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[长期酒精中毒期间大白鼠脑和肝脏中磷脂代谢若干方面的变化]

[Shifts in several aspects of phospholipid metabolism in the brain and liver of white rats during prolonged alcoholic intoxication].

作者信息

Amirkhanian L T, Karagezian K G

出版信息

Vopr Biokhim Mozga. 1974;9:43-63.

PMID:4378019
Abstract

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.

摘要

大鼠脑和肝脏中的总磷脂酸、各磷脂及乙醇胺水平在酒精中毒40天后会发生显著变化,80天后变化更为明显。在脑中,磷脂酸、总磷脂及各磷脂含量增加,乙醇胺含量降低。在肝脏中,除含肌醇磷脂外,情况正好相反,含肌醇磷脂在脑和肝脏中均显著减少。对磷脂合成初期阶段的研究表明,在酒精中毒40天及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)活性增加了数倍。这通过甘油激酶和甘油磷酸脱氢酶对其形成过程的激活,导致磷脂生成的主要产物L-α-甘油磷酸增加。尽管在慢性酒精中毒期间,肝脏中参与L-α-甘油磷酸代谢的酶活性显著增加,但其水平并未升高。这表明从L-α-甘油磷酸形成磷脂酸的过程被激活,且磷脂酸直接参与中性脂肪的生物合成。所获数据表明,慢性酒精中毒激活了脑中磷脂的生物合成过程,并加速了肝脏中磷脂的分解,导致肝脏脂肪浸润。

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