanol at a dose of 3g/kg body weight (bw). The acute administration of ethanol caused an increase in triglyceride levels in the liver during 6 h period after the treatment, in which, ethanol caused a 2.2-fold increase in hepatic triglyceride level at 4 h after the ethanol administration. In addition, the time course of serum triglyceride levels was determined. The magnitude and the pattern of changes in serum triglyceride levels in the time course were similar to those in liver triglyceride levels. A single dose of ethanol had no effect at all on activities of lipogenic enzymes G6PD and 6PGD under the condition that caused the triglyceride accumulation in the liver. Taken together, these results suggest that the increase in hepatic triglyceride levels associated with the ethanol ingestion is not likely due to the increase in fatty acid synthesis in the liver.

쥐 간에서 에탄올에 의한 간 중성지방 축적과 Lipogenic Enzyme 활성과의 관계

김문희,권오협 ( Moon Hee Kim,Oh Hyep Kwon ) 생화학분자생물학회 1992 BMB Reports Vol.25 No.6

Ethanol causes the accumulation of triglycerides in the liver. Rat liver glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase (6PGD) are lipogenic enzymes whose activities are positively correlated with the rate of hepatic fatty acid synthesis. The effect of ethanol on fatty acid synthesis in relation to levels of triglycerides in the liver was investigated by assessing activities of hepatic G6PD and 6PGD and levels of hepatic triglycerides in starved rats fed ethanol at a dose of 3 g/㎏ body weight (bw). The acute administration of ethanol caused an increase in triglyceride levels in the liver during 6 h period after the treatment, in which, ethanol caused a 2.2-fold increase in hepatic triglyceride level at 4 h after the ethanol administration. In addition, the time course of serum triglyceride levels was determined. The magnitude and the pattern of changes in serum triglyceride levels in the time course were similar to those in liver triglyceride levels. A single dose of ethanol had no effect at all on activities of lipogenic enzymes G6PD and 6PGD under the condition that caused the triglyceride accumulation in the liver. Taken together, these results suggest that the increase in hepatic triglyceride levels associated with the ethanol ingestion is not likely due to the increase in fatty acid synthesis in the liver.

급성 알콜 투여 흰쥐에서 녹두 함유 복합생약제제의 간 중성지방 축적억제 및 알콜대사 촉진효과

김문희(Moon Hee Kim),권오협(Oh Hyep Kwon),박찬구(Chan Koo Park) 대한약학회 1996 약학회지 Vol.40 No.1

An ethanol administration causes hepatic triglyceride accumulation in rats. To assess whether the herbal extract containing Phaseoli radiati semen(herbal extract) inhibits the triglyceride accumulation in the liver, we determined the hepatic triglyceiide levels in rats fed ethanol and the herbal extract. In addition, the blood ethanol concentrations and the activities of hepatic alcohol dehydrogenase(ADH) and aldehyde dehydrogenase(ALDH) were measured to determine the effects of the herbal extract on alcohol metabolism in rats. The administration of the herbal extract markedly reduced the triglyceride levels elevated by ethanol in the liver as well as in the serum. The herbal extract remarkably lowered blood ethanol concentrations in a dose-dependent manner. The ADH activities decreased by ethanol were recovered to the normal level by the herbal extract treatment. Moreover, the ALDH activities slightly decreased by ethanol increased beyond the normal level by the herbal extract treatment. We conclude that the herbal extract inhibits the hepatic triglyceride accumulation and stimulates alcohol metabolism by preventing ADH and ALDH from inhbition by the ethanol administration in the rat liver.

항체가 건조상태로 고정화된 면역진단카트의 안정화와 Shelf-Life 결정

이창우(Chang-Woo Lee),조정환(Joung-Hwan Cho),육순학(Soon-Hack Yook),권오협(Oh-Hyep Kwon),박영남(Yeong-Nam Park),백세환(Se-Hwan Pack) 한국생물공학회 1998 KSBB Journal Vol.13 No.5