[长时间酒精中毒期间大鼠大脑和肝脏磷脂代谢几个方面的变化]。

Voprosy biokhimii mozga Pub Date : 1974-01-01
L T Amirkhanian, K G Karagezian
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引用次数: 0

摘要

大鼠大脑和肝脏的磷脂酸、总磷脂和单个磷脂和乙醇胺水平在酒精中毒40天后发生了相当大的变化,80天后甚至更大。脑内磷脂酸、总磷脂和单个磷脂含量升高,乙醇胺含量降低。在肝脏中,完全相反的变化发生,除了含有磷脂的肌醇,它在大脑和肝脏中都大大减少。磷脂合成第一阶段的研究表明,在酒精中毒40和80天期间,参与l - α -甘油磷酸代谢的酶(甘油激酶、甘油磷酸脱氢酶)的活性增加了数倍。这使得磷脂生成的主要产物l - α -甘油磷酸通过甘油激酶和甘油磷酸脱氢酶激活其形成而增加。尽管慢性酒精中毒期间肝脏中参与l - α -甘油磷酸酯代谢的酶活性显著增加,但其水平并未升高。这表明了l - α -甘油磷酸形成磷脂酸的激活和中性脂肪生物合成中磷脂酸的立即包涵。结果表明,慢性酒精中毒激活脑内磷脂的生物合成过程,加速其在肝脏中的分解,导致肝脏脂肪浸润。
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[Shifts in several aspects of phospholipid metabolism in the brain and liver of white rats during prolonged alcoholic intoxication].

Phosphatidic acid, total and individual phospholipids and ethanolamine levels of rat brain and liver are changed considerably following 40 and even more so after 80, days of alcohol intoxication. In brain the content of phosphatidic acid and total and individual phospholipids is increased and that of ethanolamine reduced. In liver exactly the opposite changes take place with the exception of inositol containing phospholipids, which are considerably reduced both in brain and liver. The study of the first stages of phospholipid synthesis showed that during 40 and 80 days of alcohol intoxication activity of enzymes participating in the metabolism of L-alpha-glycerophosphate (glycerokinase, glycerophosphate dehydrogenase) is increased several fold. This brings to the increase of L-alpha-glycerophosphate, the main product of phosphatidogenesis, through activation of its formation by glycerokinase and glycerophosphate dehydrogenase. Inspite of the fact that in liver activity of enzymes taking part in the metabolism of L-alpha-glycerophosphate is considerably increased during chronic alcohol intoxication its level is not raised. This indicates an activation of phosphatidic acid formation from L-alpha-glycerophosphate and the immediate inclusion of phosphatidic acid in the biosynthesis of neutral fats. The data obtained indicate that chronic alcohol intoxication activates biosynthetic processes of phospholipids in brain and accelerates their break down in liver, bringing to the fatty infiltration of liver.

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