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Ethanol 중독 흰쥐에서 총담관결찰이 간의 Monoamine Oxidase 활성에 미치는 영향
정성광,곽춘식 ( Sung Kwang Chung,Chun Sik Kwak ) 생화학분자생물학회 1992 BMB Reports Vol.25 No.3
The activities of the hepatic monoamine oxidase (MAO) were studies when cholestasis was induced and acute ethanol intoxication developed, or cholestasis following chronic ethanol intoxication for manifestation of the biochemical background of alcohol intoxication in hepatobiliary disease. There were marked increases in the mitochondrial 5-hydroxytryptamine-MAO (5HT-MAO) and benzyla-mine-MAO (Benz-MAO) activities of the liver of the rats treated with chronic ethanol intoxication, and showed significant increase in the mitochondrial Benz-MAO after treatment with acute ethanol intoxication. When common bile duct was ligated in the rats, mitochondrial 5HT-MAO and Benz-MAO activities in the liver significantly decreased. When common bile duct was ligated after chronic ethanol intoxication and acute ethanol intoxication was done after common bile duct ligation, the activities of mitochondrial 5HT-MAO and Benz-MAO in the liver decreased more significantly than in the group only with ethanol intoxication was performed. However, the activities showed a higher degree on the same time points than the groups only with the common bile duct ligation. And microsomal 5HT-MAO and Benz-MAO activities in the liver showed significant increase when treated both with the chronic or the acute ethanol intoxication. According to the above results, the hepatic MAO seems to be an enzyme in which its activity increases in acute and chronic ethanol intoxication. And MAO in the liver is the enzyme with increased activities in ethanol intoxidation with cholestasis more than in cholestasis. The cause of the increase is the development of biosynthesis. Accordingly, these results will be the data supporting that alcoholic drink is enzymologically harmful in hepatobillary disease.
Ethanol중독 흰쥐에서 총담관결찰이 간의 Monoamine Oxidase 활성에 미치는 영향
정성광,곽춘식,Chung, Sung-Kwang,Kwak, Chun-Sik 생화학분자생물학회 1992 한국생화학회지 Vol.25 No.3
이 연구는 간담도 질환시 음주의 해로움에 대한 생화학적 배경의 일단을 밝히고자 시행한 실험으로서 급성 및 만성 주정 중독을 시킨 흰쥐에게 당즙울체를 야기시켜 간의 monoamine oxidase(MAO) 활성도를 측정한 것이다. 흰쥐에게 만성 주정 중독을 시켰을 때 간의 mitochondrial 5-hydroxytryptamine-MAO(5HT-MAO) 및 benzylamine-MAO(Benz-MAO)의 활성도는 각각 약 41% 및 약 42% 증가하였으며, 급성 주정 중독을 시켰을 때는 mitochondrial BenzMAO의 활성도가 약 35% 증가하였다. 총담관결찰로 담즙울체만 야기했을 때는 간의 mitochondrial 5HT-MAO의 활성도가 총담관결찰 후 3일에는 약 37%, 7일에는 약 38%, 14일에는 약 57% 감소하였으며, 또한 mitochondrial Benz-MAO의 활성도도 이와 같은 경향으로 감소하였다. 만성 주정 중독 후 총담관결찰로 담즙울체를 야기했을 때 및 총담관결찰 후 급성 주정 중독을 시켰을 때 간의 mitochondrial 5HT -MAO 및 Benz-MAO는 주정 중독을 시켰을 때 보다는 그 활성도가 낮았으나 담즙울체만 시켰을 때 보다는 그 활성도가 높았다. 그리고 microsomal MAO들은 주정 중독을 시켰을 때만 그 활성도가 약간 증가되었다. 이상 성적으로 보마 간의 MAO는 주정 중독시에 그 활성도가 증가되는 효소이며 또한 담즙울체시 주정 중독이 야기되면 이 효소의 활성도가 당즙울체만 있을 때 보다 증가되는 효소로 생각된다. 따라서 이 성적은 담즙울체로 간손상이 있을 때는 음주를 해서는 안된다는 것을 반영하는 자료라 할 수 있다. The activities of the hepatic monoamine oxidase (MAO) were studies when cholestasis was induced and acute ethanol intoxication developed, or cholestasis following chronic ethanol intoxication for manifestation of the biochemical background of alcohol intoxication in hepatobiliary disease. There were marked increases in the mitochondrial 5-hydroxytryptamine-MAO (5HT-MAO) and benzyla-mine-MAO (Benz-MAO) activities of the liver of the rats treated with chronic ethanol intoxication, and showed significant increase in the mitochondrial Benz-MAO after treatment with acute ethanol intoxication. When common bile duct was ligated in the rats, mitochondrial 5HT-MAO and Benz-MAO activities in the liver significantly decreased. When common bile duct was ligated after chronic ethanol intoxication and acute ethanol intoxication was done after common bile duct ligation, the activities of mitochondrial 5HT-MAO and Benz-MAO in the liver decreased more significantly than in the group only with ethanol intoxication was performed. However, the activities showed a higher degree on the same time points than the groups only with the common bile duct ligation. And microsomal 5HT-MAO and Benz-MAO activities in the liver showed significant increase when treated both with the chronic or the acute ethanol intoxication. According to the above results, the hepatic MAO seems to be an enzyme in which its activity increases in acute and chronic ethanol intoxication. And MAO in the liver is the enzyme with increased activities in ethanol intoxidation with cholestasis more than in cholestasis. The cause of the increase is the development of biosynthesis. Accordingly, these results will be the data supporting that alcoholic drink is enzymologically harmful in hepatobillary disease.