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Ethanol 대사에 미치는 Catecholamine의 영향과 Quinone Reductase의 역할

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 Effect of catecholamines and potential role of quinone reductase on ethanol oxidation 
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[한글] 동물이 여러가지 긴장상황에 처하면 ethanol 대사율이 증가하며 이런 효과는 catecholamine의 작용으로 일어날 것이라고 알려져 있다. 그러나 catecholamine의 ethanol 대사 증가작용에 대한 기절은 아직 밝혀져 있지 않으며 또 ethanol 대사에 관여하리라고 생각되는 세포질 내의 quinone reductase의 작용과는 어떤 관계가 있는지에 대해서도 잘 모르고 있다. 이에 본 실험에서는 흰쥐의 간 관류법을 이용하여 α-아드레날린성 효현제 및 그 봉쇄제, quinone reductase의 촉진제인 BHA(butylated hydroxyanisole)와 억제제인 dicumarol 등 약물들이 ethanol 대사에 미치는 영향을 추구하여 다음과 같은 결론을 얻었다. 1. Epinephrine 주입으로 ethanol 대사는 증가하였고 주입을 멈추면 감소하였으며 이 과정은 몇차례 반복될 수 있었다. 2. Epinephrine과 phenylephrine주입으로 ethanol 대사는 각각 49%, 52%씩 증가되었으며 이는 phentolamine에 의해 봉쇄되었고 isoproterenol에 의해서는 ethanol 대사가 증가하지 않았다. 3. BHA 전처치군에서의 epinephrine 주입은 대조군에서 보다 ethanol 대사를 84% 증가시켰다. 4. Dicumarol은 ethanol 대사를 완전히 억제하였으며 epinephrine의 대사증가 효과도 완전히 억제하였다. 이상의 결과로 보아 catecholamine은 ethanol 대사를 증가시키며, 이는 간세포막의 아드레날린성 α-수용체 흥분 및 quinone reductase의 기질 제공에 의한 효과로 생각된다.
[영문] Under streesful conditions, the ethanol oxidation rate in the liver is known to be increased and this is thought to be mediated by the released catecholamines. However, the involved mechanism for this catecholamine dependent enhancement of ethanol oxidation rate is not well understood. The ethanol oxidation rate is controlled by the intra-cellular levels of NAD. When quinones are givens quinone reductase catalyzes the resupply of NAD. Thus, using isolated perfused rat livers, we have studied the effects of infusing either the α-adrenergic agonists or their antagonists, as well as the dicumarol, a strong inhibitor of quinone reductase, on the rates of ethanol oxidation. We have also used livers obtained from rats pretreated with BHA, a well known inducer of the quinone reductase activity. Results showed that the ethanol oxidation rate was increased during infusions with epinephrine and the rate returned to the basal level uppon stopping the epinephrine infusion. Also, infusions with either epinephrine or phenylephrine increased the ethanol oxidation rate by 49% and 52%, respectively, and these increases would be blocked by a prior infusion of phentolamine. Infusions with isoproterenol did not increase the oxidation rate at all. In the livers obtained from BHA-pretreated rats, the ethanol oxidation rate was increased by 84% upon infusions with epinephrine. Both in the normal and the BHA-fed rat livers, prior infusion with dicumarol, not only inhibited the ethanol oxidation, but also the enhancing effect of epinephrine. Based on these results, it appears that catecholamines could increase the ethanol oxidation rate by stimulating the α-adrenergic receptors on hepatocyte membranes. In addition, the metabolites of catecholamines could sense as the substrates of quinone reductase and increase the ethanol oxidation rate by resupplying NAD.
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